18EMAWF

north west S E M I N A R S
Continuing education for the medical professional
Current Topics in Emergency Medicine

Whitefish, Montana
August 13 - 17, 2018
You must sign in every day you attend in order to receive credit.
Please bring this handout with you to the meeting.
To download lecture notes visit: http://nws.ac/18EMAWF

Northwest Seminars in joint providership with the
A.Webb Roberts Center for Continuing Medical Education of Baylor Scott & White Health
CURRENT TOPICS IN EMERGENCY MEDICINE
Whitefish, Montana
August 13 - 17, 2018
Table of Contents
Schedule��3
Faculty��4
Speaker Disclosure Information��5
Objectives��6
Hidden Killers: Plain Film Findings You Can’t Afford to Miss��8
Emergency Medicine at 29,035 ft: High Altitude Medicine��23
Emergency GI Controversies��42
Treatment of Submassive PE: Full Dose, Half Dose, or No Dose Lytics��51
Morbidity and Mortality: Life-Threatening Mimics of Mechanical Low Back Pain��64
Morbidity and Mortality: CNS Emergencies��65
Morbidity and Mortality: Infectious Disease Emergencies��73
Resuscitation Sequence Intubation��84
Novel Use of Bedside Ultrasound��92
Two for the Price of One: Trauma in Pregnancy��105
Conquering the World of Medical Education With FOAMed��116
All Bleeding Stops Sometimes: Hemorrhage Control in Trauma��123
The Zebras: Unique Presentations and Stranger Diagnoses��139
Emergent Evaluation and Treatment of Acute Delirium��151
Emergent Evaluation and Treatment of the Acute Red Eye��157
Reflections on a Combat Sabbatical: Lessons Learned in War��172
Morbidity and Mortality: Deadly Endocrinologic Disorders��192
Morbidity and Mortality: The Calm, Confused Patient��193
Beyond ACLS��194
DKA Myths��203
The material in this syllabus represents the opinion of the speaker and does not constitute endorsement or
recommendation of this information by Northwest Anesthesia Seminars, and A. Webb Roberts Center for
Continuing Education of Baylor Scott & White Health, and makes no guarantee, nor accepts liability for
omission or errors in printing. No recording or pictures allowed during the meeting.
Whitefish, Montana
August 13 - 17, 2018
SCHEDULE
Monday, August 13
Table of Contents
Participants must sign in as noted below for each day attending in order to receive credit.
0700 Registration - Mandatory Sign In - Continental Breakfast

Schedule
0725 ...................................................................................................................................................................................3
Welcome NWS Staff
0730 Hidden Killers: Plain Film Findings You Can’t Afford to Miss S.Mehta
Faculty ......................................................................................................................................................................................4
0830 Emergency Medicine at 29,035 ft: High Altitude Medicine S.Mehta
Speaker Disclosure Information ...........................................................................................................................................5
0930 Break
0945 Emergency
Objectives GI Controversies S.Rezaie
................................................................................................................................................................................6
1045 Treatment of Submassive PE: Full Dose, Half Dose, or No Dose Lytics S.Rezaie
Hidden Killers: Plain Film Findings You Can’t Afford to Miss ........................................................................................8
1145 Morbidity and Mortality: Life-Threatening Mimics of Mechanical Low Back Pain J.Williams
Emergency Medicine at 29,035 ft: High Altitude Medicine ...........................................................................................23
1245 Adjourn
Emergency GI Controversies ..............................................................................................................................................42
Tuesday, August 14
Treatment
0700 of Submassive
Registration - Mandatory PE: FullSignDose, Half Dose, Breakfast
In - Continental or No Dose Lytics .......................................................................51
0730 Morbidity
Morbidity and Mortality:
and Mortality: Life-Th CNS Emergencies
reatening Mimics of Mechanical Low Back Pain ...................................................64 J.Williams
0830 Morbidity
Morbidity and Mortality:
and Mortality: CNSInfectious
Emergencies Disease Emergencies J.Williams
....................................................................................................................65
0930 Break
Morbidity
0945 and Mortality:
Resuscitation Sequence Infectious
Intubation Disease
Emergencies ............................................................................................73
S.Rezaie
1045 Novel Use of Bedside Ultrasound
Resuscitation Sequence Intubation ....................................................................................................................................84 S.Mehta
1145 Two for the Price of One: Trauma in Pregnancy S.Mehta
Novel Use of Bedside Ultrasound ......................................................................................................................................92
1245 Adjourn
Two for the Price of One: Trauma in Pregnancy............................................................................................................105
Wednesday,
Conquering the August
World15 of –Medical
Day Open Education With FOAMed .....................................................................................116
All BleedingAugust
Thursday, Stops Sometimes:
16 Hemorrhage Control in Trauma ................................................................................123
0700 Registration
The Zebras: Unique - Mandatory
Presentations Signand In -Stranger
Continental Breakfast
Diagnoses .........................................................................................139
0730 Conquering the World of Medical Education With FOAMed S.Rezaie
Emergent Evaluation and Treatment of Acute Delirium ..............................................................................................151
0830 All Bleeding Stops Sometimes: Hemorrhage Control in Trauma S.Mehta
Emergent Evaluation and Treatment of the Acute Red Eye..........................................................................................157
0930 Break
0945 The Zebras:
Reflections on a CombatUnique Presentations
Sabbatical: Lessons and Stranger
Learned Diagnoses S.Mehta
in War .....................................................................................172
1045 Emergent Evaluation and Treatment of Acute Delirium J.Williams
Morbidity
1145 Emergentand Mortality:
EvaluationDeadly and TreatmentEndocrinologic
of the Acute Disorders
Red Eye .......................................................................................192
J.Williams
1245 Adjourn
Morbidity and Mortality: The Calm, Confused Patient ................................................................................................193
Beyond ACLS ......................................................................................................................................................................194
Friday, August 17
DKA Myths
0700 .........................................................................................................................................................................203
Registration - Mandatory Sign In - Continental Breakfast
0730 Reflections on a Combat Sabbatical: Lessons Learned in War S.Mehta
0830 Morbidity and Mortality: Deadly Endocrinologic Disorders J.Williams
0930 Break
0945 Morbidity and Mortality: The Calm, Confused Patient J.Williams
1045 Beyond ACLS S.Rezaie
1145 DKA Myths S.Rezaie
1245 Adjourn
The material in this syllabus represents the opinion of the speaker and does not constitute endorsement (20 CME / 20 CEC) or
Continuing Education of Baylor Refreshments Scottprovided during the
& White program are
Health, and intended
makes for participants
no guarantee, only. nor accepts liability for
Please note that we do not allow children or non-registered guests to sit in on the lectures.
omission or personal
Do not leave errors itemsin printing.
unattended No in therecording
meeting room;or thepictures allowed during are
hotel and NWAS/NWS/NWWT theNOT meeting.
responsible for any lost or stolen items.
3
FACULTY
Sumeru Ghanshyam Mehta, MD

Staff Physician, Greater San Antonio Emergency Physicians
Board of Directors, Greater San Antonio Emergency Physicians
Clinical Assistant Professor, University of Texas Health Science Center at San Antonio
Department of Surgery, Division of Emergency Medicine
Assistant Professor, Uniformed Services University of the Health Sciences
Department of Military and Emergency Medicine
San Antonio, Texas
Program Coordinator
Salim R. Rezaie, MD
Staff Physician, Greater San Antonio Emergency Physicians
Emergency Medicine/Internal Medicine
Creator/Founder of REBEL EM (www.rebelem.com)
Co-Creator/Founder of The Teaching Institute (www.flippingmeded.com)
San Antonio, Texas
Justin Barrett Williams, MD, FACEP

Assistant Clinical Professor, Surgery and Emergency Medicine
Interim Chief, Division of Emergency Medicine
Department of Surgery
University of Texas School of Medicine San Antonio
San Antonio, Texas
Northwest Seminars
Paul Hilliard, CRNA, President
Sandy Paxton, Onsite Coordinator
Pasco, Washington
4
SPEAKER DISCLOSURE INFORMATION
As a provider accredited by the ACCME, it is the policy of the A. Webb Roberts Center for Continuing Medical
Education of Baylor Scott & White Health to require the disclosure of the existence of any significant financial
interest or any other relationship a faculty member or a sponsor has with the manufacturer(s) of any commercial
product(s). The presenting faculty reported the following:
north west
Sumeru Mehta
Salim Rezaie
None disclosed
SNone
E disclosed
M I N A R S
Justin Williams None disclosed
Continuing education for the medical professional
NOTICE: The intent of this policy is not to prevent a speaker with a potential conflict of interest from making a
presentation. It is merely intended that any potential conflict should be identified openly so that the listeners may
Current Topics in Emergency Medicine
form their own judgments about the presentation with the full disclosure of the facts. It remains for the audience
to determine whether the speaker’s outside interests may reflect a possible bias in either the exposition or the
conclusions presented.Whitefish, Montana
august 13 - 17, 2018
You must sign in every day you attend in order to receive credit.
Please bring this handout with you to the meeting.
SYLLABUS DOWNLOAD LINK

If you would like to download the lecture notes (PDF format), please visit the following link:
To download lecture notes visit: http://nws.ac/18EMAWF

5
Whitefish, Montana
August 13 - 17, 2018
OBJECTIVES
Table of Contents
Evaluate your personal level of achievement of each objective by circling:
1 2 3 4 5
Poor Fair Adequate Good Excellent
Schedule ...................................................................................................................................................................................3
1) Hidden Killers: Plain Film Findings You Can't Afford to Miss
Faculty ......................................................................................................................................................................................4
• Review plain film radiologic findings that can lead to morbidity and mortality 1 2 3 4 5
Speaker Disclosure Information ...........................................................................................................................................5
• Review steps you can take to reduce your chance of missing critical radiologic findings 1 2 3 4 5
Objectives ................................................................................................................................................................................6
2) Emergency Medicine at 29,035 ft: High Altitude Medicine
Hidden Killers: Plain Film Findings You Can’t Afford to Miss ........................................................................................8
• Describe the pathophysiology of AMS, HAPE and HACE 1 2 3 4 5
Emergency
• Review caseMedicine at 29,035 ft
studies highlighting : High
the distinctAltitude
differences Medicine
between the ...........................................................................................23
three illnesses 1 2 3 4 5
• Review evidence-based medicine for the appropriate management of the three illnesses 1 2
Emergency GI Controversies ..............................................................................................................................................42 3 4 5
Treatment of Submassive PE: Full Dose, Half Dose, or No Dose Lytics .......................................................................51
3) Emergency GI Controversies
Morbidity
• Discussand Mortality:
the role Life-Th
of nasogastric lavagereatening
in upper GI Mimics of Mechanical Low Back Pain ...................................................64
bleed (UGIB) 1 2 3 4 5
• Review the evidence for timing of endoscopy in UGIB
Morbidity and Mortality: CNS Emergencies ....................................................................................................................651 2 3 4 5
• Discuss the role of glucagon in esophageal foreign body and review the role of PPIs in UGIB 1 2 3 4 5
Morbidity and Mortality: Infectious Disease Emergencies ............................................................................................73
Resuscitation
4) Treatment ofSequence
SubmassiveIntubation
PE: Full Dose, ....................................................................................................................................84
Half Dose, or No Dose Lytics
• Review
Novel Use oftheBedside
treatmentUltrasound
options for submassive PE 1 2 3 4 5
......................................................................................................................................92
• Discuss the best treatment options for submassive PE 1 2 3 4 5
Two for the Price of One: Trauma in Pregnancy............................................................................................................105
Conquering
5) Morbidity and theMortality:
World ofLife-Threatening
Medical Education Mimics With FOAMed
of Mechanical Low.....................................................................................116
Back Pain
• Discuss several uncommon but deadly forms of mimics of mechanical low back pain 1 2 3 4 5
All Bleeding Stops Sometimes: Hemorrhage Control in Trauma ................................................................................123
• Describe the clinical presentations of mimics of mechanical low back pain and their immediate 1 2 3 4 5
The Zebras: Unique
management priorities Presentations and Stranger Diagnoses .........................................................................................139
Emergent Evaluation and Treatment of Acute Delirium ..............................................................................................151
6) Morbidity and Mortality: CNS Emergencies
Emergent Evaluation and Treatment of the Acute Red Eye..........................................................................................157
• Discuss several uncommon but deadly forms of cerebrovascular emergencies 1 2 3 4 5
Refl•ections
Describeon theaclinical
Combat Sabbatical:
presentation Lessons
of cerebellar Learned
infarction andin itsWar .....................................................................................172
immediate management priorities 1 2 3 4 5
Morbidity and Mortality: Deadly Endocrinologic Disorders .......................................................................................192
7) Morbidity and Mortality: Infectious Disease Emergencies
Morbidity and Mortality: The Calm, Confused Patient ................................................................................................193
• Describe several uncommon but deadly forms of occult infectious disease emergencies 1 2 3 4 5
Beyond ACLS
• Describe ......................................................................................................................................................................194
a strategy for screening for occult sepsis 1 2 3 4 5
DKA Myths .........................................................................................................................................................................203
8) Resuscitation Sequence Intubation
• Discuss the HOp Killers peri-Intubation (hypotension, hypoxemia, and metabolic acidosis) 1 2 3 4 5
• Describe overcoming lung shunt physiology 1 2 3 4 5
• Use the ventilator to avoid worsening metabolic acidosis 1 2 3 4 5
9) Novel Use of Bedside Ultrasound

• Use the bedside US for novel diagnosis and procedures such as retinal detachment, pneumothorax and 1 2 3 4 5
The material in this syllabus represents the opinion of the speaker and does not constitute
lumbar puncture
endorsement or
Continuing
10) Two for theEducation
Price of One:of Baylor
Trauma Scott & White Health, and makes no guarantee, nor accepts liability for
in Pregnancy
omission or errors in printing. No recording
• Explain maternal and fetal hemodynamics and their or pictures
value allowed
in trauma during the meeting.
assessment 1 2 3 4 5
• Identify drugs which are indicated in pregnancy in trauma 1 2 3 4 5
• Discuss the indications/contraindications for emergent peripartum c-section 1 2 3 4 5
6
11) Conquering the World of Medical Education With FOAMed
• Discuss the value of FOAM for medical education 1 2 3 4 5
• Employ FOAM to attain personal learning networks 1 2 3 4 5
• Describe how to use FOAM 1 2 3 4 5
12) All Bleeding Stops Sometimes: Hemorrhage Control in Trauma

• Describe the different classifications of hemorrhage 1 2 3 4 5
• Discuss the new paradigm of hemorrhage control 1 2 3 4 5
• Identify new technology and new class of drugs that are changing the way we control hemorrhage in 1 2 3 4 5
trauma
13) The Zebras: Unique Presentations and Stranger Diagnoses

• Review cases with unusual presentations of common diagnoses 1 2 3 4 5
• Review clinical cases which presented with common symptoms but resulted in unusual diagnosis 1 2 3 4 5
14) Emergent Evaluation and Treatment of Acute Delirium

• Define delirium and describe its three forms 1 2 3 4 5
• Relate the differences between psychosis and delirium 1 2 3 4 5
• Formulate an evaluation process for diagnosing underlying medical causes of acute delirium 1 2 3 4 5
• Compose an initial treatment strategy for acute delirium in the emergency setting 1 2 3 4 5
15) Emergent Evaluation and Treatment of the Acute Red Eye

• Provide the differential diagnosis for emergencies causing an acute red eye 1 2 3 4 5
• Review specific categories and examples of emergencies causing an acute red eye 1 2 3 4 5
• Discuss initial management of emergencies causing an acute red eye 1 2 3 4 5
16) Reflections on a Combat Sabbatical: Lessons Learned in War

• Identify the sacrifices made by deployed physicians to the combat zone 1 2 3 4 5
• Discuss advances in trauma care such as tourniquet application 1 2 3 4 5
• Describe how emergency medicine is different in the combat zone compared to civilian emergency 1 2 3 4 5
medicine
17) Morbidity and Mortality: Deadly Endocrinologic Disorders

• Discuss several uncommon but deadly forms of endocrinologic emergencies 1 2 3 4 5
• Describe the clinical presentation of several deadly endocrinologic disorders and their immediate 1 2 3 4 5
management priorities
18) Morbidity and Mortality: The Calm, Confused Patient

• Identify several uncommon but deadly forms of confusion 1 2 3 4 5
• Describe the clinical presentation of confusion and its immediate management priorities 1 2 3 4 5
19) Beyond ACLS

• Discuss the importance of CPR 1 2 3 4 5
• Review options in patients with no IV access and review the evidence for epinephrine in cardiac arrest 1 2 3 4 5
• Discuss a new way to think of PEA and if the pulse check is dead 1 2 3 4 5
20) DKA Myths

• Discuss the pros and cons of ABG vs. VBG in DKA 1 2 3 4 5
• Discuss the next steps after IVFs in DKA 1 2 3 4 5
• Review the evidence for bicarbonate therapy in DKA and discuss the optimal way to dose insulin in DKA 1 2 3 4 5
• Acknowledge that euglycemic DKA is not a myth 1 2 3 4 5
7
NWAS Current Topicsinin
Current Topics Anesthesia
Emergency Medicine Nex 8
HIDDEN KILLERS:
PLAIN FILM FINDINGS YOU CAN’T AFFORD TO MISS
NWS Current Topics in Emergency Medicine Hidden Killers: Plain Film Findings You Can’t Afford to Miss 9
 Dr. Sumeru (Sam) Mehta
 Army Veteran
Welcome to…  Baylor Bear football and Spurs season ticket holder
 Been to Everest Base Camp twice
 Dr. Shadi Tolaymat
 Cardiologist
 Florida Gator (has a crush on Tim Tebow)
 Beer Connoisseur
 Dr. Ravi Karia
 Ortho Trauma at UTHSCSA
 Loves Canadian hockey
 Golf Junkie
 case‐based review of life‐threatening
diagnoses
 characteristic findings on plain radiographs of
these life‐threatening diagnoses
 the common pitfalls associated with
interpretation of these studies.
 Exponential increase imaging studies  Plain films are part of initial screening tests
 227% increase in use of CT scanning from  Fast, inexpensive and often can be performed
2000‐20081 at bedside in the unstable patient.
 ED imaging  Many catastrophic diseases have
 Plain films: 65% characteristic findings.
 CT scan: 29%  ED physician often makes initial
 Ultrasound: 4% interpretations and will help guide care
 Tremendous role for plain films in ED
1. Rao VM, Levin DC, et al. "Trends in Utilization Rates of the Various Imaging Modalities in Emergency Departments:
Nationwide Medicare Data from 2000 to 2008." JACR 2011;8(10):706‐9.
 45 yo male with CC of “chest pain”
 Sudden onset
 Stabbing
 Exam:
 HR 115 RR 16 BP 187/85 POX 95% RA
 Diaphoretic, ill appearing
 Tachycardic but o/w unremarkable
 CXR was not viewed before the patient was
catheterized.
 Catheterization revealed a dilated aortic root
and possible intimal flap.
 Catheterization was aborted and emergent
CT chest was performed showing…
 Classic teaching is looking for a “widened
mediastinum” or “abnormal aortic contour”
on CXR
 However…
 Widening only…
▪ Type A: 63% present
▪ Type B: 56% present
 Abnormal contour only 70% sensitive
 True dissections are primarily an intraluminal
event…minimal change to external diameter
 Normal to find widening or a dilated aortic
contour with…
 Chronic degeneration of the aorta which occurs
with aging
 Patients with long standing aortic valvular disease
 11‐15% of CXR with confirmed AoD were
interpreted as normal.
 Pleural effusions were noted in 19% of the
studies
 History and a good exam with high index of
suspicion.
 CT chest or TEE is required where suspicion
exists.
 24 yo male, unrestrained passenger whose
vehicle was struck at high speed on the
passenger side.
 VS: 92/56 125 22 92% on 100% NRB
 Decreased right breath sounds
 Stat portable CXR is obtained.
 Important to evaluate film technique
 Supine patient: air in pleural space collects anteriorly
and basally
 Upright patient: air collects apically
 If air collects laterally it deepens the lateral
costophrenic angle and produces the deep
sulcus sign.
 Occasionally the air collects anteromedially and
may produce an unusually sharp outline of the
mediastinal vascular structures, heart border,
and cardiophrenic sulcus
 Relatively insensitive for PTX  32 yo male thrown off his bike, landing on his

 Upright = 59% right side. Presents c/o severe pleuritic R
 Supine = 37% chest pain.
 When in doubt, CT of chest is the gold  VS: 115 24 150/95 98% RA
standard  Exam: diffuse tenderness to right chest and
 New studies suggest thoracic US (eFAST) is a right upper quadrant.
viable alternative (sens=80‐100%)  Stat CXR is ordered.
 Decubitus imaging may increase sensitive to
87%
 On a supine film, an acute effusion, such as a
hemothorax, will layer out posteriorly.
 causes the affected side to appear more
opaque compared to the other side.
 In this case, CT chest‐abd‐pel, there were
abdominal contents in the right hemithorax
 no signs of traumatic injury such as liver
laceration, rib fractures, or free fluid
 Multiple L‐sided rib fx
and deep sulcus sign.
 Comparison to R reveals
opacity of left lung c/w
hemothorax on supine
CXR
 Also radiographic signs
of pneumothorax with
shift.
 27 yo male with sudden onset of pleuritic
chest pain
 VS: 125 134/83 24 96% RA
 Exam: uncomfortable appearing, agitated
 Stat CXR was obtained…
 Pt was further questioned about events  generally has a benign course and rarely
leading up to onset of pain. causes hemodynamic compromise from
 After much prodding the patient admitted to tension physiology, as the air often
smoking crack cocaine immediately prior. decompresses into the soft tissues of the
 increase in intra‐thoracic pressure against a neck and chest
closed glottis  should be differentiated from
 Also commonly seen in asthmatics, weight pneumopericardium, which can have a
lifters, and following blunt thoracic trauma. somewhat similar appearance on radiographs
 Infant intubated for  15 yo F with chest pain

respiratory distress  Dx’d with
 hypotensive 1 hour pneumomediastimum on
post intubation. CXR
 Initial concern from  Re‐evaluation revealed
tension PTX however no crepitus on exam but
CXR revealed… pt was noted to have long
 Air does not hair in braids so CXR was
track…confined to repeated…
around the heart
 50 yo male presents from homeless shelter
with alcohol intoxication.
 During transport…he vomiting profusely
 On arrival he began c/o chest pain
 VS: 120 128/89 22 92% RA
 Exam: clinically intoxicated with slurred
speech
 Stat CXR was obtained…
 Presumed to be aspiration PNA and pt was
admitted
 Following day, pt with increased chest pain,
SOB and spiked a fever.
 CT chest was ordered…
 Perform lateral CXR whenever possible. Pleural effusions and  50 yo obese female c/o rapid onset left sided

pneumonias are more apparent.
 Appreciate the various appearances of pneumomediastinum
sharp, pleuritic chest pain and SOB.
and the clinical significance when seen with a pleural  VS: 125 128/86 26 93% RA
effusion  Stat CXT ordered…
 The majority of cases of effort‐related esophageal rupture
(Boerhaave's syndrome) occur at the left posterolateral
aspect of the distal esophagus, and commonly cause a
pleural effusion, usually left‐sided.
 In one series a history of alcohol was present in 40% of cases
of Boerhaave's syndrome, and as such should be suspected
in all intoxicated patients who are presenting with chest pain
after vomiting
 Importance of checking lateral CXR.  60 yo female with gradual onset SOB x 2

 Effusions, masses and infiltrates may be weeks.
subtle or even absent on PA alone.  Worse with exertion and supine positioning
 Always important to compared to old images  No history of HTN or cardiac disease
if at all possible.  VS 110 110/56 24 97% RA
 chest radiographs may grossly underestimate  Exam: Lungs clear to auscultation bilaterally
the severity and extent of pathology  CXR was obtained…
 Interpreted as cardiomegaly o/w NAD.
 Admitted to medical floor for work‐up of
dyspnea
 Overnight became tachypnic and
hypotensive
 Stat ECHO showed large pericardial effusion
with tamponade physiology
 Pericardiocentesis performed and taken to  Normal

OR for pericardial window. cardiomediastinal
 Pericardial fluid was malignant for silhouette
 Detection of pericardial
undiagnosed BRCA effusion is difficult.
 Retrospect review of an one year old CXR  In acute effusions, plain
showed… films may be normal.
 Role of bedside US
 62 yo female with h/o metastatic BRCA
presents with acute onset R‐sided, sharp,
pleuritic chest pain.
 VS: 130 22 96%RA 110/76
 Exam: no abdominal tenderness
 Given her h/o cancer, a pulmonary embolus
was suspected
 Stat CXR was performed while CTA was
ordered…and CXR showed...
 Pt was taken to OR…perforated ulcer.
 PHM showed large doses of corticosteroids
for her brain mets...contributed to ulcers and
lack of abdominal tenderness.
 Upright CXR is excellent for detection of
pneumoperitoneum…as little as 1‐2 ml.
 Patients should be upright for at least 5‐10
minutes to allow air to collect under the
diaphragms
 24 yo female s/p domestic assault. Was
assaulted repeatedly in the head with blunt
object.
 Pt presents with intubated pre‐hospital for
GCS 4 at scene.
 VS: 110 145/96 14 98% NRB GCS 3T
 Exam: multiple head lacerations and
contusions
 During ED course, her POX trended down and
a CXR was ordered…
 2 yo presents with 2‐d h/o low‐grade fever
and cough.
 VS: 144 28 97% RA
 Exam: Irritable
 Lungs: coarse breath sounds bilaterally (R>L)
 CXR was ordered…
 Diagnosis of child abuse can be challenging in
a busy ED.
 abused patients discharged home to the
same environment have a 50% chance of
further abuse, and a 10% chance of death
 5 or more children a day die from abuse.
 rib fractures may be very subtle on plain  Other radiographic findings of child abuse
radiographs. include periosteal reactions, metaphyseal
 look for subtle asymmetry of the rib necks, as corner fractures, and bucket handle fractures
well as sudden angulation in the ribs  Periosteal reaction, or periosteal new bone
 Rib fractures are most visible during callous
formation, which typically occurs 10‐14 days formation, may be one of the earliest
after injury radiographic findings in child abuse
 in the absence of major trauma, such as from  peak incidence is from 10‐14 days, it may
a motor vehicle accident, the probability of appear as early as 4 days from the injury
abuse in a child with a rib fracture is 71%
 Plain radiographs, particularly chest x‐rays,
still play a valuable role in the emergency
department
 Usually the first study performed
 Subtle findings may lead to early diagnosis
and treatment of potentially life‐threatening
didseases
 Be systematic in your review of radiographs
 Review old studies for comparison
 For inspiration, idea and some pictures:
 Robert Tubbs MD Alpert Medical School of Brown
University Providence, RI
EMERGENCY MEDICINE AT 29,035 FT:

HIGH ALTITUDE MEDICINE
NWS Current Topics in Emergency Medicine Emergency Medicine at 29,035 ft: High Altitude Medicine 24
To scorn all strife, and to view all life

With the curious eyes of a child;
High Altitude Illness: From the plangent sea to the prairie,
Emergency Medicine at 18,800ft and Higher From the slum to the heart of the Wild.
From the red-rimmed star to the speck of sand,
From the vast to the greatly small;
Sumeru G. Mehta, MD, MPH For I know that the whole for good is planned,
And I want to see it all.
Robert Service
Goals
• Medical Clinic at Everest Base Camp

• Introduction to High Altitude Illness
• Epidemiology
• Pathophysiology
• Treatment and Management
Nepal
• 21 million
• 60 ethnic groups
• 49 mother tongues
• $170 per capita
income
• Agriculture
• Kathmandu
• 8/10 highest peaks
• (1) Kathmandu: 1300m / 4265 ft

• (1)Lukla: 2850 / 9350
• (1) Phakding: 2640 / 8661
• (2) Namche: 3450 / 11,319
• (3) Kunde: 3840 / 12,598
• (4) Tengboche: 3860 / 12,664
• (5-7) Pheriche: 4280 / 14,042
• (8) Gorak Shep: 5170 / 16,962
• (9) Kala Pattar: 5600 / 18,373
• (9) EBC: 5340 / 17,520
Worst climbing movie EVER
High Altitude Illness High Altitude Illness

• Epidemiology “Despite the many trappings of civilization at Base
Camp, there was no forgetting that we were more
• Pathophysiology than three miles above sea level. Walking to the
mess tent at meal time left me wheezing for several
• Acclimatization minutes. If I sat up too quickly, my head reeled and
• Management vertigo set it. Sleep became elusive, a common
symptom of minor altitude illness. Most nights, I’d
• Treatment wake up three or four times gasping for breath,
feeling like I was suffocating…”
John Krakauer, Into Thin Air
Potential medical problems associated

High Altitude-Definition 1000 m = 3280 ft with high-altitude ascent
• Intermediate altitude (1500-2500m) • Acute hypoxia

• High Altitude Illness
– Physiologic changes; Pox > 90%; HAI rare • Cerebrovascular syndromes
• High Altitude (2500-3500m) • Peripheral edema
– HAI common with rapid ascent • Retinopathy
• Thromboembolism
• Very High Altitude (3500-5800m) • Sleep disorders and periodic breathing
– HAI common; Pox < 90%; Hypoxia w/ exertion • High-altitude pharyngitis and bronchitis (Khumbu cough)
• Ultraviolet exposure and keratitis (snowblindness)
• Extreme Altitude (>5800m) • Exacerbation of pre-existing illness
– Hypoxia at rest; progressive deterioration

• Cerebral and pulmonary syndromes at any
altitude over 2000m
• Usually during initial ascent
• Cerebral
– Acute Mountain Sickness (AMS)
– High-altitude cerebral edema (HACE)
• Pulmonary
– High-altitude pulmonary edema (HAPE)
Hackett et al, NEJM, 2001

• Epidemiology Max Altitude % AMS % HAPE / Reference
– AMS %HACE
• 22-25% at 2000m (6,500 ft)
• 42-53% at altitudes greater than 3000-4000m Western 3500m 18-42 0.01 Honigman,
1993
– HACE US
• 1-2% in people ascending over 4500m (14,760 ft)
– HAPE Everest 5500m 23-47 1.6/ 0.05 Hackett,
1976
• 1-2% with usual ascent rate to over 3000m (9,8000 ft) Trekkers
• 10% with rapid ascent to 4500m
– Low risk of death Denali 6194m 30 2-3 Hackett,
1986
• Trekkers = 0.0036% Climbers
• Soldiers = 0.16%
• Climbers = 17%
West, Ann Int Med; 2004

Barry, BMJ; 2003
High Altitude Illness (HAI) High Altitude Illness

• Risk Factors • Epidemiology
– Rate of ascent
– Altitude reached
• Pathophysiology
– Altitude where one sleeps • Acclimatization
– Individual susceptibility / Genetics
• Management
– Hx of HAI
– Residence of an altitude of under 900m • Treatment
– Exertion / Physical fitness
– Age (<50 for AMS)
Proposed Pathophysiological Process

of High-Altitude Illness HAI – Pathophysiology
Hackett et al, NEJM, 2001 West, Annals Int Med; 2004
HAI – Effects of High Altitude (HA) HAI – Effects of Hypoxia on Physical Performance
• Oxygen deprivation at HA is inevitable leading to • Reduced maximal oxygen consumption

hypoxia – Via elevated pulm HTN
– Oxygen is critical to normal cellular function / energy • Reduced performance results in great
• Other factors at HA (severe cold, high winds, increase in fatigue
intense solar radiation) can be nullified
• Normal myocardial contractility
• Physiologic effects of hypoxia at HA
– Hypoxia vs. ischemia
– Physical performance
– Mental performance • Genetics also play role
– Sleep
West, Ann Int Med; 2004

HAI – Effects of Hypoxia on Mental Performance HAI- Effects of Hypoxia on Sleep

• Impaired at HA • Most distressing feature of HA
• People working at an altitude of 4000m have • Frequent waking and unpleasant dreams
increased arithmetic errors, reduced attention
span, and increased mental fatigue • Periodic breathing above 4000m
– cycles of normal breathing which gradually slows,
• Brain accounts for 20% of the body’s total breath-holding, and a brief recovery period of
oxygen consumption accelerated breathing (response to increased CO2)
– Climb high, sleep low
McFarland, Physiologic adaptions; 1972
HAI – Physiology of AMS HAI - Physiology of HACE

• Precise pathogenesis not understood • End spectrum of AMS
– Brain swelling with AMS • Cerebral edema due to increased cerebral
• Mild cerebral edema? blood flow
– MRI studies with DWI, T2 and SIENA • Autopsies show cerebral edema with
• Edema is vasogenic swollen flattened gyri
• Oxidative stress?? • MRI T2 images c/w edema
• Free radicals??
Proposed Pathophysiological Process

HAI - Physiology of HACE of High-Altitude Illness
Hackett, JAMA; 1998 Hackett et al, NEJM, 2001

HAI – Physiology of HAPE HAI – Physiology of HAPE

• Non-cardiogenic form of pulmonary edema
resulting from a leak in the alveolar capillary
membrane
• Elevated incidence associated with URI and
restricted pulmonary circulation
• Hypoxic pulmonary arterial vasoconstriction
resulting in circulatory shear forces and a
consequent permeability leak
West, AnnInt Med; 2004
High Altitude Illness HAI - Acclimatization

• Epidemiology • Adaptive changes that improve the
tolerance of humans to HA and hypoxia
• Pathophysiology
– Hyperventilation
• Acclimatization – Polycythemia
• Management – Acid-base changes
• Treatment – Misconceptions
HAI - Acclimatization and Hyperventilation HAI - Acclimatization and Polycythemia
• Most important feature • Develops relatively slowly > entire process

• Increase in depth and rate of breathing not complete for several weeks
• Does not play a critical role in acute HA
• Due to hypoxic stimulation of peripheral exposure
chemoreceptors which sense low PO2
• Transient increase in erythrocyte production
• Reduces alveolar PCO2 – Due to reduced plasma volume 2/2 dehydration
• Increases alveolar PO2 – Significant insensible fluid loss
– Reduced fluid intake
– Diuresis
HAI - Acclimatization and Acid-Base Changes HAI – Misconceptions about Acclimatization

• Respiratory alkalosis with an increased pH • “acclimatization returns the
in CSF and arterial blood body to its sea level condition”
– Acute reduction in alveolar and arterial PCO2 • 4200m
– Acute HA: alveolar PO2=45mmHg
– HA acclim: alveolar PO2=54mmHg
• After 1 d, bicarbonate moved out of CSF • Severity of arterial hypoxemia
emphasized when compared to
• After 2-3 d, renal excretion of bicarbonate pts with COPD
moves arterial pH towards normal
Rahn,Am J Phys; 1949
High Altitude Illness HAI – Management of AMS

Independent Predictors of Acute Mountain Sickness
• Epidemiology
• Pathophysiology
• Acclimatization
• Management
– Prophylaxis
– Treatment
Honigman, B. et. al. Ann Intern Med

1993
HAI – Management of AMS HAI – Management of AMS

Percentage of acute mountain sickness in visitors to moderate altitudes Distribution of symptoms of acute mountain sickness in 3072 visitors
according to age, physical condition, and altitude visited
Honigman, B. et. al. Ann Intern Med Honigman, B. et. al. Ann Intern Med
1993 1993

• Common if going from sea level > 3000m • Prevention is Key
• Unusual below 2500m – avoid rapid ascent to sleeping altitudes >
• Onset 6-12 hours after arrival at altitude 3,000 m
• Resolution 1-3 d if no further ascent
• No PE findings consistent with AMS – Slow ascend allows acclimatization
• Neurological s/sx imply HACE or
alternative cause – spend 2 to 3 nights at 2,500 m to 3,000 m
before going higher
• Prevention is Key • Prophylaxis

– Day trips to higher altitude, with a return to lower – Acetazolamide
• Proven but has side effects; dosage?
altitude for sleep, aid in acclimatization
– Dexamethasone (2 mg q 6-8 hours)
• Proven but has side effects
– Over 3000m each night should be spent not >
– Gingko Biloba
300 m above the last, with a rest day every 2-3 • Controversial
days
– Theophylline
– Clonidine
– Brief exposure to high altitude prior to ascent
HAI – Acetazolamide for AMS Prophylaxis HAI – Gingko Biloba for AMS Prophylaxis
• Proven to work but what is optimal dosage? • Background

• Basnyat et al 2003
– RCT, 155 trekkers, 4243m > 4937m, AZ 125 mg BID – Oldest living tree species; used worldwide
– Pl 25%, Az 12%, NNT=8 – Used for neurocognitive disorders and peripheral
– Severe AMS: 30% v 0% vascular disease
• Dumont et al 2000
– Meta-analysis of 33 trials on AMS prophylaxis
– Reduces AMS incidence and severity of AMS
– Higher dosing Az 750 mg/d; NNT=3 • Mechanism of Action
– Az 500 mg not effective
– Flawed meta-analysis; no head-to-head comparison; studies – Not exactly known
excluded; different ascent rates – Theories include action as oxygen radical scavenger,
• Conclusion inhibition of PAF and attenuation of oxidative damage
– Optimal dosing still uncertain
– 750 and 500 mg/d clearly work; ideal for now is 5 mg/kg/d
Maakestad, WEM; 2001

HAI – Gingko Biloba for AMS Prophylaxis HAI – Gingko Biloba for AMS Prophylaxis
AMS Az GB Both Placebo • Conclusion

incidence
– Studies overall inconclusive
Gertsch, 12% 35% 14% 34% • Different dosing, timing and preperations
2004
4280m > 4928m – OTC preparations vary considerable
in 24 hours
– Harmless
Chow, 30% 65% 60%
2005 – Until further study, I would recommend…
1200m > 3800m
for 24 hours • Use in combination with Az
Mehta, 24% 40% 17% 42% • Use if no other alternative
2006 • Would not use as primary prophylaxis
2743m > 5151m
Less than 10 days
HAI – Treatment of AMS HAI – Management of HACE

• Rest and stop further ascent • Preceded by AMS
• Descend if no improvement in sx after 24 • Prodromal sx
– Early mental impairment
hours or deterioration of sx
– Change in behavior
• Analgesics and anti-emetics will relieve – Headache, N/V, hallucinations, confusion
headache and nausea • Clinical signs
• Acetazolamide 250 mg q8 hours – Ataxia, deterioration in conscious level, papilloedema
and retinal hemorrhages
• Dexamethasone 2 mg every 6 hours or 4
– Focal neurological deficits and coma may occur
mg every 12 hours
HAI – Treatment of HACE

• Descent as quickly as possible
• Oxygen administered if possible
• Acetazolamide 250 mg q8 hours
• Dexamethasone 8 mg initially then 4mg q
6-8 hours
• If descent not feasible > portable
hyperbaric bags
• Supportive care
HAI – Management of HAPE

• 2-3 d after arrival at altitude
• Clinical signs
– Early: Tachycardia, tachypnea, mild pyrexia,
basal crepitations
– Progression to: Dyspnea with exercise
progressing to dyspnea at rest; dry cough,
weakness
– Late: Severe dyspnea, frank pulmonary
edema
HAI – Treatment of HAPE HAI – Treatment of HAPE

• Descent as quickly as possible • New research
– Sildenafil 50 mg q 8 hours
• Oxygen administered if possible • Sildenafil attenuates hypoxia-induced pulmonary
• Nifedipine SR (30 mg slow release now hypertension in humans and mice
and q12 hours or 20 mg SR q 8 hours) – Salmeterol 125 mcg BID inhaled

• Prophylactic inhalation of a beta-adrenergic agonist reduces
– Consider as prophylaxis if prev hx HAPE the risk of HAPE
• If descent not feasible > portable – Nitrous Oxide

– Acetazolamide
hyperbaric bags • Az prevented HAPE in rats
• Supportive care
HAI: Pre-existing Medical Conditions and HA Case Report

• Cardiac disease • 39 yo Korean trekker found unconscious
– Anginal sx will worsen
– Risk of IHD in previously well trekkers not increase • Day 4 of trek
• Asthma
– Unaffected by travel to altitude • Was “sick” day 3 and this morning.
– Not at greater risk of HAI compared to those healthy
• Trekked 1,820 m (2800m to 4620m) without
• COPD
– Higher risk of infections, worse symptoms acclimitization
• Diabetes • PMH: none
– Hypoglycemia may be confused with HACE, vice versa
– Glucose monitors may be inaccurate at HA • Meds: Diamox (started day 1 of trek)
– Have appropriate meds/supplements available for management
• Epilepsy • All: none
– Altitude itself does not increase risk of seizures • SHx: pilot for Korean Air; married
Case Report Case Report

• Vitals: Pox: 45% RR: 32 HR: • Acute Mountain
121
Sickness
• PE:
– Gen: Severe distress, lethargic • HAPE
– HEENT: peri-oral cyanosis, • HACE
mmd, EOMI
• Treatment
– CV: tachycardic, RRR
– Descent 600 m
– Pulm: rales bilat. lower lungs
– Abd: soft
– Oxygen 2 L/min
– Neuro: confused, ataxic, non- – Dexamethasone 8 mg po
focal – Nifedipine SR 20 mg po
– Evacuate ASAP
EMS in the Khumbu EMS in the Khumbu
EMS in the Khumbu EMS in the Khumbu

EMS in the Khumbu High Altitude Illness- Summary

• Prevention is key
• Slow ascent allow adequate
acclimatization
– Over 3000m each night should be spent not >
300 m above the last, with a rest day every 2-
3 days
• Descent is always a option in HAI
• New research will expand treatment
options
View From The Summit of Mt. “Wanderlust is Incurable” Mark Jenkins
Everest
• My son, Loghan Everest Mehta

EMERGENCY GI CONTROVERSIES
Salim R. Rezaie, MD
NWS Current Topics in Emergency Medicine Emergency GI Controversies 43
Twitter: @srrezaie
Emergency GI
Controversies Facebook: REBEL EM
Email: srrezaie@gmail.com
Salim R. Rezaie, MD
No
Financial
Disclosures
www.rebelem.com
OBJECTIVES NGL in Upper GIB

Role of NGL in UGIB
Timing of Endoscopy in UGIB
Role of Glucagon in Esophageal Foreign Body
Role of PPI in UGIB

PROS NGL Before Endoscopy
≈500 Patients
Positive NGL Predictive
NGL Aspirate Prediction
Better Visualization of
HIGH RISK LESION
Aljebreen AM et al. Gastrointest Endosc 2004
Positive NGL IS NOT

Visualization
Predictive • ccc ≈250 Patients
Blood Aspirate ≈25% WITHOUT IV Erythromycin

vs
NGL
Clear/Bile Aspirate ≈15% WITH vs
IV Erythromycin + NGL
Pateron et al. Annals of Emerg Med 2011
NGL NO BETTER at…

Visualization Rebleeding
IV Erythromycin
250mg
Duration of Endoscopic
Need for 2nd EGD
Procedure
20 – 30min
Prior to Procedure
Cons Painful
≈1100 Procedures
Painful
Patients Recorded 100mm VAS
Outcomes Not Score
Improved
Most Painful Procedure was…
Singer AJ et al. Annals of EM 1999
Outcomes
NGL IS a Painful
Procedure ≈600 UGIB Patients
30d Mortality
Mean Hospital LOS
Transfusion Requirements
Timing of Endoscopy
Huang ES et al. Gastrointestinal Endoscopy 2011
NGL DOES NOT Improve

In UGIB, NGL NOT REQUIRED for…
Meaningful Outcomes
Diagnosis
Earlier Performance of Prognosis
Endoscopy Visualization
Therapeutic Effect
Laine L Jensen DM Am J Gastroenterol 2012

NGL BOTTOM LINE

NG Lavage: Indicated or Outdated?
Just
SAY NO
Timing of Endoscopy Definitions

Early vs Delayed
Endpoints
Assessed
Wake Up & EGD? Systematic Review

3 Trials 2 Trials
(1400pts) (1100pts)
1 Trial (100pts)
NO DIFF
DECREASED INCREASED
Mortality
Transfusion O2 Desat
Rebleeding
Rebleeding
Transfusion
Surgery
Surgery
BENEFIT NO BENEFIT
3:00AM Spiegel BMR et al. Arch Intern Med 2001

Endoscopy <12hr vs 12 – 24hrs Optimal Timing of Endoscopy &

Lowest Mortality
Decreased Transfusion* ≈12,500 pts
No Difference Mortality HD Stable + ASA 1 – 2: 0 – 36hrs
No Difference Need for Surgery HD Stable + ASA 3 – 5: 12 – 36hrs
*Only in patients with bloody emesis HD Unstable + ASA 1 – 5: 6 – 24hrs
Lin HJ et al. J Clin Gastroenterol 1996 Laursen SB et al. Gastrointest Endosc 2016
Resuscitate Before You

HD Unstable Intubate
1.7 – 2.4%
Resuscitate & Resuscitate & Transiently
Stabilize OR Don’t
Stabilize Stabilize
EGD <2hrs, <3hrs,

EGD 6 – 24hrs or <6hrs??? Heffner AC et al. Resuscitation 2013
Kim WY et al. Plos One 2014
TIMING OF Glucagon for Esophageal Foreign

ENDOSCOPY Bodies
BOTTOM LINE
Resuscitate Before
You Endoscopate
3 Trials with Placebo

8 Trials Since 1983 Arms
Complications
Glucagon 14.4%
vs
Placebo: 17.7% Esophageal
Pathology: 22.3%
N/V: 10.6%
Glucagon BOTTOM LINE

Question Tradition: Glucagon for
Esophageal Foreign Bodies
No Better than Placebo
PPI in Upper UGIB

Good PPI + PUD
Bad PPI + Undiff UGIB
Ugly Bolus vs Drip
GOOD (PPI + PUD) BAD (PPI + Undiff UGIB)

21 RCTs ≈2900pts 6 RCTs ≈2200pts
REDUCED Stigmata of Recent Hemorrhage

NO DIFFERENCE Mortality REDUCED Endoscopic Therapy
REDUCED Surgical Intervention NO DIFFERENCE Mortality

NO DIFFERENCE Rebleeding
REDUCED Rebleeding
NO DIFFERENCE Surgery
Sreedharan A et al. Cochrane Database Syst Rev 2010 Leontiadis G et al. Cochrane Database Syst Rev 2004
PPI Drip UGLY (PPI Bolus vs Drip)

13 RCTs
NO DIFFERENCE
Rebleeding
Mortality
PRBC Transfusion
Hospital LOS
Sachar H et al. JAMA Intern Med 2014

PPI BOTTOM LINE The Good, The Bad, and The Ugly of Proton
Pump Inhibitors in UGIB
BOLUS = Drip
TREATMENT OF SUBMASSIVE PE:

FULL DOSE, HALF DOSE, OR NO DOSE LYTICS
Salim R. Rezaie, MD
NWS Current Topics in Emergency Medicine Treatment of Submassive PE 52
Objectives
Bust n' Move: The
Critical PE Patient
Discuss Initial Management of PE
Analyze Data for Thrombolytics in

Salim R. Rezaie, MD Massive and Submassive PE
@srrezaie
No Financial
Disclosures
Initial Resuscitation
Avoid Hypoxia
& Hypercarbia
Shunt Physiology
Avoid Intubation
HFNC RV not Like LV

PEEP BiPAP
Crescent Shape
Thinner Wall
BVM
Medial Displacement of
Septum
Fluids Death Spiral

Inhaled
Nitric Oxide
Vasopressors
Inotropes
Vasodilators
Inotropes
Vasopressors
Escalating Thrombolysis
Limit IVF
Therapy
64.8%
Choice of Lytic
Mortality
25.0%
15.0%
8.1%
RV Dysfunction, No Hypotension Cardiogenic Shock Cardiopulmonary

Hypotension Resuscitation
Massive PE
YES Massive PE
Full Dose Lytics
YES
YES Thrombolysis vs Anticoagulation
YES
Recurrent
NNT = 10 PE/Death
Massive PE
Half Dose Lytics
NNH = 10Major Bleeding

Thrombolysis vs Anticoagulation
PEAPETT Trial Results of PEAPETT

96%
23 Pts Cardiac Arrest 91% 87%
0%
ROSC Survival to DC Alive at 2 Years Any Bleeding
NO DIFFERENCE
Half Dose Pulmonary Obstruction
vs Recurrent PE
Death
Full Dose
RCT of 118pts DECREASED
Major Bleeding
Submassive PE
Massive PE
BOTTOM LINE Full Dose
CDT
Half Dose
Consider Half Dose tPA
No Dose
NO
Insufficient
Evidence
Select
Select
Submassive PE
Full Dose Lytics
2 – 3%
ICH Thrombolysis vs Anticoatulation
NO DIFFERENCE
MAPPET-3 Mortality
Bleeding
DECREASED
≈250 pts HD Decomp
NNT = 7
TOPCOAT
≈80 pts DECREASED INCREASED

RV ICH
Dysfunction
NNT = 6 NNH = 40
7 Day Outcomes
PEITHO
≈1000 pts
↓HD Compromise (3-Fold)
↑ECH (5-Fold)
↑ICH (10-Fold)
Mortality NNT = 65
2014 Meta-Analysis
Major Bleeding NNH = 18
ICH NNH = 78
≈1700 pts
PEITHO PEITHO Follow Up

Follow Up
≈700 pts
NO DIFFERENCE
in Mortality or Clinical Symptoms
Unselected Patients Full Dose

BOTTOM LINE
DECREASE HD Decomp
BUT
INCREASE Bleeding
Submassive PE
Half Dose Lytics Levine et al 1990
Thrombolysis vs Anticoagulation
≈60 pts
DECREASED Clot Burden

MOPETT
0 Bleeds
120 pts
DECREASED
Pulmonary HTN Mortality
Assessment
NNT = 2
0 Bleeds
Full Dose vs Half NO DIFFERENCE

Mortality or Recurrent PE
Dose
MAJOR BLEED
NNH =
15
Half Dose One More Thing

Trials
1 ICH
Anticoagulation
453 pts 0.2% +
Lytics
=
BAD
Half
Half Dose
Dose Submassive PE
BOTTOM
BOTTOM LINE
LINE No Lytics
Equivalent to Full Dose

BUT Thrombolysis vs Anticoagulation
Less Bleeding
Submassive PE is a Spectrum of Disease

Anticoagulation
M
Alone O
R
T
A
L
I
More HD Decomp T
Y
NNH = 18 Not Sick Sick

No DOSE Submassive PE
BOTTOM LINE CDT
In Select Patients
Anticoagulation Alone Catheter Directed Therapy
Has More HD Decomp
Decreased
SEATTLE-2 Clot Burden
0 ICH
1 Major Bleed
INCREASED
Cost
Hospital LOS
DECREASED
PERFECT Trial HD Decomp
RV Strain
0 ICH or Major
Bleed
No
Age ≥65
Comparison
Arms High Risk
of Bleeding
CDT Bottom Line Putting it All Together
Safe MASSIVE PE: Consider 1/2 Dose

But… SUBMASSIVE PE: Select Pts, 1/2 Dose
CDT: Older Pts or High Risk Bleeding
INCREASED
Cost & LOS Stop Anticoagulation + Lytic
Questions
Salim R. Rezaie, MD
@srrezaie
MORBIDITY AND MORTALITY:

LIFE-THREATENING MIMICS OF MECHANICAL
LOW BACK PAIN
(No Handout Available)

MORBIDITY AND MORTALITY: CNS EMERGENCIES

NWS Current Topics in Emergency Medicine Morbidity and Mortality: CNS Emergencies 66
Learning Objectives
Morbidity and Mortality: Central • Become familiar with several uncommon but deadly
Nervous System Emergencies forms of cerebrovascular emergencies
Justin Williams, MD, FAAEM

• Describe the clinical presentation of cerebellar
Greater San Antonio Emergency Physicians
infarction and its immediate management priorities
Medical Director
Methodist Stone Oak Hospital – San Antonio
Case 1 Case 1
• 42 y/o AAF with a history of CHF, HTN, Hyperlipidemia and
CVA – diagnosed two weeks ago presents with right sided chest • Social Hx: Not provided
pain for three days, and left knee pain
• Sharp, stabbing, worse with movement and deep inspiration, • 118/113 107 16 96.6 98%RA
10/10 intensity, no prior pain similar
• Meds: Lasix, Lisinopril, Paxil, Metoprolol, ASA, Zocor, Elavil

• PE: Obese, TTP over right chest wall, walks
with limp on right and has 4/5 strength on right,
• Allergies: none left knee tender without swelling or redness, no
cording, Homan’s sign negative, o/w normal
• Fam Hx: Negative for PE or DVT
Case 1 Case 1
• Labs: • ED Course:
• CBC normal • Chest pain ascribed to musculoskeletal or neuropathic
etiology
• Renal normal
• PM anti-hypertensives given
• Coags normal
• Discharged to home with follow-up in 24 hours
• Urinalysis – 3-5 WBC, 5-10 RBC, 5-10 Squamous
• CXR – Cardiomegaly
• V/Q scan – very low probability for PE
Case 1 Case 1
• ED Course: • Nursing Documentation:

• Given anticoagulant • “CP + SOB + H/A X 3 days – worse the AM when
• Return tomorrow for BLE duplex woke up”
• “States CP worse on right side, radiates to lower
back”
• Dx: Atypical Chest Pain, LLE pain • “States slight numbness in right arm”
• “States pain is 10/10, also states slight blurred vision
with H/A”
• “Pt has slight edema of BLE extremities, + pulses”
• Rx: Ibuprofen 400-800mg PO Q8 hours X 3
days • D/C Vitals: 176/98 92 16 98.1 99% RA
Case 1 Case 1
• Return Visit • ED Course:

• Returns in 24 hours for duplex of BLE • Initially, went for venous duplex – negative BLE
• Complaining of 10/10 headache, chest pain • Noted upon return to have right sided weakness and
and“slurred speech” and right sided weakness that slurred speech
occurs when her blood pressure gets high • Given Percocet, Morphine, Phenergan, Nitroglycerin
• 190/132 112 16 96.8 97% 1.5 inches and Metoprolol X 3, and Metoprolol 50mg
PO
• Started on Nitroglycerin gtt, titrated to 150/95
Case 1 Hypertensive Disorders
• Hospital Course: • Hypertensive Urgency

• Absence of target organ damage in the presence of severe
• Diagnosed with Hypertensive Urgency elevation of blood pressure with systolic blood pressure
• Ruled out for AMI above 180 mm Hg or diastolic blood pressure frequently
greater than 110 mm Hg is considered hypertensive urgency
• Neurologic symptoms improved to baseline over course
of 40 hours
• Nitroglycerin titrated to off, Metoprolol dose increased • Hypertensive Emergency
to 200mg PO BID • Systolic blood pressure above 180 mm Hg or diastolic blood
pressure frequently greater than 120 mm Hg with acute or
• Subsequently readmitted for hypertensive crisis ongoing vital target organ damage, such as damage to the
brain, kidney, or heart, in the setting of severe hypertension
is considered a hypertensive emergency
Hypertensive Disorders Hypertensive Encephalopathy
• Hypertensive encephalopathy describes the • Cerebral autoregulatory response is

transient migratory neurologic symptoms overwhelmed
associated with the malignant hypertensive state
in hypertensive emergency • Acute rise in systemic blood pressure exceeds
the individual's cerebral autoregulatory range
• Hydrostatic leakage across the capillaries
• Head CT alone (without Lumbar Puncture) may within the central nervous system
be appropriate in the setting of marked
hypertension, with headache and neurologic
symptoms (but beware)
Hypertensive Encephalopathy Hypertensive Encephalopathy
• Progression of vascular pathology leads to • Lower mean arterial pressure by 25% into cerebral
generalized vasodilatation, cerebral edema, and autoregulatory blood flow range
papilledema
• Nitroglycerin, Nitroprusside, Hydralazine and
Enalaprilat common agents
• In chronically hypertensive patients,
autoregulation is altered and shifted upward to
maintain a relatively constant cerebral blood • Without treatment, the 6-month mortality rate for
flow at a higher mean arterial blood pressure hypertensive emergencies is 50%, and the 1-year
range mortality rate approaches 90%
Case 2 Case 2
• 42 y/o AAM found at home intermittently combative, • 230/117 108 30 85%RA 101.5F
covered in feces, urine. EMS called secondary to sister • SaO2 91% NRB
finding the patient non-conversant, and minimally
responsive (baseline MS normal). Had not been seen in
two days – electricity turned off to apartment X 2 days. • PE: Combative, snoring respirations, covered in feces
• Head AT/NC, Gaze disconjugate, pupils 3mm bilaterally
• PMHx: HTN, venous stasis ulcers BLE, OSA reactive
• PSHX: None pertinent • CTAB, RRR, Tachycardic
• Meds: MVI, Calcium, Ibuprofen • Intermittently combative, garbled unintelligible speech,
• All: NKDA localizes BUE
Case 2 Case 2
• IV, O2 , Monitor • WBC 15
• Intubated for respiratory status and combativeness • Bicarb 33, Cr 1.5, Glu 147, BE +9
• Neuromuscular paralysis with Vecuronium • Lactate 2.3

• CKMB 8.9, TnI <0.5
• CXR: LLL infiltrate
• 7.26 / 72 / 255
• Head CT: Preliminary read negative
• LP: Clear
• Resuscitated with 3L NS
• Rocephin, Vancomycin, Azithromycin given • Admit vitals: 130/75 87 12 100% (100% O2)
Case 2 Case 2
• Admitted to MICU – Dx: Pneumonia
• Patient brought to Radiology for immediate Head
• Started on Acyclovir for possible viral meningitis CT
• TnI increased to 0.8 – started on ASA, Metoprolol,
Heparin
• While in CT – resident paged stat from…
• 4am – CPAP trial initiated
• 5:45am – failed CPAP – now unresponsive, fixed
pupils, loss of gag
• Thoughts?
Case 2 Case 2
• Over-read Head CT (next AM):
• Initial read Head CT without contrast (evening): • There is extensive abnormal attenuation identified within
• The ventricles are prominent. There is no intracranial the left cerebellum. Marked mass-effect upon the fourth
hemorrhage. There is mild periventricular white matter disease. ventricle is noted. There is effacement of the
quadrigeminal plate cistern.
• The ventricles are mildly prominent. Additional zones

diminished attenuation are suspected within both frontal
lobes although this is not definitive. There is some sulcal
effacement noted.
• Large left cerebellar infarct with mass-effect.
• Early hydrocephalus.
Cerebellar Infarction Cerebellar Infarction

• Neurosurgery consult obtained
• Considered IVC placement
• Deferred secondary to devastating neurological impairment
• Brain death exam performed – coded during exam
• Resuscitated
• Family withdrew care, Organ sharing alliance notified
Cerebellar Infarction Cerebellar CVA

• Coroner Report: • Outcome frequently not based upon size of infarction, but
• Left Cerebellar Necrosis location
• Hypertensive heart disease with 800ml serous pericardial

• Patients with large infarction, but open ventricles – observe
effusion
• Bilateral pulmonary edema and congestion • Patients with effacement of 4th ventricle – surgical drainage
or decompression
• Surgical drainage or decompression often lifesaving before

herniation
Cerebellar CVA Cerebellar CVA

• Most common mechanism of cerebellar infarctions
• 3 month mortality – 40%
in young individuals:
• Arterial occlusion as a result of intracranial vertebral
artery dissection (40%), mainly PICA
• Best outcomes in normal 4th ventricle, normal GCS (80%
good outcome)
• Embolism from a cardiac source primarily from patent
foramen ovale and rheumatic valvular disease.
• 0% good outcome with diminished GCS <8, and

effacement of 4th ventricle • Hematologic disturbances and migraine were responsible
for a few cases
F. Barinagarrementeria, L. E. Amaya, and C. Cantu. Causes and Mechanisms
of Cerebellar Infarction in Young Patients. Stroke, December 1, 1997; 28(12):
2400 - 2404.
Case 3 Case 3
• 61 y/o Female – found in bathtub unresponsive by • Head CT 2:10am: LEFT CEREBELLAR VERMIS,
husband at 12:10am, last seen 5:30-6pm. EMS BRACHIUM PONTIS, AND BILATERAL
arrival 12:43 FSBS 105, withdrew to pain THALAMIC LOW ATTENUATION
• Arrival in ED 1:20am – GCS 7 - Intubated for CONCERNING FOR ACUTE INFARCT,
airway protection given 5mg Versed then started on POSSIBLY DUE TO BASILAR ARTERY
Versed gtt THROMBUS. A FOLLOW UP HEAD CT OR
MRI WITH DIFFUSION WEIGHTED IMAGING
• Labs normal IS RECOMMENDED FOR FURTHER
EVALUATION.
Case 3 Top of the Basilar Syndrome

• Dx: Top of the Basilar
• Diagnosis on chart: CVA / Cerebellar infarct Syndrome
• MICU consultation note time: 5:30am • Blockage of the distal portion
of the basilar artery – most
• In MICU – patient noted to have“non-reactive commonly by embolism
pupils”by MICU resident – Neurology consulted
• Results in infarction of rostral
• Primary patient care transferred to Neurology in brainstem and cerebellar
AM hemispheres
Top of the Basilar Syndrome Top of the Basilar Syndrome

• Distal basilar blockage results in infarction of Posterior Cerebral (PCA)
and Superior Cerebellar arteries (SCA)
• “Top of the Basilar” Syndrome (Anton Syndrome):
• Somnolence
• Results in infarction of midbrain, thalamus, hypothalamus and superior • Memory defects
cerebellum
• Confusion
• Can also affect cerebrum – specifically portions of the hippocampus, • Mutism
parietal, temporal and occipital lobes
• Visual hallucinations
• Bilateral loss of vision with unawareness or denial of
blindness
• Vertical gaze paralysis
• Skewed deviation of the eyes
Posterior Circulation Strokes Posterior Circulation Strokes
• Posterior Circulation Strokes

• Posterior circulation stroke
• 5D’s
• Intraarterial TPA an option up to 24 hours post event
• Dizziness
• Diplopia
• New England Medical Center Posterior Circulation
Registry
• Dysarthria
• 66% initially experienced TIA with 59% progressing to
• Dysphagia
CVA
• Dystaxia
• TIAs are usually multiple, occur over several months and
increase in frequency prior to CVA
Posterior Circulation Strokes Posterior Circulation Strokes
• Posterior circulation stroke • Hospital course complicated by worsening mental

• New England Medical Center Posterior Circulation status and septic shock
Registry
• Trach and PEG placed
• Following CVA – 2.3% mortality, with 75% with minor or
no deficit upon discharge (provided they are treated)
• Patient discharged to LTAC
• Worse outcome if CVA is embolic (58% major disability)
• Decreased LOC, abnormal pupils and quadraparesis are • Unresponsive, some RUE flexion to painful stimulus
predictors of poor outcome (but not always, with
intervention)
• Questions?
• Comments?

INFECTIOUS DISEASE EMERGENCIES
NWS Current Topics in Emergency Medicine Morbidity and Mortality: Infectious Disease Emergencies 74
Learning Objectives
Morbidity and Mortality: Occult • Become familiar with several uncommon but deadly
Infectious Disease Emergencies forms of Occult infectious disease emergencies

• Describe a strategy for screening for occult sepsis
Medical Director
Case 1 Case 1
• 52 y/o AAM – facial swelling for 1.5 days
• 89/60 131 20 96.1 97%
• Swelling over left maxillary area
• PE:
• No fevers, trismus, drooling, odynophasia • ENT: No buccal space infection, induration over left canine, no
trismus, no erythema or exudate
• PMHx: MRDD, Hypertension, CAD, IDDM, • O/W normal
Rheumatoid arthritis, Gout, Sepsis X 2, Respiratory
failure, C-Diff Colitis, Adrenal Insufficiency, RTA type II
• Labs:
• Meds: Lisinopril, Lasix, Pepcid, Neurontin, Risperidal, • WBC 13.2 o/w normal with normal diff
Diclofenac, Trileptal, Iron, ASA • Na 134 K 4.8 Cl 112 HCO3 13 BUN 24 Cr 1.5 Glu 77
• Repeat renal prior to D/C, after intervention - unchanged
• Normal cardiac markers
• Allergies: NKDA
Case 1 Case 1
• Return Visit 48 hours:
• ED course: • “I don’t feel well”
• Given 2 liters of fluid with BP 90/70, HR 100 • Facial swelling and pain improved
• General painless malaise, and non-productive cough
• I+D of Canine space without return of pus
• Followup arranged with PMD • 90/60 120 18 100.2 90%RA
• Discussed with OMFS – dental clinic will call patient • PE: general malaise, o/w normal
• Clindamycin for 10 days • Labs:
• Discharge vitals: 90/65 93 22 98.1 96% RA • WBC 11.8 - 21% Bands
• Renal - HCO3 10, BUN 40, Cr 2.4
• Lactate 0.8
• Ammonia 132
• CXR: R>L bibasilar ASD
Case 1 Case 1
• Return Visit 48 hours: • Hospital Course:

• ED course: • Admitted to MICU – never intubated, pH 7.18
• BP trended down to 72/42 • Started on hydrocortisone for adrenal insufficiency
• 2L Normal Saline Bolus • Continued on Vancomycin, started on Unasyn for
facial cellulitis
• R Subclavian TLC and R radial Arterial Line • Rehydrated for ARF
• Cefepime, Vancomycin, Tobramycin • Started on Bicitra for RTA Type II
• Quantitative sepsis resuscitation initiated • Facial CT – negative for abcess
• MAP in 50’s – started on Levophed • Admitted 6 days – third course of sepsis
Case 1 Occult HIV Infection

• Post-Hospital Course
• Re-admitted for sepsis in September and October • Recurrent episodes of infection or sepsis – consider
• Discharged after admission for fourth course of Sepsis ordering HIV screen
• What diagnostic test was performed that revealed cause of

recurrent sepsis episodes?
• Not all hypotension is just sepsis – consider stress
dose steroids
• HIV positive – CD4 count 136
Occult HIV Infection SIRS / Sepsis Diagnosis
• Pay close attention to abnormal vital signs and lab • SIRS

values • (Systemic Inflammatory Response Syndrome)
• 2/4 criteria necessary for diagnosis

• Know the SIRS criteria by heart, and think twice • Temp > 38 or < 36
about sending someone home if they meet SIRS • HR > 90
criteria • WBC > 12,000 or < 4,000 or > 10% bands
• RR >= 20 or PCO2 <= 32
SIRS and Sepsis Sepsis Definition
Global Tissue • Sepsis

Bacteremia
Hypoxia
Other
• SIRS + infection
• (documented or highly suspected)
Fungemia Trauma
INFECTION SEPSIS SIRS
• Severe Sepsis
Burns
• Sepsis + organ dysfunction
Viremia
Other Pancreatitis
• Septic Shock
• Severe Sepsis + persistent hypotension
Case 2 Case 2
• 18 y/o G3 P1021 with RLQ abdominal pain X 4-5 days. • SocHx: Sexually active without OCP / Barrier contraceptives
LNMP one week ago. Radiates to back and associated with
dysuria and frequency
• ROS: Denies h/o STD
• PMHx: Ectopic pregnancy – 2 months ago s/p L salpingo- • 117/84 109 18 97.8 100%RA
oophrectomy, Asthma, SCD, Bipolar d/o, R forearm abscess
• PE: Mild distress, obese abdomen, RLQ TTP, voluntary

• Meds: Keflex Allergies: Morphine - itching guarding, no rebound, open os with “serosanguinous”
drainage, no CMT, R adnexal TTP, no mass
Case 2 Case 2
• Labs: • ED Course:
• Parenteral narcotics and toradol given with minimal relief of
• POC renal - normal pain
• U/A – small LE, no micro mentioned • Patient“got ornery”about pain not being treated – wanted
• BHCG negative to leave – given 10 Percocet and Motrin
• LE noted but not treated – Urine micro not noted
• CT A/P with PO/IV: normal appendix, R ovarian cyst
2.5cm, incidental umbilical hernia
• Differential noted: Ectopic, Appendicitis,
UTI/pyelonephritis, Trauma, Ovarian Cyst
• D/C vitals: 118/75 90 16 97.8 99%RA • Dx: Right ovarian cyst, Incidental umbilical hernia,
Abdominal Pain NOS
Case 2 Case 2
• Return Visit: • Return Visit:

• Returned 24 hours later • DNA probe noted to be GC and Chl positive from prior
visit, wet prep positive for Trichomonas
• Notes BLQ abdominal pain with vaginal discharge and • U/A - + nitrates, small LE, many bacteria, 5-10 WBC,
dysuria – began two days ago –“mucousy”discharge 3-5 Sq Epi
• WBC 14 Hb 12 Hct 39 Plt 275 Segs 85%
• 71/46 142 20 102.7 97%RA • Renal: Bicarb 18 Glucose 128
• AXR: No free air
• PE: Purulent vaginal discharge with CMT, R>L
adenexal TTP
Case 2 Pelvic Inflammatory Disease
• ED Course: • PID afflicts more than 1 million women each year and
generates annual health care costs of approximately $ 4.2b
• 2 L NS
• Ampicillin, Gentamicin, Clindamycin • 250,000 hospitalizations per year
• Tylenol, Toradol, Morphine, Phenergan
• Admitted to OB/GYN
• Clinical symptoms:
• Bilateral lower abdominal pain
• Dx: PID, possible TOA, UTI
• Vaginal discharge
• Did well as inpatient
• Low back pain
• Irregular vaginal bleeding
Pelvic Inflammatory Disease Pelvic Inflammatory Disease
• Gonorrhea and chlamydia associated • Fewer than 50% of women with acute PID
infections are more likely to cause symptoms have a white blood cell (WBC) count more
toward the end of menses and in the first 10 than 10,000
days following the menstrual period
• Clinical diagnosis of PID can be difficult and • An elevated WBC count is not a CDC
imprecise due to the nonspecific nature of criterion for diagnosing PID
the presenting signs and symptoms
• Due to the serious potential complications of • Institute empiric treatment of PID when a patient
untreated PID and the endemic prevalence has all of the following minimal clinical criteria in
the absence of an established cause other than PID:
of the infection, the Centers for Disease
• Lower abdominal tenderness on palpation
Control and Prevention (CDC) has adopted
• Adnexal tenderness
an approach to maximize diagnosis by using
• Cervical motion tenderness
minimal criteria
• Additional criteria, especially in women with more • Facultative anaerobes consistent with the
severe clinical signs, can be used to increase the endogenous vaginal and perineal flora have been
specificity of the diagnosis identified as potential etiologic agents in PID.
• Oral temperature more than 38.3°C (101°F) These include the following flora:
• Abnormal cervical or vaginal discharge • Gardnerella vaginalis
• Elevated erythrocyte sedimentation rate (ESR) • Streptococcus agalactiae
• Elevated C-reactive protein • Peptostreptococcus species
• Laboratory documentation of cervical infection with N • Bacteroides species (other than Bacteroides fragilis)
gonorrhoeae or C trachomatis • Genital Mycoplasma and Ureaplasma species
• Coliforms
Case 3
• 55 y/o Male with h/o pancreatitis, gout and

IVDA presents complaining of headache and
RUQ abdominal pain
• Last used IV drugs six hours ago – now with mild
headache and mild RUQ abdominal pain
• 144/113 158 24 101.9 95%
• CXR: Right basilar atelectasis
• Given tylenol, 3L NS and azithromycin PO
• Dx: Pneumonia
• HR 106 upon discharge
Case 3
• Represents 24 hours later with left sided chest

pain to same physician
• 156/102 101 18 96.9 97%RA
• Chest pain reproducible upon palpation
• CXR: Slight worsening of right basilar atelectasis –
note states ASD
• EKG unchanged
• Given 30mg toradol – good relief of pain
• Discharged home with Dx: Chest Pain NOS – likely
chest wall strain – Ibuprofen for pain
Case 3 Case 3
• Represents two days later with chest pain and • Admitted to floor – started on IV Fluoroquinolone for
tachycardia pneumonia
• Left sided with radiation to left neck and arm with • Fever to 103 on floor one day post admission with
SOB, N/V and DOE mental status changes
• 146/102 132 20 99.5 96%RA • LP performed – elevated opening pressure, with
• EKG: unchanged elevated WBC with neutrophil predominance
• CXR: right basilar atelectasis resolved • Started on vanc, ceftriaxone, unasyn and acyclovir
• Given ASA, NTG, morphine, ativan • Intubated on floor for respiratory failure
• Admitted to Internal Medicine service • Blood cultures grew out Klebsiella
• MRI of spine performed secondary to prominent left
sided weakness on neuro exam
Case 3 IVDA Associated Infections
• Radiology reading: • Gordon RJ and Lowy FD. Bacterial Infections in

• 1) EPIDURAL ABSCESS EXTENDING FROM C3 TO T1 WITH
MODERATE LEFTWARD CORD COMPRESSION MOST Drug Users. N Engl J Med 353;18 November 3,
SEVERE AT THE C6-C7 LEVEL.
• 2) C6 AND C7 VERTEBRAL BODY EDEMA AND
2005
ENHANCEMENT. ALTHOUGH THIS MAY BE REACTIVE,
OSTEOMYELITIS IS NOT ENTIRELY EXCLUDED. THERE IS
NO ASSOCIATED DISC ENHANCEMENT AT THE C6-C7
LEVEL.
• Hospital course
• Epidural abscess drained by neurosurgery
• Tracheostomy placed required persistent ventilation for respiratory
failure
• Transferred to LTAC for rehabilitation
IVDA Associated Infections IVDA Associated Infections
• Be concerned for bacteremia in any IVDA with fever or • Skin, soft-tissue, and skeletal infections
abnormal vital signs • Staphylococcus aureus (including community-associated
MRSA)
• Be on the look for immunocompromise
• Streptococcus species — groups A, C, and G
• Discovery of one infection should trigger further examination • Streptococcus anginosus (milleri)
for other sources of infection • α-hemolytic streptococci
• Most common: • Pseudomonas aeruginosa
• Skin and soft tissue • Other gram-negative bacteria (Escherichia coli, enterobacter,
klebsiella, proteus, serratia)
• Musculoskeletal
• Oral anaerobes (bacteroides species, Eikenella corrodens,
• Endovascular fusobacterium species, peptostreptococcus species)
• Pulmonary • Mycobacterium tuberculosis
• Sexually Transmitted
IVDA Associated Infections IVDA Associated Infections
• Infective endocarditis • Pulmonary infection Community-acquired pneumonia

• S. pneumoniae,
• S. aureus (including community-associated MRSA)
• S. aureus,
• Streptococcus species (groups A, B, G, and others) • Haemophilus influenzae,
• P. aeruginosa • Klebsiella pneumoniae
• Other gram-negative bacteria • Chlamydia pneumoniae
• Mycoplasma pneumoniae
• Toxin-mediated disease • Legionella pneumophila
• Oropharyngeal flora (i.e., due to aspiration)
• Clostridium botulinum
• Opportunistic pulmonary infections (associated with HIV disease)
• C. tetani • M. tuberculosis (including multidrug-resistant tuberculosis)
• Other clostridia species (C. sordellii, C. novyi, C. • M. avium complex
perfringens) • P. aeruginosa
• Group A streptococcus • Nocardia species
• S. aureus • Rhodococcus equi
IVDA Associated Infections Case 4
• Sexually transmitted infections • 38 year old WF with complaint of low neck/upper back pain
for 7 days
• Chlamydia trachomatis
• No known injury
• Neisseria gonorrhoeae
• Treponema pallidum • Recently moving furniture
• C5-T1 region posteriorly
• “Aching Pain” 10/10 without medication, with Vicodin and
Ibuprofen 2/10
• Vital Signs: 105/70 87 18 98.2

Case 4 Case 4
• Worse with movement in all directions • Past Medical History:

• Ectopic Pregnancy - Remote
• Occasional difficulty swallowing
• No recent fevers, sorethroat, chest pain, shortness of

breath • Medications:
• Vicodin and Ibuprofen PRN
• Convinced to come in by family – did not want to
come
• Allergies:
• None
Case 4 Case 4
• Social History: • Neck pain as above, worse with movement
• Drinks EtOH occasionally • Occasional difficulty swallowing

• Uses Cocaine frequently, last 2-3 weeks ago • No sorethroat
• Denies current or past IVDU • No fevers, chills
• Smokes two packs per day tobacco
• No chest pain
• No SOB
• Family History: • No headache
• None pertinent
• No weakness, numbness, paresthesias, gait disturbances,
bowel/bladder incontinence
Case 4 Case 4
• General: Disheveled, thin, frail, sleepy white • Neck:

female, easily arousable, A+OX4 • No LAD
• Eyes: WNL • Normal Thyroid
• (+) TTP over posterior midline and paraspinal
• HEENT: structures at C5-C7
• Multiple healing scabs and scars on face
• Full range of motion with pain
• Clear oropharynx
• No tonsilar edema, erythema, exudate, or • Cardiopulmonary: WNL
cobblestoning
Case 4 Case 4
• Skin: Rash on face, o/w WNL • β-hcg – negative U tox - Cocaine
• Musculoskeletal: WNL • U/A – Mod LE, Mod Bact, 10-20 Squamous

Epithelial, 20-50 WBC, (+) Trichomonas
• Neurologic: Normal sensation, no gait disturbance,
normal speech, normal strength • \ 11.4 /
• Psychiatric: Somewhat oppositional, sleepy but • 7.8 -------- 242 N 76 L 14.7 o/w WNL
arousable, intact judgement
• / 33.6 \
• ESR 60 CRP 14.7
Case 4 Case 4
• CXR: WNL • What would you do now?
• Cervical Spine Series:

• Wet read: Normal
Case 4 MRI
• MRI recommended upon consultation with

Neuroradiologist (Fellow)
• Pain control with Motrin and Tylenol PO

Case 4 Case 4
• Wet Read: Normal • Patient called and returned by EMS

• Retroread (8:30am next morning):
• Retropharyngeal edema/soft tissue swelling from C1-C6 with • Admitted to ENT with Neurosurgery, Infectious
small focal abcess at C5-C6 Disease consultations
• Enhancing epidural phlegmonous tissue from C4-C5 to C6 level, • Placed in Miami J collar
without any focal epidural abcess or cord compression, most
consistent with inflammation / infection • PICC placed – IV Unasyn given
• Non-visualization of the anterior longitudinal ligament with • Discharged to Nursing Facility – Unasyn for 4 weeks
questionable extension of the infection / inflammation into the
C5-C6 intervertebral disc
Retropharyngeal Abscess Retropharyngeal Abscess

• ENT consultation is mandatory
• Clinical Presentation
• Sore throat, fever, neck stiffness, and stridor • Operative drainage and airway management
• Bacterial Causes
• Aerobic organisms, such as beta-hemolytic streptococci and
• Originally thought to be a disease primarily of Staphylococcus aureus
• Anaerobic organisms, such as species of Bacteroides and Veillonella
children • Gram-negative organisms, such as Haemophilus parainfluenzae and
Bartonella henselae
• Incidence in adults is rising
• Treat with antibiotics for oropharyngeal flora
• Clindamycin
• Extended spectrum penicillins
Retropharyngeal Abscess
• Complications • Questions?
• Airway obstruction
• Mediastinitis (up to 50%)
• Aspiration pneumonia • Comments?
• Epidural abscess
• Jugular venous thrombosis
• Necrotizing Fasciitis • Thank you.
• Sepsis
• Erosion into Carotid Artery
RESUSCITATION SEQUENCE INTUBATION

Salim R. Rezaie, MD
NWS Current Topics in Emergency Medicine Resuscitation Sequence Intubation 85
Critical Care Updates:

Twitter: @srrezaie
Resuscitation Sequence Intubation Facebook: REBEL EM
Salim R. Rezaie, MD
@srrezaie
No
Financial
Disclosures
www.rebelem.com
John
92/57
143 HOp Killers

38
Oxygenation (Hypoxemia)
84% RA
102.1
Credit to Scott Weingart

Resuscitate Before You Hypotension Kills

Intubate
11.7
in –254.0%
- 60
Intervention 1: Sedatives Low &

Paralytics High
OR
Succinylcholine
2mg/kg IV
Ketamine Rocuronium
0.5mg/kg IV 1.6 mg/kg IV
Intervention 2a: Push Dose

Pressors Intervention 2b: Peripheral Pressors
+
Epinephrine
10mcg/mL
1mL Epi
9mL Saline (100mcg/mL)
Peripheral Pressors Bottom Line

12 - 24 Hr 18
6 - 12 Hr 9
4 - 6 Hr 2
Proximal PIV
<2 – 4 hrs
2 - 4 Hr 3
< 2Hr 4
Extravasation Events
Rapid Sequence Awake Intubation

Intervention 3: Awake Intubation
EZ-Atomizer MADgic Device
Tongue Depressor Intubate w/ ETT
Credit to Scott Weingart

Oxygenation Kills
Push Dose Epi

+
ROCKETamine
Ketamine 0.5mg/kg IV
Rocuronium 1.6mg/kg
NO DESAT Shunt Physiology

02 Sat
≥95%
Credit to Richard Levitan
Intervention 1: BVM + PEEP Valve Apneic CPAP Recruitment
If 02 Sat
≤95%
Intervention 2: DSI DSI Evidence

Mean O2 Sat Increase
89.9%
to
98.8%
ZERO Complications
Intervention 3: BUHE Intubation

BUHE Evidence
Intubation Related Complication
Supine vs BUHE
22.6% 9.3%
NC 15LPM
+
BVM 15LPM
+
PEEP Valve
15cmH20 pH Kills
Bicarbonate Therapy: Animal Bicarbonate Therapy: Human

Trials Trials
↑ Serum pH BUT ↓Intracellular pH ↑ Serum pH BUT NO ↑ BP or Pressor
Response
Bicarbonate Therapy Bottom Intervention 1: VAPOX

Line
No Improved Hemodynamics Ventilator-Assisted
PreOxygenation
Before Induction Medications

SIMV + PSV
RR TV Fi02
0 8cc/kg 100%
PS PEEP IF
5-10 5 30
EtCO2 Monitoring
Induction
Push RSI Meds

Jaw Thrust
RR = 12
Intubation
Intubate
Ventilator-Assisted
RR = 30 PreOxygenation
IF Rate = 60
Check ABG
Resuscitation Sequence
Intubation Questions?
Oxygenation (Hypoxemia)
NOVEL USE OF BEDSIDE ULTRASOUND

NWS Current Topics in Emergency Medicine Novel Use of Bedside Ultrasound 93
You Can Do That With Ultrasound?

Novel Uses of Bedside Ultrasound
You Can Do That With Ultrasound? Goals
Novel Uses of Bedside Ultrasound Review novel uses of bedside
ultrasound
Review literature supporting these
Sumeru Mehta, MD, MPH, FACEP uses
Review technique
Review normal and abnormal
You Can Do That With Ultrasound?

Novel Uses of Bedside Ultrasound Evolving Applications
No COI with Sonosite Inc. •Chest Trauma
Not covered •Pneumothorax
Physics and instrumentation •ICP monitoring
Hands on practice •Retinal Detachment
Regional anesthesia using ultrasound •FLASH exam
Other emerging applications
•Lumbar puncture
Chest trauma… Ultrasound For Pneumothorax

 Year Author N Sens
 2005 Blavis 53 98%
 2004 Knudson 328 92%
 2002 Rowan 27 100%
 2001 Dulchavsky 382 95%
 1999 Lichtenstein 187 100%
 1996 Sistrom 27 73%
 1995 Lichtenstein 111 95%
 1987 Wernecke 28 100%
Ultrasound For Pneumothorax Ultrasound For Pneumothorax
 Technique
 HF probe
 Pt is supine
 357 patients (47 with occult PTX)  Sag in 3rd-4th IC

space
 Pleural line
 3 signs were observed:
 Rib shadow
 Lung sliding  Pleural lung sliding
 To-and-fro
 A-line movement of visceral
 Lung point  Comet tails
 Hyperechoic
 Feasibility was 98% reverberation atrifacts
 Seashore sign
 For diagnosis for occult PT, US reduced the need for CT
Ultrasound For Pneumothorax:

Seashore Sign
L Lung - Normal R Lung w/ PTX
Case 1
 CC: L spont pneumo
 PMH: Spont L pneumo X 6
 VS: 117/67 68 97.9 (O) 18 100%RA
 PE: slightly diminished on left
 CXR: no PTX
 Options:
 Discharge with negative CXR
 Admit for serial CXR and consult
 CT Chest to r/o occult pneumothorax
 Ultrasound to r/o occult pneumothorax
Right lung Right lung
Left lung Left lung
Case 2 Left
 CC: " lung collapse again", right sided
shoulder and chest pain. Symptoms began
@08:00am this am.
 Past Medical History: right pneumothorax
 VS: 139/78 86 17 98% RA 98.7
 PE: decreased bs in upper lobe of right lung
Left Right
Right Left lung
Right lung Ultrasound for ICP Monitoring

 Emergency Department Sonographic Measurement of
Optic Nerve Sheath Diameter to Detect Findings of
Increased Intracranial Pressure in Adult Head Injury
Patients. Annals of Emergency Medicine 49(4). Tayal et al.
 59 pts with CHI – blinded prospective

 8 pts with CT evidence of elevated ICP and OND > 5 mm
 US optic nerve findings were 100% sen and 63% spec
 Gold std: CT findings by blinded radiologist c/w elevated
ICP
New study
 A review of 8 papers.
 “In patients with head injuries, a bedside US measurement of the ONSD > 5
mm has high sensitivity and specificity for detecting raised ICP
 Systematic review and meta-analysis
 Six studies
 231 patients
 Conclusion: US of ONSD showed good diagnostic accuracy
 Confirmed threshold of ONSD > 5 mm to detect ICP > 20 cm H2O for detecting ICH
 Using direct measurements of ICP as measured by ventriculostomy.
Ultrasound for ICP Monitoring Ultrasound for ICP Monitoring
Ultrasound for ICP Monitoring Ultrasound for ICP Monitoring
3mm
<5 mm
Ultrasound for ICP Monitoring Technique
Technique
Ultrasound for Retinal Detatchment
 Risk factors
 advancing age, previous cataract surgery, myopia, and trauma
 S / Sx
 light flashes, floaters, peripheral visual field loss, and blurred
vision
 Early intervention facilitates prevention of retinal
detachment after formation of retinal breaks and
improves visual outcomes of retinal detachment surgery
Cornea
Iris
Vitreous
Retina
Optic nerve
c L
V
FLASH examination FLASH examination

Focused  2001. The American Journal of Emergency Medicine, 19(4). Rose
Limited
et al.
 Prelude to a larger prospective study
Assessment by  Describes the utility of US to rule of pericardial effusion, free

fluid in the abdomen, and AA.
Sonography In Undifferentiated  Three cases were presented.
Hypotension
Randomized Controlled Trial of Immediate vs. Delayed Goal-directed Ultrasound to

Identify the Etiology of Nontraumatic Hypotension in Emergency Department Patients .
2004. Academic Emergency Medicine 11()5. Jones et al.
FLASH Protocol
 Subcostal
 Tamponade (RV collapse)
 IVC
 BACKGROUND: Utility of a clinical algorithm incorporating goal-directed
 Look at size and collapse
US protocol in the ED evaluation of non-traumatic symptomatic  >50% collapse is abnormal suggesting low intravascular volume
undifferentiated hypotension.
 Parasternal Long axis cardiac view
 METHODS:Randomized controlled trial of immediate versus delayed goal-  LV function(judged by visual inspection of gross wall contraction)
directed US.  Apical 4-chamber view
 The US protocol consisted of seven torso (cardiac and abdominal) views.
 Visual estimation of ventricular size and qualitative function
 Group 1 (immediate US) received US protocol at time 0.
 Hepatorenal recess view
 Group 2 (delayed US) received US protocol 15-30 min later.  Free intraperitoneal fluid
 RESULTS: 184 were included. At 15 min, correct final diagnosis in 80% of  Pelvis
group 1, versus 50% of group 2.  Free intraperitoneal fluid
 CONCLUSION: Incorporation of a goal-directed ultrasound protocol in the  Abdominal Aorta
evaluation of non-traumatic symptomatic undifferentiated hypotension results  Aneurysm
in fewer viable diagnostic etiologies and more accurate physician impression of
final diagnosis.
IVC measurement technique IVC measurement technique
FLASH Protocol Bad Tattoo # 1
 Free fluid present ? Y/N

 What is the RV size? Normal or Dilated
 Pericardial effusion? Y/N
 Tamponade physiology Y/N
 Aortic aneurysm? Y/N
 Free fluid present Y/N
 Evidence of IVC collapse? Y/N
 LV function
Hyperdynamic/NL/impaired
Bad
US-Guided Lumbar Puncture
Tattoo
#2
How Good Are We???
% of n
First Pass 33
Simple Re-direction 22
New Skin Puncture 20
26%
Second Interspace 17
Failure 9
Strout et al, Journal of Emergency Nursing, 2004
* N = 90
How Good Are We???

% of % of
patients* patients**
Head to Head…
First Pass
33 42
55%
vs.
Simple Re-direction
22 33 75% Success Failure
New Skin Puncture
20 20 Palpation 73% 27%
Second Interspace
17 0 26% *
Failure
9 4
vs. Ultrasound 96% 4%*
4% Nomura et al, ACEP 2005 * p=0.003
*Strout et al, Journal of Emergency Nursing, 2004. N = 90 N = 66
** Ferre et al, Journal of Emergency Medicine, 2009. N = 39
Transverse Midline Saggittal Midline

Spinous Process
Spinous process
Lamina TW Sweeney©
TW Sweeney©
Dura
Subarachnoid
Spinous Process Space
Midline
Paramedian Find L4-L5 Interspinous Space
Lamina Lamina
TW Sweeney©
TW Sweeney©
Epidural
Ligamentum
Space flavum
Subarachnoid space
Dura
Transverse Midline of L4 Spinous Process Identify True Midline

The Key = Shadow and Mark
Mark Midline Sagittal Midline

Mark Middle of Interspinous Space Sagittal Paramedian
Measure Depth Ready to go…

Measure depth to dura mater as estimate of minimum needle distance
 Site of needle insertion… X-marks the spot
 Angle of needle advancement
 Depth to the dura

4.5 cm
Technique… Upcoming Application of Ultrasound

 Regional anesthesia
 Airway confirmation
 Musculoskeletal
 Fractures, tendon injuries,
 US in space??
 FAST at MACH 20: Clinical Ultrasound Aboard the
International Space Station. J of Trauma
How can you incorporate this into your

clinical practice…to improve your game? Yes…”we talkin’ about practice.”
Ultrasoundpodcast.com
Sonosite.com
One minute ultrasound
Practice
Practice
Practice
TWO FOR THE PRICE OF ONE: TRAUMA IN PREGNANCY

NWS Current Topics in Emergency Medicine Two for the Price of One: Trauma in Pregnancy 106
Introduction
 Maternal and fetal well-being
Two for the Price of One:
Trauma in Pregnancy
 Team approach to care
Sumeru G. Mehta, MD, MPH, FACEP
 Stress on providers
Topics Covered Pregnancy and Trauma
 Epidemiology
 Frequent cause of non-ob maternal death
 Physiology
 6-7% of all pregnant women experience some “accidental” injury
 Management
 Contributes to fetal death > maternal death
 Special Issues  Common initial episode of domestic violence
 PITFALLS
Etiology of Severe Trauma in Pregnant Women Maternal Death due to Medical Causes and Injuries
(Lavery and Staten-McCormick, 3/95) Dannenberg et al ‘95
5% Other
Causes Number % of total
MVA 409 63.9
7% Drug OD
Falls 123 19.2 12% MVA
Penetrating 64 10.0
Blunt 37 5.8 13% Suicide
Burns 7 1.0 61%
Maternal Mortality 12 1.9 39%

Fetal Mortality 55 10.0 63%
Homicide
N=115
Fetal Death Predictors of Fetal Compromise

 Obstetrical findings  Fetal death
 Vaginal bleeding  ISS – 30
Maternal death #1 cause of fetal death  Uterine tenderness  Direct utero-placental
injury
 Uterine contractions
 Maternal pelvic fracture
 Maternal shock  Review of 4 case series
 Ruptured membranes  Severe maternal head
 Pelvic fx, retroperitoneal  6 maternal deaths / 57 fetal
injury
deaths
hemorrhage,  Cardiotocographic  Maternal acidosis
 Remaining 51:
 80% fetal mortality signs
 1/2 minor trauma
 Abruptio placenta  Fetal tachycardia
 abruptio placenta
#2 cause of fetal dealth  Fetal bradycardia
 25% direct fetal injuries
 Late decelerations
Predictors of Pregnancy Outcome Predictors of Pregnancy Outcome

 Retrospective review (1986-1996)  Potential Predictors of non-viable pregnancy
outcomes:
 61 pts hosp post-trauma  Maternal hypotension
 Most 3rd trimester (59%)  Fetal bradycardia
 MVC most common
 1 maternal death and 8 feto-neonatal deaths
 Other maternal and fetal physiologic variables
 Maternal factors are poor measures of fetal well-being and are
 ISS unable to predict fetal outcome
 Hypotension
Baerge-Varela, Y, Zietlow, SP, Bannon, MP, et al, Trauma in pregnancy, Mayo Clinic
Proceedings, 2000;75(12): 1243-48.
Trauma in Pregnancy Cardiovascular Alterations
 Epidemiology  High Flow/Low Resistance State

 Increased CO (HR, SV)
 Physiology  20-30%, 1-1.5 L/min by 10 wks
 Decreased SBP and DBP until 3rd trimester
 Management  Down 10 -15 mm Hg
 Drop in HCT 31-35%

 Special Issues
 Decrease in CVP
 PITFALLS
Hematologic Alterations Respiratory Alterations

 Decreased Lung Capacity
 Increased  RV, minute ventilation diminished
 Blood Volume  TV increased
 Dilutional Anemia
 Chronic Compensated Respiratory Alkalosis
 WBCs
 Progesterone stimulation of respiratory centers
 Clotting Factors:
 Increased RR, HCO3 excretion
 Fibrinogen, VII, VIII, IX, X  No change or slight increase in pH
 ESR
 Elevated diaphragm ~ 4 cm
 Release of thromboplastic material
 Increased maternal O2 consumption
Gastrointestinal Alterations Trauma in Preganncy

 Physiologic Ileus  Epidemiology
 Decreased motility and gastric emptying
 Physiology
 Displaced intra-abdominal contents
 LESS reliable peritoneal signs  Management

 Increased alk phos (x 2)  Special Issues
 PITFALLS
Management:
Trauma Protocol Maternal Assessment and Treatment
A  ATLS...Alter based on maternal physiology

B  100% O2, fluids, L lat. decubitus position
 Hx: LMP, EDC, current and previous pregnancy status, seat belt
C use
D  PE: Fundal height, uterine tenderness or contractions, fetal
mvmt, PELVIC (amniotic fluid, vaginal bleeding, bony injuries) or
E not?
 Fetus
Airway Difficulties in the

Fetal Assessment and Treatment Parturient
 Rx: OOOOs, mom
 Everywhere
 Fo2-HgB dissociation curve shifted to L
 Uterine hypo-perfusion precedes maternal shock  Tongue, supraglottic tissues, airway lumen
 PE: FHT, fetal movement  Mucosal engorgement and friability
 Tests  Increased aspiration risk

 Ultrasound: fetal HR, ? Abruption
 Blind nasal intubation: relatively contra-indicated
 Electronic monitoring: fetal distress, uterine irritability
 As few attempts as possible!
Intubation Concerns RSI

• Partially compensated  Cricoid pressure
Buffering capacity
respiratory alkalosis  Pre-oxygenation
• Increased mO2  Induction agent

 Thiopental or etomidate
consumption Rapid onset hypoxia
• Decreased lung  Paralytic agent
capacity  Succinylcholine
 Vent settings
• Decreased GI motility  Pco2 = 30 mm hg
& gastric emptying
Aspiration risk
• Displaced intra-
abdominal contents
Cardiovascular Compromise: Fetal

Compromise Mechanical compression
 Uteroplacental mass passive low-resistance

 10% systemic blood volume by term
 Flow based on maternal perfusion pressure Lateral  CO reduced 10-30%
Supine Compression of great

 α and β adrenergic agents 
vessels
 Vasoconstriction
 Decreased uterine blood flow
Support maternal circulation Avoid infra-diaphragmatic venous access

CPR During Pregnancy
 Defibrillation NOT contraindicated

Avoid  Vasopressors should be used despite utero-placental
vasoconstriction
Aorto-caval  Before 24 wks: no change

 After 24 wks:
compression  Avoid aorto-caval compression
 L lateral decubitus, manual displacement, wedges/cushions
 Chest compressions higher on sternum and with patient
tilted 30-450
 Consider emergent cesarean section
RADS absorbed per study in unsheilded

Radiation... how much is OK? gravid uterus
 < 5-10 Rads total thought  Effect on fetus depends on:

to be safe  Developmental stage: STUDY Dose range (Rads)
organogenesis 9-60d C-spine negligible
 15 Rads  Exposure time Chest AP 0.0003-0.0043
 6% severe MR  Dose delivered Pelvis AP 0.142-0.486
 <3% childhood CA  Dose absorbed Abdomen AP 0.133-0.451
 15% small head size IVP 0.202-0.815
Spine AP 0.154-0.527
Femur 0.0016-0.012
Cystography 0.135-0.441
CT Head <0.05
CT Thorax <1.0
CT Upper abdomen <3.0
CT Lower abd/Pelvis 3-9
Risk of radiation
 Any radiation is slight increased risk
 Early pregnancy
 0-2 wks gestation
 Slight increased risk for SAB but NO increased risk for
congenital malformations (not dose dependent:
stochastic effect)
 2-15 wks gestation
 Small increased risk of teratogenic mutations with
exposure to intermediate and high dose radiation (dose
dependent: deterministic effect)
How about Ultrasound?

 No risk of radiation exposure
 US is Non-teratogenic
 Few studies looking at ability to detect
intraperitoneal fluid in pregnant patient
 Goodwin H, et al. J. Trauma 04/01
 127 pts, 7 intra-abd inuries, 6 hemoperit.
 5/6 identified with US
 Sensitivity 83% (95% CI 36-100%)
 Specificity 98% (95% CI 93-100%)
 Similar to non-pregnant patients
Trauma in Pregnancy Trauma Unique to Pregnancy
 Epidemiology  Increased risk of fetal-maternal hemorrhage
 Abruptio placenta
 Physiology
 Uterine rupture
 Management  Massive retroperitoneal hemorrhage
 Special Issues
 PITFALLS
Feto-maternal Hemorrhage Keep It Simple

 Transfusion of fetal blood into maternal circulation
 4.5 X > injured (10-30% traumas)
 Significant in >30% severe trauma Give RhoGAM to all Rh
 90% inconsequential
 Results: fetal anemia, IUFD, isoimmunization of Rh – negative women.

mother (0.1 CC fetal blood)
Leave the KB test to the Consultant.

Abruptio Placenta
 Premature separation of placenta from uterine wall
 40-50% severe injuries, 1-6% minor
 Most common cause fetal/neonatal loss after trauma
 Classic signs (< 50%) : vaginal bleeding, uterine
cramping/contractions, maternal hypovolemia,
expanding uterine size, FHR abnormalities
 Death rate: maternal <1%, fetal 20-30%
 Soon after traumatic event
 Within 48 hrs
 26% concurrent
Detection of Placental Abruption Uterine Rupture
 Cardiotocographic monitoring
 Detects contraction
Rare > 0.6%
 Monitors FHR
 Acts as VS for mother Prior C-Section
 Begin as soon as Mom is stabilized
 4 hours if NO abnl Sx/Sx (after 22-24 wks)
 Extend to 24 hrs if > 4 contractions in 1 hr Maternal mortality – 10%
 US not helpful (0nly 50% sensitive)
Fetal mortality – 70%
Retroperitoneal
Uterine Rupture Hemorrhage
Maternal hypotension Pelvis fractures

Lethal to fetus
Lethal to mother
Acute Abdomen
Maternal Injury Emergent/Perimortem C-section
 Seat Belts
 Decrease maternal  When ACLS fails and fetus may be viable
injury and ejection
 Goal: delivery within 4-5 minutes of arrest
 3-point restraint
 Consider viability of fetus
 Improper application
 Institution dependent
 Abruption / fetal injury
 Proper placement  Consider if arrest due to untreatable problem
 Should not cross the
uterus
Perimortem C-section
• Most experienced.
• CPR initiated at the time
of arrest and continued
through the procedure. 42 8
7
• Timing
• Delivery within 5 min
3
• Gestational age
• Wt directly correlates with 1
survival
Katz VL at al. Obstet Gynecol. 1986
Perimortem C-section
Abuse and Pregnancy...Morbidity Trauma in Pregnancy

 5.5-17% women are victims of abuse during  Epidemiology
pregnancy (McFarlane ‘92, Hilliard ‘85, Berenson ‘91, Amaro ‘90)
 Long term sequelae are not clear  Physiology

 Abuse during pregnancy is a strong indicator of  Management
ongoing or prior abuse
 >1/2 of women abused during pregnancy had been  Special Issues
victims of prior abuse
 Battering during pregnancy is associated with an  PITFALLS
increased risk of homicide
Pitfalls Pitfalls
 Failure to recognize and treat supine hypotension.  Neglect of maternal injuries
 Inadequate volume replacement  Failure to recognize abruption
 Failure to recognize intra-abdominal injury  Failure to monitor fetus

Questions??
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NWS Current Topics in Emergency Medicine Conquering the World of Medical Education With FOAMed 117
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ALL BLEEDING STOPS SOMETIMES:

HEMORRHAGE CONTROL IN TRAUMA
NWS Current Topics in Emergency Medicine All Bleeding Stops Sometimes: Hemorrhage Control in Trauma 124
Hemorrhage Control in Trauma Outline

Sumeru Mehta, MD, MPH • Epidemiology
• Prediction models
• Coagulopathy
• Resuscitation
• Rational for products
• Summary
• Conclusions
1 2
Injury Severity Score Successful Strategy for

NTDB=10 L1TC=12 Severe=15+ Combat=23
Region Injury AIS Square Top 3

Hemorrhage Control includes…
• EMS/ED
• Anesthesia
Head and Cerebral 3 9
Neck Contusion • Surgery
• ICU
Face No injury 0
• Transfusion / Blood bank
Chest Flail Chest 4 16
• Very small numbers
Abdomen Minor liver Cont 2 25 – 1-2% of all civilian trauma admissions
Spleen rupture 5 – High mortality
Extremity Femur Fx 3 • Can not be done in isolation
– Has to work equally well at 1200 and 0200
External No injury 0
3 4
Coagulopathy of Trauma 55%
…..Balance…..
40%
Coag
Majority (90%) are

Pro-thrombotic Minority (<5%) at 5% Hyper Norm Hypo
Need risk of MT
anticoagulation
Bleeding / Death 0 0.5 1 1.5 2 3 4 5 6 7
DVT / PE Days
Brohi K. Acute Traumatic Coagulopathy, J Trauma, 2003

Gando S. Activation of the TF Dep Coag Pathway in ARDS Patients after Trauma. 1999.
Deb S. LR and Hetastarch but Not Plasma after Rat Hemorrhagic Shock Is Associated with Immediate
Lung Apoptosis. J Trauma 2000.
Coagulopathy of trauma is dynamic Napolitano LM. SIRS Score Predicts Mortality and LOS in Trauma Patients. J Trauma 2000.
Kaufmann CR. Usefulness of TEG in Trauma Patients. J Trauma. 1997.
5 6
Geerts WH. A Prospective Study of DVT and PE after Major Trauma. NEJM, 1994.
UTHSC-Houston 1999-2008
Demetriades D, et al Trauma fatalities: time and Trauma admissions = 36,028 and 2394 deaths = 6.6%
Early deaths (≤ 24 hrs) = 1398 or 58%
location of hospital deaths. JACS. 2004.
• 1993 to 2002.
• 2,648 hospital trauma deaths. 30
– head (43%), chest (28%) and abdomen (19%) 25 72 hrs = 72%

• 37% of victims had no vital signs present on % 20 24 hrs = 58%
30 days = 97%
6 days = 92%
admission 15
• Deaths caused by head trauma peaked at 6 to 24 10

hours 5
• Deaths caused by chest or abdominal trauma 0

(47%) peaked at 1 to 6 hours.
7 Deaths from day 31-171 = 68/2394 = 3% 8
Ann Surgery 2007
Causes of Death
Potentially Survivable
• Improved methods of intravenous or intra- 100
cavitary, noncompressible hemostasis combined 90
with rapid evacuation to surgery may increase 80
70
survival. 60
– 50% of causes of death still associated with truncal
Percent
Group 1
50
Group 2
hemorrhage 40
• Structured analysis (PI) identified improved 30
methods of truncal hemorrhage control as a 20
principal research requirement.

10
9 0 10
Hemorrhage Extremity Torso Ax/neck/groin
Cost of Hemorrhage: Relationship between

Transfusion and the War: 2001-2007 RBC’s Transfused, ISS and Mortality
Total # Total # Average # Low High RBC’s
Units Pts Units/Pt transused to
Transfuse Transfuse
d d 685/3287 (21%)
WB 6,001 1,035 5.8 1 48 patients with an
ISS 14 (9-25)
RBC’s 85,429 14,706 5.8 1 143
and 87/685
Platelets 3,723 1,540 2.4 1 29
(13%) mortality.
FFP 41,666 6,469 6.4 1 98
Cryo 11,456 1,034 11.1 1 114
11 12
Western Trauma, J Trauma, 2007
• 1124 casualties receiving atleast 1 unit

• 420 pts (37%) received MT
– MT: 10 U / 24 hr or 50% blood volume over 3 hrs.
– Pts with 2/4 variable had 54% incidence of MT
– HR > 110 HGB < 11
– SBP < 110 BD <=-6
13 14
Comparison of three MT prediction studies Summary of Epidemiology

Study Variables ROC value • Truncal Hemorrhage is a unresolved
problem
McLaughlin et al. SBP, HR, pH, Hct 0.839
• MT can be reliably predicted (very early)
Yücel et al. SBP, HR, BD, Hgb 0.892
with standard tests
Male, +FAST, long
bone/pelvic fracture
NEED
• Rapid Effective Early Dx and Intervention
Moore et al. SBP, pH 0.804
ISS>25
15 16
The Lethal Triad after 2003

Coagulopathy
Develops
over Time - Acidosis Hypothermia
1997 Death
Coagulopathy
Cosgriff N, et al. Predicting life-threatening coagulopathy in the massively transfused patient: Brohi K, et al. J Trauma, 2003.
17 MacLeod J, et al. J Trauma 2003 18
Hypothermia and acidosis revisited. J Trauma. 1997.
J Trauma, 2003.
J Trauma, 2003.
• Derangements in coagulation occur rapidly after trauma

even after adjusting for ISS
• By the time of arrival at the ED, 1/3 of trauma patients
had a coagulopathy associated with a poor outcome 19 20
The Probability of Death with 95% CI by INR
0.5
0.45
0.4
0.35
0.3
Probability
Prob. of Death
0.25 Low
Upper
0.2
0.15
0.1
0.05
0
1 1.5 2 2.5 3 3.5
INR
21 22
How to Resuscitate? How to Resuscitate?

• Its not just raise the BP • Controlling coagulopathy of hemorrhage in
• Not just the hole in the blood vessel that needs truncal trauma is paramount
rapid suture
• Hemorrhage control via the ideology of
• Reverse the systemic endothelial injury damage control resuscitation (DCR)
– Reverse permeability – Blood vs crystalloid
– Prevent edema – Ratios of pRBC’s : plasma : platelets
– Repair the endothelium – Recombinant factor VIIa
• Dampen the systemic inflammatory response – Thawed plasma
• Prevent and Reverse coagulopathy – Platelets
23 24
Which one to use, start, how

The Lethal Triad after 2003 much, stop, iatrogenic acidosis?
NS LR
Acidosis Hypothermia
Death
Coagulopathy
Brohi K, et al. J Trauma, 2003.
MacLeod J, et al. J Trauma 2003 25 26
DCR components
• Stop bleeding
• Hypotensive resuscitation
• Minimize crystalloid
• Use plasma to resuscitate patients
• Rapid progress in trauma care occurs during a war.
• Increased platelet use
• Damage control resuscitation addresses diagnosis and
treatment of the entire lethal triad immediately upon • Reverse hypothermia and acidosis
admission.
• Hemostatic adjuncts
J Trauma, 2007. 27 28
Resuscitation Hypotensive Resuscitation

1. Damage Control Resuscitation • Time honored technique developed by military
• Hypotensive resuscitation
physicians during WWI and WWII
• Hemostatic resuscitation • Maximizing the resuscitation benefit to the
mitochondria while minimizing rebleeding by
avoiding “popping the clot.”
2. When surgery and resuscitation • Supported by a significant body of scientific data.
techniques are both focused on stopping • Approach preserves the resuscitation fluid within the
bleeding vascular ssytem
• Resuscitation and surgery becomes much • Logistically sound by preventing needless waste of
easier blood and fluids.
29 30
Hemostatic Resuscitation Typical 24 hour Resuscitation

• Damage Control Resuscitation is centered on the
philosophy of Damage Control Surgery
– “staying out of trouble rather than getting out of trouble”
• THEN • NOW
• Damage control philosophy can be extended to – 20 liters of LR – 3-5 liters of LR
resuscitation
– focus on restoring normal coagulation and minimizing crystalloid.
– 15 RBCs – 7 RBCs
– Traditional resuscitation dilutes the already altered coagulation – 5 FFP – 6 FFP
system and likely increase multiple organ failure.
• Aggressive, physiologically sound, hemostatic
– 0 platelets – 1 platelets
resuscitation techniques should be performed in parallel
with equally aggressive surgical hemostasis
Associated with decreased edema, MOF
and improved survival
-Hess JR, Holcomb JB, Hoyt DB. Damage Control Resuscitation: The need for specific blood
products to treat the coagulopathy of trauma. Transfusion, May, 2006. 31 32
-McMullin NR, Holcomb JB, Sondeen JL. Hemostatic Resuscitation. Shock, 2006.
Shock, 2006 Arch Surg 2003
• HYPOTHESIS: Normal resuscitation, compared with

• Aggressive crystalloid-based resuscitation strategies supranormal, requires less crystalloid volume, decreasing
and large-volume resuscitations may be deleterious. the incidence of intra-abdominal hypertension (IAH) and
– Development of cardiac and pulmonary complications abdominal compartment syndrome (ACS).
• Future resuscitations research focus on improvement • 1999-2001, n = 85 vs 2001-02, n = 71

in fluid composition and adjuncts.
• CONCLUSION: Supranormal resuscitation, compared with
• Recent interest in early use of vasopressor agents to normal resuscitation, was associated with more lactated
support hemodynamics. Ringer infusion, decreased intestinal perfusion (higher
GAPCO2), and an increased incidence of IAH, ACS,
multiple organ failure and death.
33 34
Blough, et. al. Arch Surg 2003. Summary

• Truncal Hemorrhage is an unresolved
problem
• MT can be reliably predicted (very early)
with standard tests
• Coagulopathy is present on admission and
can be made worse by iatrogenic injury
NEED
• Rapid, Effective and Early Intervention
35 36
OK, so what are we going to

actually do with all these data?
37
A symposium held at the U.S. Army Institute of Surgical Research, 26-27 May 2005
38
• If clinically evident coagulopathy is • Reviewed massive transfusion protocols from

prevented by the early use of FFP, well-developed trauma systems in Denver,
Houston, Helsinki, Sydney, and Baltimore.
subsequent blood product consumption is
likely to be less. • This group them presented a massive
transfusion protocol based on the best data from
• In massive transfusion, early 1:1:1 their review.
– pRBC : plasma : platelets are indicated – 1:1:1 (RBC : plasma : platelets)
– The ratio is associated with improved outcomes
39 40
1 : 1 : 1 Ratio
• Be very clear about volumes of the 1:1:1
• 1 unit of plasma (250 cc)
• 1 unit of RBC’s (450 cc) • Compared low (1:8), medium (1:2.5) and high
(1:1.4) plasma:RBC ratio in patients requiring
• 1 unit of platelet (50 cc) massive transfusion
• A high plasma : RBC ration was independently

associated with improved survival to hospital
discharge and decreased death from hemorrhage
41 42
Mortality by Plasma : RBC Ratio Comparison of the primary causes of

n = 252 MT’s (2003-2004) death in each plasma : RBC ratio group
100
70 65% 90 Time to death

aLow = 2 hrs (1-4)
60 P < 0.05 80
bMed = 4 hrs (2-16)
cHigh = 38 hrs (4-155)
50 70
Mortality
*P < 0.05
40 60
34%
30 50
20 19% 40 *
16231
53 30
10 162 7
6
20
0 2
4
(Low) 1:8 (Medium) 1:2.5 (High) 1:1.4 10

2.5
1 1 1
0.5
0
Borgman MA, et. accepted, J Trauma, Oct, 2007. 43 Low n=20 Medium n=18 High n=31 44
Demographics
Massive Transfusion Resuscitation
Four Year Review of 1:1 Transfusion Ratio
UNPUBLISHED DATA Current (06-07) Previous (04-05)
# pts 95 97
Age yrs 37 2 392
ISS 28 1.2 29  1
Kenneth M. Jastrow III, Ernest Gonzalez,
INR admission 1.62 .08 1.8 
Rosemary Kozar
0.2
University of Texas at Houston
INR 24 hrs 1.36 .02 1.4 
0.03
45 46
Outcomes
• UNPUBLISHED DATA
Current Previous
• Compare in-hospital mortality to:
FFP:PRBC – Early transfusion of plasma and/or plts
first 24 hrs 1:1.1 1:1.5 – Time-varying plasma:RBC and plt:RBC ratios
first 6 hrs 1:1.3 1:2.4 • 905 patients
• Increased ratios of plasma:RBC and plt:RBC
were independently associated with decreased 6
Mortality 15% 30%
hr mortality
• After 24 hours, the ratios were not associated
47 48
Conclusions
Patients arrive to the ED coagulopathic
Coagulopathy is associated with mortality

J Trauma, 2005
• Pro-hemostatic drug used to treat coagulopathy

Our previous protocols resulted in a persistent • Given after the 8th unit of PRBCs
coagulopathy and FFP deficit on arrival to ICU • Decreased PRBC use in blunt trauma
• Decreased ARDS in blunt patients
Implementing a 1:1 ratio on arrival to the ED has • Safe (= 3% complication rates)
decreased MT mortality by 50% – No increased complications
49 50
May 2007
• Patients requiring a massive transfusion and receiving • When comparing rFVIIa (+) to rFVIIa (-) patients
rFVIIa were identified. – 24 hour mortality was 7/49 (14%) and 26/75 (35%), (p=0.01)
– 5,586 admitted, 292 (5.2%) required a MT – 30 day mortality was 15/49 (31%) and 38/75 (51%), (p=.03).
• 97 of these (33%) received rFVIIa.
• 17 received rFVIIa early and 44 received rFVIIa late. • SBP was higher in the rFVIIa (+) group
• Fewer units of pRBCs were given to the early rFVIIa • The use of rFVIIa was associated with improved early and late
group. survival after severe trauma and massive transfusion.
– 16.7 early vs 21.7 late, p=0.03 • rFVIIa was not associated with increased risk of thrombotic
• There were no differences in mortality, ARDS, infection or events.
thrombotic events between groups.
51 52
Kaplan – Meier Curve of 24 hour mortality for Kaplan – Meier Curve of 30 day mortality for
rFVIIa + patients vs rFVIIa – patients. rFVIIa + patients vs rFVIIa – patients.
P value = 0.004 by the log rank test. p value = 0.02 by the log rank test.
53 54
• Higher rate of MT in rFVIIa group

- A large number of patients who met criteria for rFVIIa did not receive it. • Higher rate of overall complications
- rFVIIa group tended to be sicker 55 56
No association with improved survival or increased risk of

complications
• How do we eliminate clinical

judgement??
• Propensity matching…
– No significant difference in mortality
57 58
• Phase 3 randomized clinical study

– Pharmaceutical sponsored • Arterial and venous thromboembolic events (and
• 573 pts (481 blunt 92 penetrating) RF) were similar
•
• Enrollment stopped 2/2 unexpected low
• 560 patients monitored for AE after rFVIIa or
mortality and difficulties with enrollment
placebo
• Mortality=11% (rFVIIa) vs 10.7% (placebo)
• rVIIa reduced blood product use but did • Higher reporting of AMI/STEMI but not
not affect mortality. No significance in AE. thromboembolism
59 60
Summary Summary
• Recombinant fVIIa use in trauma remains very • Truncal Hemorrhage is an unresolved problem
controversial
• MT can be reliably predicted (very early) with
• Anecdotal observations in clinical practice:
standard tests
– No incidence of acute graft failure in patients who
underwent vascular repair post rFVIIa • Coagulopathy is present on admission and can
– Became SOP in our resuscitation (ED and OR) of be made worse by iatrogenic injury
trauma patients. • Increased plasma saves lives
– Use in conjunction with the idea of “Damage Control
Resuscitation” in the MT patient
• Why?
– Over 300 doses given without any acute (24 hours)
systemic adverse events.
61 62
• Acidosis and hypothermia

Annals of Surgery, May 2007
cause a clinical
coagulopathy with
different thrombin
generation kinetics.
• Confirm the need to
prevent or correct
hypothermia and acidosis
and indicate the need for
improved techniques to
monitor coagulopathy in
the trauma population.
63 64
AJP Endo Metab, 2005
The acute changes in coagulation (hypo) after

hemorrhagic shock are related to the increased FIBRINOGEN: FALLS FIRST
degradation of fibrinogen
and FALLS FAST
A deficiency of fibrinogen develops earlier
than any other hemostatic abnormality when
plasma-poor RCCs are used for the
Hypothermia caused a deficit in fibrinogen availability replacement of major blood loss.
and a delay in thrombin generation, consequently
inhibiting coagulation function. 65 66
Overall Mortality vs. Fibrinogen Ratio Category Fibrinogen (gm) and Mortality
50
45
40
p < 0.001
35
30
Mortality % 25
20
15 n=55
10
n=197
5
0
0 to < 0.2 > 0.2
Grams Fibrinogen/RBC Ratio
67 68
Source of Fibrinogen
• 1 unit of FFP
– 400mg fibrinogen in 250 mls
• 1 six-pack of platelets
– 100mg/u x 6units = 600mg in 300mls
• 1 unit of apheresis platelets
– 200mg in 100ml up to 500mg in 250ml
• 1 unit of cryoprecipitate
– 250mg fibrinogen in 10ml
• 1 unit of fresh whole blood
– 1000mg fibrinogen
• 1 unit PRBCs
– < 100mg fibrinogen
Ref: MAJ Simon Clayton MD, and Dr. John Hess. 69 70
Thawed Plasma Other adjuncts…

• FFP that is kept for up to 5 days at 4°C
• Platelets either in the form of fresh whole blood (FWB) or
• Can be present upon arrival in the in the ED aPLT are associated with improved survival at 48 hours
– can be used as a primary resuscitative fluid and 30 days. (Cosgriff et al, Perkins et al, Cinat et al.)
• This approach not only addresses the
metabolic abnormality of shock, but initiates
reversal of the early coagulopathy of trauma
• Multiple centers are now using this product
– Decreases waste by 60-70% • A higher platelet: pRBC ratio was associated with
improved early and late survival and decreased
hemorrhagic death.
71 72
Whole Blood…magic bullet?? Component Therapy vs What we bleed
Plt
5.5x1010
50 mL FFP
PRBC
Hct 55% 80% 500 mL
335 mL 275 mL
Warm
Hct: 38-44%
So Component Therapy Gives You
1U PRBC + 1U PLT + 1U FFP Plt: 150-400K
•Hct 29% Coags: 100%
•Plt 87K
•Coag activity 65% 1000 mg
•950 mg fibrinogen Fibrinogen
73 74
•Armand & Hess, Transfusion Med. Rev., 2003
Mechanism Recommendation
• What is amazing is how little is actually • Use prediction models or clinical judgement for
known about this early coagulopathy and early implementation of a MT guideline
therefore how best to treat these patients – Over triage, start early
– Decrease crystalloid use
– Treat and prevent hypothermia and acidosis
• Leading potentially preventable cause of
death in trauma patients • MT protocol initiated after max of 2 units pRBC
– 1:1:1 ratio of RBC, plasma and platelets
– Increased fibrinogen and platelets save lives
• There are no relevant animal models of – Use rFVIIa in patients with ongoing coagulopathic
shock induced coagulopathy bleeding
75 76
“The Future”
Need Randomized trials
Dried / Lyophilized Components
• No prospective data in the massive • Lyophilized Fibrinogen
– Used for trauma patients in Austria
transfusion arena – Approved in US
• Frozen, FD platelets or Lyophilized Platelets
– human studies and animal trials (LP)
• Lots of expert opinion and confounded – European countries in Afghanistan
retrospective studies • Dried plasma
– animal studies
– Including our own – Human trials
– Approved in many EU countries, used in Afghanistan
• RBCs
– Stem cell derived-DARPA
– lyophilized RBC’s
77 78
• Various individual recombinant coagulation proteins
Summary
Prior Coordination and Cooperation
• ED staff • Uncontrolled Hemorrhage is a major
• Anesthesia problem
• Surgery – MT is only 2% of all civilian trauma admissions
• ICU • Predictive models are here
• Transfusion / Blood bank – Rapid dx of MT patients who are in shock and
• Can not be done in isolation coagulopathic
• Very small numbers – Must start plasma and platelets much earlier
– 1-2% of all civilian trauma admissions – How early??
– High mortality
79 80
How do you make early blood

Summary
products happen?
• Use blood products early and as a primary • Focus on improving coagulation status while
resuscitation fluid preventing rebleeding
– Perform standard metabolic resuscitation
• O- RBCs—in the ED – Minimize impact on the already primed inflammatory
• AB or A plasma—in the ED system
• Decrease crystalloid use
• Platelets—in the ED?
– Thawed plasma allows a early 1:1 ratio
– Increase platelet use improves outcome
• Prehospital?? – rFVIIa decreases blood use and probably improves
survival
– RBC and FFP on helicoptors being studied now
81 82
Summary Acknowledgements…
• Use physiology (not tradition) to drive • Thank you to…
diagnosis and interventions – Dr. John Holcomb
– Dr. Phil Spinella
• Don’t make the presenting problems – Dr. Jeremy Perkins
worse with repeated iatrogenic injury. – Dr. Charles Fox
• Understand risks and benefits of all

products
83 84
pH= 6.9 BD=18 BP 74/40 HR 140’s INR 1.8
85
THE ZEBRAS: UNIQUE PRESENTATIONS

AND STRANGER DIAGNOSES
NWS Current Topics in Emergency Medicine The Zebras: Unique Presentations and Stranger Diagnoses 140
UNIQUE PRESENTATIONS AND STRANGER

DIAGNOSES When you hear hoofbeats, think
horses not zebras.”
Dr. Theodore Woodward
Sumeru (Sam) Mehta, MD, MPH
The University of Texas Health Science Center San
Antonio
THE EMERGENCY DEPARTMENT IS LIKE THE

PLAINS OF AFRICA. Typical Diet of the King:
EM Physician is the King Abdominal Pain – NOS
Headache
Chest Pain
Diabetic complications
Malingering
Medication refills
DAILY GRIND OF THE ER…WE LIVE FOR: ELUSIVE CREATURES

• 1) THE ACUTE RESUSCITATION
• 2) THE INTERESTING CASE
HOW DO YOU CATCH A ZEBRA IN THE DAILY

TYPICAL RESIDENT WORK-UPS GRIND OF THE ER?
1. You will never see a zebra if you don’t think

about it.
2. If something does not fit the clinical picture…

investigate further!
CASE 1: CC-ABDOMINAL PAIN

• 27 yo female presents with right sided abdominal pain. • Labs: WBC 18K, + UTI, Lactate 4.9
VS: HR 130, T 101, BP 70/40
HPI/ROS: Pain x 3 days, waxing and waning, now constant. + EDC: 2 L IVF, CX, ABX, Early Goal Directed
fevers, + dysuria Therapy
PMH: None
PSH: None
FH/Social HX: Neg Diagnosis: Urosepsis…?
PE: Pale and diaphoretic, ill appearing, soft non-tender
abdomen, R CVA tenderness.
HOW MANY HEALTHY 27 YEAR OLDS HAVE

UROSEPSIS??
Obstructed UVJ Stone with Pyonephrosis
PERCUTAENOUS NEPHROSTOMY CASE 2: CC-RECTAL BLEEDING

• 59 yo male presents with weakness and rectal bleeding
x 12 hours
• VS: BP 80/40, HR 120, Afib w RVR on monitor

HPI/ROS: Large amounts of BRBPR, Mild Nausea, Mild Diffuse
Abdominal Pain
PMH: HTN, CAD, Afib, PVD
FH/Social HX: Smoker
Meds: Lopressor, HCTZ, Coumadin
PE: Pale and diaphoretic, ill appearing, mildly distended
abdomen, Frank Blood on Rectal Exam
• EDC: IVF, PRBC, Treated for GI Bleeding
Labs: H/H 5/15 INR 4
Diagnosis: GI bleeding…?
• Perhaps…JUST PERHAPS, this is

more than your average GI Bleed.
EXCUSE ME SIR, HOW DID YOU GET THAT

SCAR?
AORTOENTERIC FISTULAE
< 1% AAA REPAIRS
ERODES INTO DUODENUM
MASSIVE GI BLEED
CASE 3: CC-MVC
• 60 yo male restrained driver MVC rollover with LOC at
scene
VS: BP 80/40, HR 120, Sats 80%

EMS: C-Collar, Spine Immobilizer, Intubated
Primary Survey: Seatbelt sign on Chest and Upper
Abdomen, Crepitance to Right Chest Wall
• CT Head: Neg
CT C-Spine: Neg
CT Chest/Abd/P: PTX
ETOH: 350
EDC: Ventilator Management awaiting SICU

bed.
• EDC: 3 Hours Later Sedation Held for Neuro

Check…Patient with Right Sided Hemiparesis
Repeat Head CT negative
Diagnosis: Stroke…?
• Why Would a Trauma Patient Have a Stroke?
Now you see both carotids

Now you don’t
CAROTID DISSECTION
• High C-Spine Injuries
Dissecting flap causes thrombosis and emboli
Anticoagulation, INR
Must Consider Vascular Injuries in Trauma Patients

With Focal Neuro Defecits
CASE #4: CC: VERTIGO

• 64 yo male presents with headache and vertigo
HPI: Chronic HA’s x 4 yrs with a change in his headache x 1

month.
Right sided HA, some subjective vision changes. Intermittent

fever x 1-2 months. Sig historical Alternans.
Had CT and LP 1 week ago. and states it was normal.

Increasing HA, now can’t walk because of pain and dizziness.
• PMH: HTN, DM, Sarcoidosis, Chronic HA’s • Old results reviewed from previous ED visit for r/o SAH
/ Meningitis:
• Meds: Metformin, Motrin, Tylenol, Enalapril,
Depakote, Neurontin Temp 101
SH: Food service worker, no travel CT head negative
Vitals: BP 190/80 TEMP 98.6 WBC 14
Exam: TRUNCAL ATAXIA LP results: glucose 60, Protein 70, RBC 350 – 4, WBC
2, Gram Stain neg, Culture neg, VDRL neg, Opening
Pressure Normal
• CT: Negative
Labs: Negative
Persistent Truncal Ataxia when standing
Old Guy Can’t Walk – Admit to Medicine…Good

Luck!!
CASE #5 CC: LE WEAKNESS

• 59 yo female with h/o chronic low back pain who had a VITALS: 122/69 78 20 99.0 100% RA
neurostimulator placed for pain control in her LS 6 EXAM: AxOx3 but intermittently inappropriate; neuro: B LE
weeks ago who now presents with B LE weakness, weakness (2/5 R and 3/5 L); urinary incontinence
urinary incontinence and inability to walk. Foley placed
Labs unremarkable
HPI: seen 1 d ago at OSH for HTN and nausea.
ROS: No chest pain, SOB, BLE paresthesias
PMH: HTN, chronic neck/back pain
PSH: prior back and neck surgeries
FH/SH: Nurse; denies IVDA
Unable to perform MR D2 neurostimulator so CT of T and With normal MR, neurosurgeon suspected weakness was
LS with contrast performed effort related so rehab placement initiated and...again
- negative begrudgelingly, neurology was consulted.
Discussed with neurosurgeon…begrudgelingly admitted CT Head: “Suggestion of small L > R anterior cerebral
the patient...for observation only artery infarcts.”
2-3 days later, pt remained weak in LE extremities so NS MR Brain/ MR Angio: “Acute/subacute areas of infarction
was removed to perform MR... involving the bilateral posterior frontal and anterior parietal
lobes…diminished flow of left vertebral artery due to
MR TS/LS w/wo contrast: post op changes; nothing acute stenosis or occlusion.”
CASE #6 CC: DIZZY AND LIGHTHEADED
ECHO: PFO
• 83 yo male with h/o HTN who presents 2 days status
post pacemaker placement 2 days ago for SSS. Now
presents dizzy, LH, with nausea. Denied CP or SOB
ROS: weakness,
PMH: HTN, SSS
PSH: remote prostate surgery
FH/SH: Military retiree
VITALS: 104/60 60 16 97.6 95% RA

Intermittent hypotension with SBP between 79 and 93 which
responded to fluids
EXAM: AxOx3; CTAB, PM insertion site is C/D/I; RRR with no
murmurs; abd soft ntnd; neuro nonfocal
CXR: “Cardiomegaly. PM appears appropriate. NAD”
LABS: Unremarkable
BEDSIDE ECHO: moderate to large pericardial effusion

DX: Acute Pericardial Tamponade
Pt underwent emergency pericardiocentesis and
placement of pericardial tube for drainage. Over 600 cc of
bloody fluid was obtained and SBP improved from 70 t0
120 immediately post procedure.
CASE: #7 CC: BLACK TOE

• 50 yo male presents with toe discoloration
HPI: Toe discoloration x 1 week not improving with

antibiotics that PCM prescribed.
ROS: no pain, no fevers
PMH: DM, HTN
PSH: appy, stab wound
FH/SH: smoker
DIAGNOSIS: INFECTED TOE…?

CASE #8 CC: RIGHT FLANK PAIN

• 32 yo male presents with right flank pain x 12 hours.
HPI: Began after lifting a heavy box. No neurologic

symptoms. Moderate groin swelling. Unable to walk
because of severe pain.
PMH/PSH: Hemophilia a – monthly spontaneous joint
and muscle bleeds
Meds: None currently
Allergies: Factor VIII
LARGE PSOAS MUSCLE BLEED
CASE #9: CC: BACK PAIN

• 49 yo male presents with acute onset upper
back pain
HPI: Awoke with upper back pain that radiates around to his
shoulders. No trauma. No chest pain. Intermittent paresthesias
in all 4 extremities. Ambulates with difficulty because of extreme
pain.
PMH: HTN, CAD, Afib
PSH: None
Meds: Coumadin, Labetalol
SH/FH: Smoking, Occasional IV Cocaine
• VS: BP 190/110, HR 122, Temp 98.6 • EDC: EKG Normal

Equal Bilateral BP’s X-rays Normal
Afib on the monitor BP control, Pain Control
Labs: INR 9, otherwise normal
Physical Exam: Moderate Distress. Patient Chest CT r/o Dissection Pending
cannot find a comfortable position. Otherwise a
normal examination.
• After 16 mg Dilaudid, patient asleep with TURNOVER

continued 12/10 pain
Plan: CT Chest pending, Pain control, trial of
ambulation and hope for the best!
Diagnosis: Drug Seeking…?
Re-examination: Asleep with persistent
tachycardia. Has not been able to urinate while in
Discharge, Admit or Turnover? the ED.
SPONTANEOUS EPIDURAL HEMATOMA

COMMENTS OR QUESTIONS?
EMERGENT EVALUATION AND TREATMENT

OF ACUTE DELIRIUM
NWS Current Topics in Emergency Medicine Emergent Evaluation and Treatment of Acute Delirium 152
Excited or Hyperactive
Delirium
Acute Delirium: Deadly Medical
Illness Masquerading as Psychosis

Medical Director
Learning Objectives Case Scenario
• Define delirium and describe its three forms • Called to gas station at 12AM
• Relate the differences between psychosis and delirium • Man harassing customers
• Formulate an evaluation process for diagnosing underlying • Upon arrival – disoriented, angry white male swinging at
medical causes of delirium
police resisting detainment
• Compose an initial treatment strategy for acute delirium in the

emergency setting • How do you initially proceed (non-pharmacologically)?
Objectives Acute Delirium Definition
• Describe the symptom complex of Acute Delirium • “Acute Confusional State”

• Not a disease, but a complex of signs caused by a
medical illness
• Formulate an evaluation process for diagnosing
underlying medical causes of Acute Delirium
• Latin Roots
• De – away from
• Lirium – furrow in a field
• Compose an initial treatment strategy for Acute
• “going off the ploughed track”
Delirium in the Emergency Setting
Acute Delirium Signs Acute Delirium
• Disturbance of consciousness • Psychosis = psychiatric cause
• Change in cognition
• Delirium = direct physiologic cause of a medical
illness (organic cause)
• Internists may use the term “encephalopathy”
• Disturbance develops over hours or days and fluctuates
• Differentiated from Psychosis / Dementia • Medical condition must cause a change from the
• Caused by a medical condition person’s baseline cognition level
Types of Delirium Case Scenario
• Hypoactive • How do you determine whether this person is

suffering from psychological versus medical illness?
• Hyperactive
• What common medical illnesses / conditions can
cause this sort of behavior?
• Mixed
Psychiatric Versus Medical Acute Delirium Causes

• Risk Factors
• Age > 75 years
• Males
• Poor Baseline Cognitive Functioning
• CNS Pathology
• Sensory Impairment
• Severe Illness
• Metabolic Disorders
• Trauma
• Sleep Deprivation
• Over Sedation
• Medication Side Effects
• Poorly Controlled Pain
• Substance Abuse and Withdrawal
Acute Delirium Case Scenario
• Most Common – Substance Abuse / Withdrawal • What sort of medical / pharmacological

interventions are appropriate?
• Acute Intoxication
• Cocaine
• Which medications do you need to avoid and why?
• Amphetamines
• Synthetics
• Substance Withdrawal
• Alcohol and benzodiazepine withdrawal most prominent
Physical Restraint Physical Restraint
• Medically necessary • If the patient is handcuffed, he or she should not be

handcuffed to the stretcher to avoid injury if there is a
collision
• Ordered by a physician
• Depending on local policies, law enforcement may be

• Needed to ensure the individual’s safety required to accompany the patient in the ambulance
• Used only after less restrictive interventions have been • If a peace officer is not riding in the ambulance, EMS
considered and determined to be ineffective or are judged providers should have the means to remove the handcuffs
unlikely to protect the individual or others from harm from the patient
Physical Restraints Treatment
• Restrained patients should not be transported in a prone • DONT

position • Dextrose
• Oxygen
• Narcan
• Thiamine
• Patients should not have their arms and legs tied behind their
backs
• Assure safety of the patient and personnel
• Patients should not be placed between restraining items

• Physical Restraint
• Nothing should be placed over the patient’s face, head or neck • Attempt to elicit the underlying cause of the delirium
Treatment Treatment
• T-A-DA • Benzodiazepines
• Can exacerbate certain causes of delirium
• Tolerate • Midazolam 5mg IM
• Lorazepam 2mg IV increments / escalating increments
• Anticipate
• Don’t Agitate
• Haloperidol
• 2‐10mg IVP q30min, then 25% of loading dose q6h
• Watch QTc prolongation
• Correct electrolytes
• Discontinue / investigate for anticholinergic agents
• Droperidol
• 5mg IM
• Watch QTc prolongation
• Pharmacologic Restraint • Correct electrolytes
Treatment Case Scenario
• Atypical Antipsychotics • What is the expected course of treatment and length

• Second line unless known allergy to prior agents of treatment in the ED?
• Olanzapine (10mg PO / SL initial dose)
• PO dosing is unrealistic in Hyperactive Delirium
• What sort of diagnostic tests are required to
medically clear this patient?
• Ketamine
• 4-5mg/kg IM
Evaluation Evaluation
• Pregnancy test in females
• Comprehensive H + P with collateral information • Chemistry panel and LFT’s
• Complete blood count
• TSH
• Detailed physical exam looking for signs of trauma,
• Urine toxicology screen for drugs of abuse
examination for toxidromes and evidence of
infection • Alcohol level
• Serum osmolality and VBG if toxic alcohols or metabolic derangement suspected
• If potential suicidal gesture – consider acetaminophen level

• High index of suspicion for CNS pathology or • Head CT if concern for trauma of CNS pathology
metabolic derangement
• Lumbar puncture if concern for infectious encephalopathy
Disposition Clinical Scenario
• Admission to general medical floor for observation • After pharmacologic sedation with Midazolam and
if vital signs normal and sensorium has not cleared Droperidol, the patient awakes with normal vital signs on
the medical floor eight hours later
• Admission to Intensive Care Unit if vital sign • The patient is contrite, and admits to abusing large
abnormalities persist, or concern exists for quantities of cocaine
decompromise or airway impairment
• The patient desires inpatient drug treatment for his

addiction and is transferred to a treatment facility
Summary Questions?
• Delirium is an altered sensorium due to a medical • Thank you

condition as opposed to a psychiatric condition
• Most common initial treatment for excited delirium is a • Any feedback?

typical antipsychotic (phenothiazine derivative) in
combination with a benzodiazepine, given IM
• Diagnosis of the underlying medical condition is

paramount
EMERGENT EVALUATION AND TREATMENT

OF THE ACUTE RED EYE
NWS Current Topics in Emergency Medicine Emergent Evaluation and Treatment of the Acute Red Eye 158
Learning Objectives
The Acute Red Eye • Provide the differential diagnosis for emergencies
causing an acute red eye

• Review specific categories and examples of
Greater San Antonio Emergency Physicians emergencies causing an acute red eye
Medical Director
• Discuss initial management of emergencies causing
an acute red eye
True Ophthalmologic
Emergencies
• GLOBE PENETRATION
• CHEMICAL BURNS
• CENTRAL RETINAL ARTERY OCCLUSION
• ACUTE ANGLE CLOSURE GLAUCOMA

Red/ Painful Eye
• Anatomy
• History/ Exam
• Specific Topics
Anatomy Anatomy
• Eyelids--specialized skin folds containing the tarsal • Lacrimal gland

plate (a fibrous band, elevates lid) and muscles • lacrimal fossa, temporal aspect under upper lid
• loose connective tissue-- swells easily • tears pass across eye to lacrimal puncta, (upper and
• highly vascular lower) at lid margins to the respective canthi - to duct
• orbicularis oculi- circumferential, closes lids, CN VII
• levator palpebrae, CN III, superior tarsal muscle,
sympathetic nervous system - elevates eyelid
• sensory- CN V,1st&2nd div. Supra/infraorbital nerve
Anatomy Anatomy
• Conjunctiva • Sclera
• Transparent membrane, lines the inner surface of • dense white connective tissue capsule,
the lids (palpebral conjunctiva) and covers the nourishment from vessels in the episclera, lying
anterior surface of the eye (bulbar conjunctiva) between conjunctiva and sclera
except over cornea
• Iris
• Cornea
• an optical diaphragm which when acted upon by
• transparent, avascular structure, exquisitely pain the muscles of the ciliary body change pupil size,
sensitive forms the anterior aspect of the uvea
• sclera joins cornea at limbus
Anatomy The Red and/or Painful Eye
• Anterior chamber • Eye complaints comprise 3-10% of ED visits

• fluid filled area between the iris and and posterior
surface of the cornea
• 75% caused by: conjunctivitis, corneal or
• Lens conjunctival foreign body or corneal abrasion
• Vitrious
• Retina • Studies show majority of cases ED diagnosis

is concordant with Ophthalmology, missed
diagnoses rarely cause significant problems
History History
• Four cardinal complaints • Time course

• change in vision • acute, or chronic with exacerbation
• change in appearance • how long - minutes, hours, days
• pain or discomfort • constant or intermittent
• intense light exposure, FB
• trauma
• The patient may complain of one or more of these

• Pain or discomfort
• burning, FBS, itching, aching
• location, unilateral or bilateral
History History
• Visual changes • Associated Symptoms

• what are they, constant, intermittent • photophobia, pain with EOM, nausea/vomiting or
abd pain, headache, fevers, floaters, URI
• Discharge symptoms
• what kind, AM matting
• Ocular Hx ( in addition to usual PMHx)
• Any exposures, FB, trauma • contact lenses!!!
• Chemicals, allergens, makeup (new or shared) • surgery
• welding, tanning booths, metal on metal
• medications
• other eye problems--glaucoma, cataracts,etc
Exam
• Visual acuity
• Inspection/External examination
• Pupillary reactions
• Ocular motility
• Visual field testing
• Slit lamp
• Intraocular pressure
• Direct ophthalmoscopy
Inspection Visual acuity
• Move from out to in • Vital sign of the Eye

• Done at 20 ft, best vision (use corrective lenses or
• Equal - proptosis or enophthalmos pinhole, will should correct to 20/30)
• Lids-ptosis, swelling, ecchymosis or • if unable to do at 20 ft ---go to 10ft (10/200)
erythema, lashes, blepharospasm • if not finger count>>perceive motion>>light
perception
• Position, equal light reflex
• can use pocket card at 14in
• Conjunctiva and sclera-- red, swollen, • Do bad eye first ( no cheating)
discharge, unilateral or both, FB
Visual Acuity Pupil Exam
• <6 mo- OK if able to track light at 1-3 ft • Pupil exam

• steady fixation~ 20/40 • shape
• unsteady fixation ~ 20/100 • round, irregular, teardrop (rupture)
• no fixation~ 20/400 • size
• equal, anisocoria (physiologic us not >1mm, equal light
reactions)
• pilocarpine test
Pupil Exam
• Reaction
• equal, APD (Marcus-Gunn pupil)
• swinging light test
• abnormal eye does not perceive light, appears to dilate
when light directed into it
• indicates pathology distal to optic chiasm
Pilocarpine Test Exam
• Unilateral dilated (mydriatic) pupil • Ocular motility

• instill 0.125% pilocarpine (1 gtt 1% in 7gtts NS) • 6 cardinal positions of gaze
• Adie’s pupil (efferent defect) will constrict, normal pupil
will not
• In no change, instill 0.5% pilocarpine then if needed with • Visual field testing
1% • confrontational, Amsler grid
• if a rxn with 0.5%-- underlying pathology
• if no rxn-- pharmacologic dilation
• Direct ophthalmoscopy
Exam Specific Topics
• Slit lamp and/or Fluorescein staining • Acute Angle Closure Glaucoma

• make sure pt not wearing contact lenses • Conjunctivitis
• Intraocular pressure • Anterior Uveitis (Iritis)
• palpation, Schiotz, applination, tonopen
• Keratitis
• contraindicated in globe perforation, abrasion, FB,
trauma, active infection • Corneal Abrasions/Foreign Bodies
• Normal 10-20mm Hg,
• Acute angle closure glaucoma--50-70mm Hg
• Subconjunctival Hemorrhage
• Scleritis/ Episcleritis
Acute Angle Closure

Glaucoma
• Aqueous humor produced by ciliary body- flows from
posterior chamber to anterior chamber
• IOP determined by balance of production and removal of
aqueous humor
• Pts have shallow angle (usually hypermetropic), also
increases with age
• narrow angle causes a resistance to flow of fluid out of the
anterior chamber
• Attack us. Precipitated by pupillary dilatation

• increases outflow obstruction, maximal at mid-dilation
Presentation
• Increasing IOP bulges iris forward>>increasing

block
• IOP may exceed 70 mm Hg
• damages corneal endothelium, lens, iris, retina and
optic nerve
• Any pupil dilation can precipitate

• emotional stress, anticholinergic or
sympathomimetic medications, dim lighting,
iatrogenic (instilling dilating drops)
Presentation Exam
• Sudden onset of eye pain and blurred vision • Unilateral visual decrement
• “halos” around lights due to corneal edema
• Conjunctival injection (perilimbal, ciliary flush)
• May be accompanied by nausea and vomiting and
• Cornea appears hazy or“milky”
abdominal pain
• may be the predominant symptom • Fixed, mid-dilated pupil
• Increased IOP
Treatment Treatment
• Call Ophthalmology • Topical Beta-blockers (betaxolol, timolol)

• Decrease pressure-outcome more dependent on • decrease aqueous production
duration than absolute pressure • onset in 30 min, peak 1-2 hrs
• decrease production of aqueous humor • use with caution in COPD, CHF, conduction abn
• reduce vitreous humor volume
• facilitate aqueous outflow
• Acetazolamide (carbonic anhydrase inhibitor)
• decreases aqueous production
• use in conjunction with beta-blockers
• 500mg initially the 250mg q6h, PO, IM, IV
Treatment Conjunctivitis
• Hyperosmotic agents • Bacterial, Viral, Allergic, Fungal,

• reduce vitreous humor volume Chlamydial
• oral glycerol-1ml/kg (with lemon juice)
• Inflammation of the conjunctival membrane
• oral isosorbide
• IV mannitol, 1-1.5 mg/kg • Typically gradual onset, unilateral or
bilateral
• Pilocarpine 2-4% q 15min for 1-2 hrs
• facilitates aqueous outflow, pulls iris from angle • Itching, burning, pain, FBS, AM mattering
• VA usually not affected, pupils normal,
diffuse injection, +/-- chemosis or lid edema
Bacterial Conjunctivitis
• All age groups, usually purulent D/C with am

mattering, no nodes, varying conj. injection, painless
• Primarily skin contaminants
• Strep. Pneumo> Staph. Aureus>>Hemophilus
sp.(25%)> Proteus, Klebsiella (10%)
• Gram Neg organisms in older pts,
immunocompromised, diabetics and preexisting
external eye disorders
• Think of GC with copious pus -- do gram stain and
cx
Treatment
• Treatment
• topical antibiotics; recommend polytrim or
erythromycin oint, avoid gent or neomycin and
sulfas; consider Pseudomonas in contact lens
users.(use fluroquinolone)
• Don’t patch or use steroids
• warm soaks/compresses
• avoid cross contamination
• F/U if not better in 3-5 days or worse
Viral Conjunctivitis
• Majority of “pink eye”
• usually less pus, more watery discharge (epiphoria)
• frequently have pre-auricular adenopathy
• up to 50% will have associated URI sxs

EKC
• Epidemic Keratoconjunctivitis
• adenovirus type 3&7;children and young adults
• fever, pharyngitis, cervical adenitis, follicular conjunctivitis
• Extremely contagious
• starts as usual pink eye, after 5-7d
• eye pain, photophobia, decreased VA
• marked inflammation, chemosis and epiphoria
• occ. corneal infiltrates
EKC
• Lasts 2-8 weeks
• Refer to Ophthalmology
• Avoid spread of infection

• wear gloves, wash hands!!!
• Terminal room cleaning
• sterilize instruments
• patient education
Herpes
• Simplex (HSV)
• primary (children) or usually reactivation
• tearing, chemosis, mucoid discharge, subconjunctival
hemorrhages and injuction
• Slit lamp with staining reveals dendritic keratitis

with or without ulceration
• Tx: consult ophtho, topical and/or oral antivirals
consider topical abx, Viroptic and acyclovir, NO
STEROIDS
Herpes
• Zoster
• dermatitis involving V1 branch of CN V has 70%
chance of ocular involvement
• lesion at the tip of the nose – Hutchinson’s Sign
• conjunctivitis, iritis, ulcers +/- skin lesions
• Consult Ophthalmology
• Steroids, oral acyclovir, topical antibiotics
Allergic Conjunctivitis
• Often seasonal, involves intense itching

• type I hypersensitivity reaction
• Usually unilateral, may be both eyes

• edema, chemosis, mild photophobia
• less intense conj. Injection
• may have assoc. AR sxs
• Tx: cool compresses, topical and/or oral

antihistamines
Anterior Uveitis (Iritis) Iritis
• Uvea consists of iris, ciliary body and • Exam

choroid-- becomes inflamed • perilimbal injection
• small poorly reactive pupil (inflamed iris)
• Most idiopathic, other causes are systemic • cell and/or flare in anterior chamber on slit lamp
inflammatory disorders, infections, exam
malignancies and trauma • Tx: long acting cycloplegic (cyclogel)
• Pts present with unilateral painful red eye • reduces pain and photophobia, help reduce
scarring
with photophobia (direct and consensual),
• Consult Ophtho- may advise topical steroid
decreased visual acuity, no discharge • Follow up in AM
Keratitis
• Inflammation of the cornea

• Corneal ulcer-- a white spot with overlying
epithelial defect
• multiple etiologies, bacterial, viral (herpetic)
• consider Pseudomonas in contact lens wearer
• UV keratitis-- intense light exposure, eg. welding,
sun gazing, snow blindness
• sunburn of the cornea, intense pain, FBS and photophobia
4-8hr after exposure, see injection, diffuse punctate
staining
• Treat with pain meds, cycloplegics, consider antibiotics
and patching
Foreign Body/ Corneal

Abrasion
• Common in ED
• FB removal after topical anesthesia
• Irrigation, Q-tip, needle or spud (with slit lamp)
• look in fornices, evert lids
• if epithelial defect present tx with abx for 2-3 days,
consider patching ( no patch in contact lens wearer),
cycloplegics and pain meds
• may have persistent foreign body sensation even if none
found
• Follow up in 1-3 days, no driving (loss of binocular
vision)
Subconjunctival Hemorrhage
• Rupture of small vessel under clear conjunctiva

• smooth, sharply demarcated area, painless
• usually due to minor trauma, valsalva, etc
• consider coagulopathy and uncontrolled hypertension or
ruptured globe
• Ensure no hyphema or foreign body
• Treat with cool compresses as needed, reassurance
• resolution in 2-3 weeks
Scleritis/Episcleritis
• Scleritis--inflammation of the sclera

• deep violaceous injection, edema, severe deep eye pain
• 3 types- diffuse, nodular, necrotizing
• Treatment by Ophthalmology, topical NSAIDS,
steroids
• Episcleritis-- more superficial, localized

inflammation, less pain
• Treat with topical decongestants, oral NSAIDS
• referral to Ophthalmology
Summary
• Perform a complete exam

• Visual acuities on everyone
• Don’t always need IOP
• Consider sight threatening problems

• Be liberal with pain meds and topical antibiotics,
don’t prescribe steroids, avoid patching
• Call Ophthalmology with any questions
Questions?
• Thank you
REFLECTIONS ON A COMBAT SABBATICAL:

LESSONS LEARNED IN WAR
NWS Current Topics in Emergency Medicine Reflections on a Combat Sabbatical: Lessons Learned in War 173
Reflections On a DISCLAIMER
Combat Sabbatical
 Views expressed here are
Sumeru Mehta, MD, MPH
solely mine and not
shared by the United
States Army or
Department of Defense
“When you reach the end
9/11 of your rope, tie a knot in

it and hang on.”
Thomas Jefferson
“Do what you can,

with what you have,
where you are.”
Theodore Roosevelt
Eastridge et al. JTrauma 2006.
OIF Medical Assets 10th Combat Support Hospital(CSH)
 Level III / Combat  Ft. Carson, Colorado

Support Hospitals
 October 2005 to October 2006
– Baghdad, Mosul,
– Balad  Baghdad, Iraq
– Talil, Tikrit, Kirkuk, – Ibn Sina Hospital
BIAP
 20 physicians (4 EM)
 Level I and II
throughtout  67 nurses / 36 LPN (16 EM)
 71 medics and others (21 EM)
10th CSH Assets Epidemiology (10/05-10/06)
 4-6 fully functional OR’s  6,300 ED visits

 Two CT scanners USH with 3886 trauma visits
 24/7 radiology  19,046 blood products
 Blood bank support / whole blood 15,673 at all other Level III combined
drives  8,695 OR procedures
 Team approach > “Mascal”  262 deaths
>95% survival rate
Patient Population Trauma By Mechanism

0%7% 1% 4%
1% 1% 4%
7%
34%
25%
40%
43%
32%
US Soldiers Iraqi Military MVC IED GSW
Iraqi Civilian Security Internee MORTAR FALL BLAST

DOD Civilian US Contractor OTHER RPG
NON US Contrator Coalition Force
Trauma By Location Civilian and Combat Comparison

Combat Casualties are Different than Civilian
8% 3% 16%
4%
2% 6%
4%
13%
23%
21%
Shoulder/Chest Abdomen
Head/Neck Upper Extremity
Lower Extremity Back/Spine
Buttocks/Rectum Groin/Pelvis
Face Eyes
Trauma Center Staffing

Who comprised our team?
Civilian vs Military
Ranks of nurses and medics upon
deployment Average Age of Nurse Average Years of Expereince
10 50 18
16
8 40 14
12
6 30 10
Y e a rs
Ye a rs
8
20
4 6
10 4
2 2
0 0
0 Civilian Military Civilian Military
E2 E3 E4 E5 E6 E7 O1 O2 O3 O5
Rank
MAJ Dodson
MAJ Mehta
LTC(P) Mazur CPT(P) Steinbruner
“…when again touched, Trauma 101 (Day # 1)

as surely they will be,
by the better angels
of our nature.”
Abraham Lincoln
“Experience is simply the

name we give our
mistakes.” "A watershed moment..."
Oscar Wilde
Trauma Care In A Combat Environment

Civilian vs Traditional
Trauma Model
 Current ATLS model  ATLS teaches “Vertical” approach
– Single provider
Inadequate resources and staffing
– A then B then C
 Combat ATLS  Our approach was “Horizontal”
Audible in theatre – Multiple providers
 pre-assigned roles and responsibilities
– Team leader
 coordinates activity
 Observes, synthesizes data, forms definitive care plan
– ABC Tasks occur simultaneously
Egoless Medicine The Team
 Biggest problem with ATLS….  Civilian Model:  Military Model:

– You…. – Nurse
 Why was the “team” so important?
– Attending/Fellow – Medics (2)
 Role of emergency physicians – Anesthesia – You…..
 Role of surgeons – Bigillion nurses
– Techs
 “Egoless Medicine” in the Trauma Room
– Clerks
– Resp. Techs
– EKG. Techs
Standard Trauma Team 10th CSH - Trauma Team

1. Command Physician
2. Trauma Nurse
1/2 2/3
1. Command Physician 7 3. Medic
2. Primary Resuscitator 3
4. X-ray Technician 2 3
3. Anesthetist 2 5
4. Assistant Surgeon
4
5. Trauma Nurse 8 3
6. Recorder
9 4
7. Respiratory Technician
8. X-Ray Technician
9. Lab Technician 1 6
Pre Deployment Planning:

Non-Physician Role Expectations
AKA Battle Drills
 Pre Deployment preparation  Civilian
 Exposure, VS, peripheral access,
Physician leadership
medications/blood
Invest heavily in Medics  Combat (all under physician supervision)
Identifying skilled people early  Above plus…
Identify non skilled people early  Femoral blood sample, rapid infuser, central
access, I/O
 Role identification
 Ventilator management, airway management
 Expanded roles  Tourniquets, coordination for diagnostics/OR
 Sedation and paralytic management
60 Days in the CSH Trauma Care In A Combat Environment

Procedures from 01Apr06-01Jun06
 ABCDE changed to AAABBB
20
18  Initial team approach?
# of times procedures
16 – Simultaneous
14 Assess
performed

12 RN
10 MEDIC
– Physician
8 – Abnormal
Total
6 – Not a physical exam
4  Access
2
0 – Get access fast, within 30 sec
Intubation Central A-Line Chest  Airway
Line tube – Have someone monitor, give O2
Types of procedures
Trauma Care and Evaluation Trauma Care and Evaluation
 Assess  If yes……..
– Not a primary survey  Intubate
– Abnormal: – Premixed drugs:
 Succinylcholine
 Mentation
 Etomidate
 Breathing  Fentanyl
 Body parts  Versed
 Vecuronium
 Once airway secure…  Primary survey: focused

 BBB – Penetrating head, abdominal, chest.
– Stop any Bleeding – Deformed limbs.
– Blood Products/Damage control resus. – Eye injuries……
– Begin Primary Survey – FAST
 If no obvious OR
indications
 Secondary survey…..  Pearls

– Look for holes. – I/O’s are the bomb…
– X-ray or CT any hole. – Cric kits are too time consuming
 Scalpel and ETT
– Patient never left until the x-rays/CT were
– Intubation……you can always extubate
done.
– Strap hangers and crowd control
– Blood, blood and more blood
– FAST / Ultrasound
– Tourniquets
“Practice random acts of

kindness and senseless
beauty.”
Anonymous
Lessons Learned
“Those who do not learn
Tourniquets
from history are doomed 
Ultrasound
to repeat it.”

 Performance Improvement / Research

Voltaire  Trauma Care
Blood Products
Damage Control Resuscitation
Tourniquets Tourniquets
SAVES
 Apply as soon as possible
 May use tourniquet before other measures
 Use approved before improvised
LIVES
 Place proximal to stop bleeding and pulse
 Apply second (or third) tourniquet if pulse
persists
 Tourniquets loosen with time and transport
 Trial release in ED with stable patient
 232 pts
– 309 limbs
– 428 tourniquets
 Tourniquet use was
strongly associated with
survival
 4 cases of palsies EMT
– All resolved or in
process of resolving
 No amputations solely SOFTT
from tourniquet use CAT
Bedside Ultrasound
 Sonosite 180  Level I-III

Total ultrasounds: 621
 Utilized primarily 
– FAST: 401 (65%)
for: –
 46 positive (11.5%)
RUQ: 38 (6%)
– FAST, FB, Fx, – Aorta: 5
– Renal: 38 (6%)
cardiac, procedural, – Pelvic: 15
IVC – Soft Tissue: 64 (17%)
– Procedural: 6
 Teach medics/RN’s – Other: 7
 Adequate views on 98% on exams
 Critical asset at  Diagnostically relevant in 78% of the studies
22% were returned to duty without evacuation or admission based
Level I/II

on initial US findings and clinical exam
Performance Improvement/ Blood Products, Coagulopathy

Research and Resuscitation
Research at 10th CSH Ongoing theatre
 Damage Control Resuscitation
 
– Ultrasound research
– Personal protective gear
–
–
rFVIIa
Tourniquets – Body armor extensions
– Begins pre-hospital with
– Burn – Kevlar helmet revisions hemorrhage control
– Multiple case studies / – Hemostasis
case reports – Battlefield tourniquets – Prevent and treat hypothermia
 PI at 10th CSH – Hemostatic dressings
– Prevent and treat acidosis
– Aeromedical – Recombinant factor VIIa
– JTTS – Resuscitation – Prevent and treat coagulopathy
– Burn flow sheets – O2 therapietics /
hemoglobin based O2
carriers
Holcomb et al. JTrauma 2006.

Blood Products, Coagulopathy

Lethal Triad and Resuscitation
– Transfusion of plasma, RBCs, and
platelets in a 1:1:1 ratio
– Minimize crystalloids
HYPOTHERMIA COAGULOPATHY – Emphasizes endpoints (INR, BD, Temp,
SBP, Hgb)
 Indicator of poor outcomes(massive
transfusion/death)
ACIDOSIS – Recombinant Factor VIIa as an adjunct??
Select Clinical Papers Select Clinical Papers
 rFVIIa decreased 30-d mortality in severely injure combat

 Early administration of rFVIIa reduced RBC adminstration by casualties requiring massive transfusion
20% in massive transfusion patients.
 Early rFVIIa use with DCR does not improve 24 survival

 rFVIIa was effective for controlling hemorrhage and reversing  rFVIIa group had better pH, INR, BD upon presentation to the
coagulopathy for severe vascular injury ICU
 Early graft failures unrelated to rFVIIa
Massive Transfusion
Coagulopathy
Protocol
 Recognize patients at risk…immediately  “Code Red” blood in the ED
 Begin treatment in the ED…immediately – 4 U PBC, 2 U thawed plasma
 Avoid dilution of coagulation proteins  Multiple Belmont use
– Avoid NS / LR
 Fresh whole blood
 Achieve resuscitation end points
– Normothermic, NL INR, SBP > 90, Hgb >= 11,  Specific component therapy
BD <= 6  Recombinant fVIIa
 Massive transfusion protocol
Predictors of Death
 Depressed GCS at EMT admission



pH < 7.0
BD ≥ 20
“War is Hell.”
 INR ≥ 2.0 William T. Sherman
 EMT thoracotomy
 Emergent, unplanned return to the OR
pH=6.9 BD=18 BP 74/40 HR 140’s INR 1.8
Friend
Patriot
Surgeon

DEADLY ENDOCRINOLOGIC DISORDERS


THE CALM, CONFUSED PATIENT

BEYOND ACLS
Salim R. Rezaie, MD
NWS Current Topics in Emergency Medicine Beyond ACLS 195
Twitter: @srrezaie
Facebook: REBEL EM
Beyond ACLS
Salim R. Rezaie, MD
@srrezaie
EM Other Specialities
Disease Manifestation
Probability of Error
Time
www.rebelem.com
CPR
Epi
C
IV
POCUS Pulse P
R
P
RATE E
P
R
R
100 – 120/min 2015 AHA CPR E
F
S
Guideline U
S
S
DEPTH Update I
U
R
O
2in - 2.4in E
N
RECOIL TIME
Allow Full Recoil
PAUSE = Decreased Perfusion
INTERRUPTIONS
Minimize Pauses
Cunningham LM et al. AJEM 2012
Neuro Intact Outcome
CPR: Man or Machine?

5 RCTs
R.I.P.
>10,000 Pts with OHCA
vs NO DIFFERENCE
ROSC
Survival
Survival with Good Neurologic Outcome
Mechanical CPR NOT Dead NO IV Access
15g Needles
Humeral
Head IO Infusion Rates Under Pressure
(300mmHg): Cadaver Study
Outcome Humerus Proximal Tibia

Mean Flow Rate 57.1 mL/min 30.7 mL/min
1st Attempt Success 100% 81%
Proximal
Tibia
Distal
Tibia
PMID: 25757113
1st Attempt Success Time to Access (min)

100% 8.00
91%
90% 7.0
7.00
80%
6.00 5.8
70%
60% 5.00 4.6
51%
50% 43% 4.00
40%
3.00
30%
20% 2.00
10% 1.00
0%
0.00
Tibial IO Humerus IO PIV Tibial IO Humerus IO PIV
Reades R et al. Ann Emerg Med 2011 Reades R et al. Ann Emerg Med 2011
IO vs PIV
Higher
Success Rate
Faster Access
Achieved
8 RCTs
Class I (Strong)
Benefit>>>Risk
IV Epinephrine
Class IIa (Moderate)
Benefit>>Risk
↑ ROSC 50%
Class IIb (Weak) 1mg q3 – 5min
Benefit≥Risk
No ↑ Survival 75%
Class III (No Benefit)
Benefit=Risk
MAYBE ↑ Mortality 25%
Reasonable
PARAMEDIC-2 Active
Class III (Harm)
Risk>Benefit
Dirty “Epi” Drip
WTF + = 1 mcg/mL
Epi Drip
Epi Drip in OHCA
0.5mcg/kg/min
100kg Patient
50mcg/min
250mcg over 5min Cognitive Support Support Avoid Post

Offload CPP CPP ROSC BP
H ? H ?
≈1/3 of
PEA Cardiac
Arrest Cases
T
?
Poor
Prognosis
? H T H
Narrow Complex PEA

Pulseless Electrical Activity
Cardiac Tamponade
Narrow Complex QRS Wide Complex QRS
Acute MI*
QRS <0.12 QRS ≥0.12
Tension PTX
Mechanical RV Problem Metabolic LV Problem
Acute PE*
Acute Myocardial Infarction*
Pulmonary Embolism* Mechanical Hyperinflation
Wide Complex PEA
Hyperkalemia IV Calcium; Shift
Sodium Channel Blocker

Sodium Bicarbonate
Toxicity
K+ 9.0 1 amp CaGluc + 1 amp Bicarb
Cognitive Offload Not in Trauma

No Outcomes Data
Less to Remember
PE & MI Narrow or Wide QRS
Pros Cons
Is the Pulse Check Dead? Pulse

Checks
Manual Pulse Check Pseudo-PEA vs PEA
>5sec 43%
>10sec 4%
Arterial Line TTE

Cardiac Activity
on TTE
ROSC = 51.6%
No Cardiac
Activity on TTE
ROSC = 2.4%
EtCO2 at 20 Min Caveats of EtCO2

<10 - 15mmHg = No ROSC
10 – 20mmHg = CPR
>20mmHg = ROSC ETT Dislodged
Respiratory Causes
<10mmHg at 20min
Survival = 0.8% PE
Summary
Beyond ACLS
Salim R. Rezaie, MD
@srrezaie
Questions
DKA MYTHS
Salim R. Rezaie, MD
NWS Current Topics in Emergency Medicine DKA Myths 204
Twitter: @srrezaie
DKA Myths Facebook: REBEL EM
Salim R. Rezaie, MD
@srrezaie
No Financial
Disclosures
www.rebelem.com
86/52
136
97%
30
99.1
Accucheck
CRITICAL HIGH
ABC’s
Labs
Myth #1: We Should Get ABGs

Instead of VBGs in DKA
2010 Review ABG vs VBG pH

3 Trials = 265 Pts 200 Pts Presumed DKA
Mean pH Diff = 0.02 Treatment Change 2.5%

Mean Bicarb Diff ≈ -2.0 Disposition Change 0.5%
ABGs
VBG ABG
Painful
Complications
Start Insulin
Now?
Myth #2: After IVFs the Next Step is

to Start Insulin
Insulin Therapy
VBG K+
pH = 6.9
Bicarb < 5 Insulin ATPase Cell
K+ = 2.8 Na+
Glucose = 843
Keep it Simple
Serum PO K+ IV K+ Insulin
K+ Infusion?
Serum PO K+ IV K+ Insulin Serum PO K+ IV K+ Insulin

K+ Infusion? K+ Infusion?
>5.0 NONE NONE YES <3.5 40 x1 20 - 40 NO
After IVF, Replace

Electrolytes First
Serum PO K+ IV K+ Insulin
K+ Infusion?
3.5 –
20 x1 10 - 20 YES
5.o
VBG
pH = 6.9
Myth #3: Once the pH is <7.1 Give Bicarb < 5
Bicarbonate K+ = 2.8
Glucose = 843
American 2011 Systematic Review
Diabetes 44 Trials
Association 400 Pts
Bicarb vs NO Bicarb
Last Update: 2009
2013 Retrospective Study

Results
86 Patients
Metabolic Acidosis Bicarb vs NO Bicarb

Increased HypoK+
No Study with pH <6.85
Results
Metabolic Acidosis
Time on Insulin
Time to Hospital Discharge
VBG
pH = 6.9
Bicarb < 5
Myth #4: We Should Bolus Insulin K+ = 2.8
Before Starting an Infusion
Glucose = 843
Bolus Insulin No Differences

vs
NO Bolus
Goyal et al. 2008

Hypoglycemia
Insulin Drip
0.05 – 0.1 U/kg/hr
6% vs 1%
Refuted By
Case Series
Bonus Myth: Euglycemic DKA (euDKA) DOES Case Reports
NOT Exist
Risk Factors
euDKA Recognition
Anion Gap Acidosis
Food Restriction Euglycemia
Partial Treatment
Vomiting
↓ Gluconeogenisis
SGLT-2 Inhibitors 32%
CHECK FOR KETONES

Treatment Take Home Points

IVF
VBG NOT ABG
Electrolytes
Insulin
After IVF, Replace Electrolytes 1st
Dextrose Just Say NO to Bicarb & Bolus Insulin

Containing euDKA is Not a Myth
Solutions
Thank You
2018 Schedule
10/3, 2018 Gatlinburg, Tennessee EKG Interpretation Seminar
10/4-7, 2018 Gatlinburg, Tennessee Anesthesia Spectrum + ACLS/PALS
10/8-12, 2018 Gateway, Colorado Clinical Anesthesia Update

10/15-27, 2018 13-Day Vietnam and Cambodia Land Tour Anesthesia Update
10/22-26, 2018 Springdale, Utah (Zion National Park) Clinical Anesthesia Update
10/26-29, 2018 New York, New York Topics in Emergency Medicine
Presented by Northwest Seminars
10/28 - 11/2, 2018 Maui, Hawaii Anesthesia Topics
10/29 - 11/10, 2018 12-Night Western Mediterranean Cruise Clinical Concerns in Anesthesia
10/31, 2018 Key West, Florida EKG Interpretation Seminar
11/1-4, 2018 Key West, Florida Keys in Anesthesia + ACLS/PALS
11/3-4, 2018 Orlando, Florida Ophthalmic Block Hands-on Workshop
11/4-9, 2018 Providenciales, Turks and Caicos Islands Current Topics in Anesthesia
11/4-9, 2018 Port Maria, Jamaica Topics in Emergency Medicine
11/11-16, 2018 Port Maria, Jamaica Reviews for Anesthesia Professionals
11/12-16, 2018 Maui, Hawaii Topics in Pediatric Emergency Medicine
11/15-18, 2018 Key West, Florida Topics in Emergency Medicine
11/18-30, 2018 12-Night Southern Caribbean Cruise Clinical Concerns in Anesthesia
24 Credit Program!
11/27-30, 2018 Napa Valley, California Relevant Topics in Anesthesia
11/28 - 12/1, 2018 Nassau, Bahamas Current Anesthesia Topics
12/2-7, 2018 Palm Beach, Aruba Topics in Emergency Medicine
12/4-7, 2018 Savannah, Georgia Current Topics in Anesthesia
24 Credit Program!
12/6-9, 2018 Palm Beach, Florida Topics in Emergency Medicine
12/10-20, 2018 10-Night East Asia Cruise: Hong Kong, Japan, Taiwan, Topics in Anesthesia
and the Philippines 24 Credit Program!
12/10, 2018 Las Vegas, Nevada EKG Interpretation Seminar
12/11-14, 2018 Las Vegas, Nevada Cardiothoracic and Vascular Anesthesia Update + ACLS/
PALS
12/13-16, 2018 Phoenix, Arizona Current Topics in Emergency Medicine
12/17-20, 2018 Key Biscayne (Miami), Florida Current Topics in Anesthesia
12/30, 2018 - 1/6, 7-Night Eastern Caribbean Holiday Cruise Topics in Anesthesia
2019
* Preliminary 2019 Schedule

1/8-11, 2019 Phoenix, Arizona Current Topics in Anesthesia
1/14-18, 2019 San Juan, Puerto Rico Relevant Topics in Anesthesia
1/17-20, 2019 Sarasota, Florida Update in Obstetrical Anesthesia
1/20 - 2/3, 2019 14-Night Antarctica Cruise Topics in Anesthesia
1/27 - 2/1, 2019 Port Maria, Jamaica Reviews for Anesthesia Professionals
1/28 - 2/1, 2019 Lake Tahoe (Truckee), California Anesthesia Update
2/3-8, 2019 Guacalito de la Isla, Nicaragua Anesthesia Update
2/4-8, 2019 Sun Valley, Idaho Topics in Emergency Medicine
2/5-8, 2019 Las Vegas, Nevada Anesthesia Update + ACLS/PALS
2/11-14, 2019 Kona, Hawaii Anesthesia Update
2/14-17, 2019 Orlando, Florida Current Topics in Anesthesia
2/17-27, 2019 10-Night Brazil Cruise Clinical Concerns in Anesthesia
2/17-28, 2019 Ecuador & The Galapagos Islands Land and Sea Tour Clinical Concerns in Anesthesia
2/18-21, 2019 Orlando, Florida Topics in Emergency Medicine
2/21-24, 2019 Charleston, South Carolina Current Challenges in Anesthesia + ACLS/PALS
2/25 - 3/1 2019 Jackson Hole, Wyoming Anesthesia Update
2/28 - 3/3, 2019 Tucson, Arizona Anesthesia Update
3/4-8, 2019 Lake Tahoe (Stateline), Nevada Topics in Emergency Medicine
3/5-15, 2019 10-Night New Zealand Cruise Clinical Concerns in Anesthesia
3/6-9, 2019 Anaheim (Disneyland), California Anesthesia Update
3/7-10, 2019 Dallas, Texas Anesthesia Update + ACLS/PALS
3/10-17, 2019 7-Night Eastern Caribbean Cruise Current Anesthesia Practice
3/11-14, 2019 Duck Key, Florida Topics in Emergency Medicine
3/11-15, 2019 Park City, Utah Topics in Anesthesia
3/11-15, 2019 Maui, Hawaii Update in Critical Care
3/17-24, 2019 7-Night Mexican Riviera Cruise Clinical Concerns in Anesthesia
3/18-22, 2019 Whistler, British Columbia, Canada Current Topics in Anesthesia
3/21-24, 2019 Duck Key, Florida Current Challenges in Anesthesia
3/24-29, 2019 Cozumel, Mexico Anesthesia Update
Scuba Diving Available!
3/25-28, 2019 Bonita Springs, Florida Topics in Emergency Medicine

3/25-29, 2019 Kauai, Hawaii Topics in Emergency Medicine
3/25-29, 2019 Park City, Utah Update in Critical Care
3/28-31, 2019 Memphis, Tennessee Anesthesia Update + ACLS/PALS
3/31 - 4/5, 2019 Providenciales, Turks and Caicos Islands Topics in Emergency Medicine
4/2-5, 2019 Monterey, California Topics in Anesthesia
4/3-6, 2019 Hilton Head, South Carolina Relevant Topics in Anesthesia
4/7-12, 2019 Providenciales, Turks and Caicos Islands Current Topics in Anesthesia
4/8-11, 2019 Virginia Beach, Virginia Update in Obstetrical Anesthesia
4/8-17, 2019 9-Night Pacific Coastal Cruise Clinical Concerns in Anesthesia
4/8, 2019 Las Vegas, Nevada Business Concepts in Healthcare
4/13-14, 2019 Orlando, Florida Ophthalmic Block Hands-On Workshop
4/14-21, 2019 7-Day Eastern Caribbean Cruise Topics in Anesthesia
4/16-19, 2019 Vancouver, British Columbia, Canada Current Anesthesia Practice
4/21-28, 2019 7-Night Western Caribbean Cruise Topics in Emergency Medicine
4/25-28, 2019 Destin, Florida Topics in Anesthesia + ACLS/PALS
4/25-28, 2019 New Orleans, Louisiana Anesthesia Update
4/28 - 5/3, 2019 Ambergris Caye, Belize Giant Strides Anesthesia
4/29 - 5/2, 2019 Bonita Springs, Florida Current Topics in Anesthesia

5/6-9, 2019 Monterey, California Topics in Emergency Medicine
5/6-17, 2019 11-Night Western Mediterranean Cruise Clinical Concerns in Anesthesia
5/9-12, 2019 Chicago, Illinois Topics in Anesthesia + ACLS/PALS
5/13-16, 2019 Brooklyn, New York Anesthesia Update
5/16-19, 2019 Kissimmee, Florida Update in Critical Care
5/20-23, 2019 Indian Wells, California Topics in Anesthesia
5/20-24, 2019 San Juan, Puerto Rico Topics in Emergency Medicine
5/21-24, 2019 Austin, Texas Anesthesia Update
5/23-26, 2019 Philadelphia Pennsylvania Current Challenges in Anesthesia
5/27-31, 2019 Reykjavík, Iceland Current Anesthesia Practice
6/3-6, 2019 Duck, North Carolina Anesthesia Update
6/3-14, 2019 11-Day Iceland & Ireland Cruise Topics in Anesthesia
6/5-8, 2019 Boise, Idaho Relevant Topics in Anesthesia
6/10-13, 2019 Lake Oconee (Greensboro), Georgia Topics in Anesthesia
6/10-14, 2019 Yosemite, California Anesthesia Update
6/13-16, 2019 Key West, Florida Topics in Anesthesia
6/17-21, 2019 Jackson Hole, Wyoming Relevant Topics in Anesthesia
6/17-21, 2019 Grand Cayman, Cayman Islands Anesthesia Update
6/19-22, 2019 Cincinnati, Ohio Anesthesia Update + ACLS/PALS
6/20-23, 2019 Nashville, Tennessee Update in Critical Care
6/24-27, 2019 Las Vegas, Nevada Anesthesia Update
6/25-28, 2019 Savannah, Georgia Topics in Emergency Medicine
6/26-29, 2019 Washington, D.C. Relevant Topics in Anesthesia
6/30 - 7/7, 2019 7-Night Alaska Hubbard Glacier Cruise Clinical Concerns in Anesthesia
7/11-14, 2019 St. Pete Beach, Florida Topics in Emergency Medicine
7/14-21, 2019 7-Night Bermuda Cruise Current Anesthesia Practice
7/14-21, 2019 7-Night Alaska Cruise Topics in Emergency Medicine
7/15-19, 2019 Falmouth (Cape Cod), Massachusetts Topics in Anesthesia
7/17-20, 2019 Myrtle Beach, South Carolina Current Topics in Trauma Anesthesia
7/8-12, 2019 Honolulu, Hawaii Anesthesia Update
7/8-12, 2019 Whitefish, Montana Anesthesia Update
7/22-25, 2019 Clearwater Beach, Florida Current Topics in Anesthesia
7/24-27, 2019 Portland, Oregon Pediatric Anesthesia Update
8/1-4, 2019 Huntington Beach, California Current Topics in Emergency Medicine
8/4-11, 2019 7-Day Glacier Discovery Northbound Cruise Topics in Anesthesia
8/5-9, 2019 Banff, Alberta, Canada Clinical Topics in Anesthesia
8/12-16, 2019 Whitefish, Montana Topics in Emergency Medicine
8/19-23, 2019 Anchorage, Alaska Topics in Emergency Medicine
8/19-30, 2019 11-Night Amalfi Coast & Greek Isles Cruise Clinical Concerns in Anesthesia
8/21-24, 2019 Boston, Massachusetts Anesthesia Update
9/9-13, 2019 Budapest, Hungry Anesthesia Update
9/15-27, 2019 12-Night Iberian Adventure Cruise Current Topics in Anesthesia
9/18-21, 2019 Sedona, Arizona Current Anesthesia Practice
9/19-22, 2019 Hilton Head, South Carolina Relevant Topics in Anesthesia + ACLS/PALS
9/23-26, 2019 Sedona, Arizona Topics in Emergency Medicine
9/23-27, 2019 Jackson Hole, Wyoming Clinical Anesthesia Update
9/30 - 10/3, 2019 Amelia Island, Florida Anesthesia Update
10/2, 2019 Gatlinburg, Tennessee EKG Interpretation Seminar
10/3-6, 2019 Gatlinburg, Tennessee Anesthesia Spectrum + ACLS/PALS
10/7-10, 2019 Newport, Rhode Island Current Topics in Anesthesia
10/7-11, 2019 Springdale, Utah (Zion National Park) Topics in Emergency Medicine
10/14-17, 2019 Kansas City, Missouri Anesthesia Update + ACLS/PALS
10/14-18, 2019 Maui, Hawaii Topics in Emergency Medicine
10/28-31, 2019 Middleburg, Virginia Anesthesia Update
11/4-7, 2019 Providenciales, Turks and Caicos Islands Emergency Medicine Update
11/7-10, 2019 Key West, Florida Keys in Anesthesia
11/10-15, 2019 Maui, Hawaii Relevant Topics in Anesthesia
11/10-15, 2019 Port Maria, Jamaica Reviews for Anesthesia Professionals
11/14-17, 2019 Key West, Florida Topics in Emergency Medicine
11/16-23, 2019 7-Night Eastern Caribbean Cruise Anesthesia Update
11/17-22, 2019 Providenciales, Turks and Caicos Islands Anesthesia Update
12/3-6, 2019 Savannah, Georgia Current Topics in Anesthesia
12/3-6, 2019 Los Angeles, California Topics in Emergency Medicine
12/5-8, 2019 White Sulphur Springs, West Virginia Topics in Anesthesia
12/8-13, 2019 Palm Beach, Aruba Topics in Anesthesia
12/9, 2019 Las Vegas, Nevada Business Concepts
12/9-12, 2019 Charleston, South Carolina Update in Critical Care
12/12-15, 2019 South Beach (Miami) Florida Topics in Emergency Medicine
12/16-19, 2019 South Beach (Miami) Florida Anesthesia Update
12/29, 2019 - 1/5, 7-Night Eastern Caribbean Cruise Current Anesthesia Practice
2020

1/14-25, 2020 11-Night Great Barrier Reef Cruise Anesthesia Update
2/3-7, 2020 Lake Tahoe (Truckee), California Anesthesia Update
2/20-23, 2020 Charleston, South Carolina Anesthesia Update + ACLS/PALS
2/26-29, 2020 Orlando, Florida Anesthesia Update
3/2-5, 2020 Duck Key, Florida Topics in Emergency Medicine
3/9-12, 2020 Duck Key, Florida Anesthesia Update
3/9-13, 2020 Jackson Hole, Wyoming Anesthesia Update
3/11-14, 2020 Anaheim (Disneyland), California Anesthesia Update
3/12-15, 2020 Dallas, Texas Anesthesia Update + ACLS/PALS
3/19-22, 2020 Tucson, Arizona Anesthesia Update
3/29-4/3, 2020 Providenciales, Turks and Caicos Islands Anesthesia Update
4/19-24, 2020 Providenciales, Turks and Caicos Islands Emergency Medicine Update
4/30 - 5/3, 2020 New Orleans, Louisiana Anesthesia Update
5/18-21, 2020 Rancho Mirage (Palm Springs), California Anesthesia Update
6/2-5, 2020 Sedona, Arizona Update in Critical Care
6/8-12, 2020 Kapolei (O’ahu), Hawaii Anesthesia Update
6/23-26, 2020 Williamsburg, Virginia Anesthesia Update
7/13-17, 2020 Honolulu, Hawaii Emergency Medicine Update
7/22-25, 2020 Portland, Oregon Topics in Emergency Medicine
8/3-7, 2020 Sunriver, Oregon Anesthesia Update
8/3-7, 2020 Anchorage, Alaska Anesthesia Update
9/12-15, 2019 Gulf Shores, Alabama Anesthesia Update
9/14-17, 2020 Sedona, Arizona Topics in Emergency Medicine
9/21-24, 2020 Amelia Island, Florida Anesthesia Update
9/23-26, 2020 Sedona, Arizona Anesthesia Update
10/12-16, 2020 Maui, Hawaii Topics in Emergency Medicine
11/8-13, 2020 Maui, Hawaii Anesthesia Update
12/1-4, 2020 Napa, California Anesthesia Update
12/8-11, 2020 Savannah, Georgia Anesthesia Update
12/17-20, 2020 Key Biscayne, Florida Anesthesia Update

3/15-19, 2021 Whistler, British Columbia, Canada Anesthesia Update
3/18-21, 2021 Tucson, Arizona Anesthesia Update
3/21-26, 2021 Cozumel, Mexico Anesthesia Update
4/8-11, 2021 Memphis, Tennessee Anesthesia Update + ACLS/PALS

7/12-16, 2021 Falmouth (Cape Cod), Massachusetts Anesthesia Update
9/27-30, 2021 Amelia Island, Florida Anesthesia Update

* Dates, locations, and topics are subject to change without notice.
New locations are being added daily.

Visit our website for up-to-date location and conference schedules.
north west
S E M I N A R S
Northwest Anesthesia Seminars
www.nwas.com www.northwestseminars.com
info@nwas.com info@northwestseminars.com
(800) 222-6927 | (509) 547-7065 | Fax (509) 547-1265

Rev 6/25/18
Frequent Attendee Points
Program
We value your patronage and have a simple program to reward
you. Our Frequent Attendee Points (FAP) program gives you an
added bonus for money spent on our seminars, as well as hotel
reservations and cruise cabins booked through our in-house
travel agency, Northwest Worldwide Travel.
How it works
Frequent Attendee Points for seminar tuition are calculated at
ten percent (10%) of the cost of the seminar. For example, if your
tuition is $800, you would earn 80 Frequent Attendee Points.
You also receive 1.5% of the cost of the net room rate for your
hotel room or cruise cabin booked through Northwest Worldwide
Travel. For example, if you spend five nights at a hotel for $185
per night, would earn you 13.88 Frequent Attendee Points.
Frequent Attendee Points can only be applied to a full tuition

cost; no partial tuition can be credited. There is no dollar value
to Frequent Attendee Points for anything other than Northwest
Seminars course tuition. Frequent Attendee Points cannot be
transferred or gifted to another person; no partial credit can be given.
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(800) 222-6927
www.northwestseminars.com

18EMAWF

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north west S E M I N A R S

Continuing education for the medical professional

Current Topics in Emergency Medicine

To download lecture notes visit: http://nws.ac/18EMAWF

0700 Registration - Mandatory Sign In - Continental Breakfast

Sumeru Ghanshyam Mehta, MD

Justin Barrett Williams, MD, FACEP

SYLLABUS DOWNLOAD LINK

To download lecture notes visit: http://nws.ac/18EMAWF

9) Novel Use of Bedside Ultrasound

12) All Bleeding Stops Sometimes: Hemorrhage Control in Trauma

13) The Zebras: Unique Presentations and Stranger Diagnoses

14) Emergent Evaluation and Treatment of Acute Delirium

15) Emergent Evaluation and Treatment of the Acute Red Eye

16) Reflections on a Combat Sabbatical: Lessons Learned in War

17) Morbidity and Mortality: Deadly Endocrinologic Disorders

18) Morbidity and Mortality: The Calm, Confused Patient

19) Beyond ACLS

20) DKA Myths

 Relatively insensitive for PTX  32 yo male thrown off his bike, landing on his

 Infant intubated for  15 yo F with chest pain

 Perform lateral CXR whenever possible. Pleural effusions and  50 yo obese female c/o rapid onset left sided

 Importance of checking lateral CXR.  60 yo female with gradual onset SOB x 2

 Pericardiocentesis performed and taken to  Normal

EMERGENCY MEDICINE AT 29,035 FT:

To scorn all strife, and to view all life

• Medical Clinic at Everest Base Camp

• (1) Kathmandu: 1300m / 4265 ft

Worst climbing movie EVER

High Altitude Illness High Altitude Illness

Potential medical problems associated

• Intermediate altitude (1500-2500m) • Acute hypoxia

High Altitude Illness High Altitude Illness

Hackett et al, NEJM, 2001

High Altitude Illness High Altitude Illness

West, Ann Int Med; 2004

High Altitude Illness (HAI) High Altitude Illness

Proposed Pathophysiological Process

Hackett et al, NEJM, 2001 West, Annals Int Med; 2004

• Oxygen deprivation at HA is inevitable leading to • Reduced maximal oxygen consumption

West, Ann Int Med; 2004

HAI – Effects of Hypoxia on Mental Performance HAI- Effects of Hypoxia on Sleep

McFarland, Physiologic adaptions; 1972

HAI – Physiology of AMS HAI - Physiology of HACE

Proposed Pathophysiological Process

Hackett, JAMA; 1998 Hackett et al, NEJM, 2001

HAI – Physiology of HAPE HAI – Physiology of HAPE

West, AnnInt Med; 2004

High Altitude Illness HAI - Acclimatization

HAI - Acclimatization and Hyperventilation HAI - Acclimatization and Polycythemia

• Most important feature • Develops relatively slowly > entire process

HAI - Acclimatization and Acid-Base Changes HAI – Misconceptions about Acclimatization

Rahn,Am J Phys; 1949

High Altitude Illness HAI – Management of AMS

Honigman, B. et. al. Ann Intern Med

HAI – Management of AMS HAI – Management of AMS

HAI – Management of AMS HAI – Management of AMS

HAI – Management of AMS HAI – Management of AMS

• Prevention is Key • Prophylaxis

• Proven to work but what is optimal dosage? • Background

Maakestad, WEM; 2001

AMS Az GB Both Placebo • Conclusion

HAI – Treatment of AMS HAI – Management of HACE