Emergency Medicine

Residents’ Association of Michigan

ITE Review Course

February 9, 2024

Virtual
Zoom Call
 In-Training Review Course

Friday, February 9, 2024

8:30 – 8:45 am Welcome – Intro to ITE/Boards/Study Prep Guide Angela Pugliese, MD

8:45 – 9:15 am Trauma 1 Jamie Hope, MD
9:15 – 9:45 am Abd/GI Caroline Dowers, MD
9:45 – 9:50 am Break
9:50 – 10:20 am Cardiovascular 1 Matt Hysell, MD
10:20 – 10:50 am Toxicology Bram Dolcourt, MD, FACEP
10:50 – 11:10 am Procedures Neha Sykes, MD
11:10 – 11:15 am Break
11:15 – 11:35 am EMS/Disaster Robert Dunne, MD, FACEP
11:35 – 12:00 pm Renal/GU Meghan Liroff, MD
12:00 – 1:00 pm Lunch/Visit Vendors Breakouts
1:00 – 1:30 pm Trauma 2 John Joseph, MD
1:30 – 2:00 pm Neuro Fadi Kasyouhanan, MD
2:00 – 2:20 pm Pediatrics Dan Nguyen, MD
2:20 – 2:30 pm Break
2:30 – 3:00 pm Cardiovascular 2 Dawn Jung, MD
3:00 – 3:30 pm Thoracic/Respiratory Dave Betten, MD, FACEP
3:30 – 4:00 pm OB/GYN Kirk Trentham, MD

- Schedule is subject to change -

 EMRAM ITE Review Course
February 9, 2024
Virtual Zoom Call

FACULTY

David Betten, MD, FACEP John Joseph, MD

Sparrow Health System Beaumont Royal Oak
bettend@[Link] jjoseph6@[Link]

Co-Course Director Dawn Jung, MD

Daniel DeWeert, MD Beaumont Royal Oak
Henry Ford Hospital [Link]@[Link]
DDeweer1@[Link]
Fadi Kasyouhana, MD
Bram Dolcourt, MD, FACEP Beaumont Royal Oak
DMC – Detroit Receiving Hospital [Link]@[Link]
bdolcourt@[Link]
Meghan Liroff, MD
Caroline Dowers, MD Henry Ford Hospital
Henry Ford Health MLIROFF1@[Link]
cdowers1@[Link]
Dan Nguyen, MD
Robert Dunne, MD, FACEP Beaumont Royal Oak
St. John Hospital and Medical Center [Link]@[Link]
rkdunne@[Link]
Co-Course Director
Jamie Hope, MD Angela Pugliese, MD
Beaumont Royal Oak Henry Ford Hospital
[Link]@[Link] apuglie1@[Link]

Matthew Hysell, MD Neha Sykes, MD

Spectrum Health - Lakeland Detroit Receiving Hospital
[Link]@[Link] nsykes1@[Link]

Kirk Trentham, MD
Sparrow Hospital – Lansing
trentham@[Link]
Carol Rivers’ Emergency Medicine Review Products
Eleventh Edition Just Released!

Free Shipping Offer to Michigan In-Service Participants

Use code FREESHIPMI24 prior to checkout. Valid through: 2/29/24

Rivers’ Textbook Rivers’ Package (text & flash cards)

FREE Includes access to eBook Includes access to eBook & eCards
SHIPPING Non-Member Resident - $200.00 Non-Member Resident - $250.00
EMRA Resident - $150.00 EMRA Resident - $200.00

A trusted and successful tool utilized for decades!

• Comprehensive, content-focused, 2-volume textbook
• Ideal study-tool for certification and In-training exam preparation
• 500 + Questions/Answers
• eBook access provided through a robust, searchable, web-based portal.
• Hundreds of Images including color images in Cutaneous Disorders
• End of Chapter Clinical Scenarios
• Updated guidelines and ACEP clinical policies
• Flash Cards also available!

Contact Ohio ACEP

info@[Link] | (614) 792-6506 | [Link] [Link]/rivers
EMRAM ITE Review – Lecture Content Guide

Trauma 1

a. Hemorrhagic shock – Not as simple as blood out, blood in

i. Trauma remains a leading cause of death worldwide
ii. Half of trauma deaths are attributed to hemorrhage
iii. Hypovolemic shock occurs when there is a decreased intravascular volume to
the point of cardiovascular and end organ compromise (ie, tissue-perfusion
mismatch)
iv. Disproportionate in young adults and children (YPLL)
v. Many factors contribute
1. Patient age
2. Physiologic reserve
3. Comorbidities
4. Anticoagulant use
5. Baseline hypertension may mask hypotension
6. Use of Beta-blockers, CCB, other medications that might mask
hemodynamic changes or blunt body’s natural physiologic response to
the stress
vi. Total circulating blood volume for healthy 70 kg patient = 5000 mL

vii. Classes of shock (I-IV)

1. Class I
a. <15% volume loss (<750 mL)
b. Minimal tachycardia, normal BP, normal pulse pressure, < 2 sec
cap refill, normal RR
c. UOP 30 cc/hr or more
d. Slightly anxious
2. Class II
a. 15-30% blood volume (750-1500 mL)
b. HR > 100, BP normal, pulse pressure down, cap refill 2-3 sec,
resp rate 20-30
c. UOP 20-30 cc/hr
d. Mildly anxious
3. Class III
a. 30-40% blood volume (1500-2000 mL)
b. HR >120, hypotension, lower pulse pressure, cap refill 3-4 sec,
30-40 RR
c. UOP 5-10 cc/hr
d. Anxious and confused
4. Class IV
a. > 40% (>2000 mL)
 b. Pulse > 140, severe hypotension and low pulse pressure, cap
refill > 5 sec, RR > 40
c. UOP negligible
d. Confused, lethargic, obtunded

viii. Acute management – Pitfalls

1. Ensure there are not other contributing factors that need to be
alleviated (tension PTX, cardiac tamponade, etc) for the resuscitation
2. Hypothermia – Coagulopathy – Acidosis: “vicious cycle” of hemorrhagic
shock – the lethal triad!
3. Iatrogenic effects – Treatments can worsen hypothermia, coagulopathy,
and acidosis!
4. Loss of 02 carrying capacity + hypovolemia → SIRS response and
acidosis, which leads to end organ dysfunction, including hepatic
dysfunction (can’t make clotting factors), renal dysfunction (can’t make
urine)
5. Massive blood loss (in and of itself) leads to coagulopathy, in addition
that caused by treatment
6. Crystalloids – lead to coagulopathy by diluting clotting factors. Also,
often room temperature, which worsens hypothermia, which worsens
coagulopathy…while in a cold trauma room!
7. Blood transfusion – if not warmed, worsens hypothermia. Transfusion
products contain citrate, which chelates calcium → hypocalcemia, liver
cannot clear citrate due to end organ damage → hypocalcemia leads to
decreased calcium-dependent vasoconstriction (which adds in with the
SIRS-mediated loss of vasoconstriction) → hemodynamic instability
8. Vasoplegia (loss of vasoconstrictive response) – caused by
hypocalcemia, then removal of sympathetic drive with RSI meds
worsens this, so they get hemodynamic collapse.
9. Abdominal compartment syndrome – tissue edema, intraabdominal 3rd
spacing, hypovolemia and hypotension = increased abdominal pressure
→ worsens venous return and leads vascular collapse and death if not
recognized and treated (may need to do paracentesis, NGT and foley to
evacuate intraabdominal contents as much as possible, consider
laparotomy)
10. TRALI and TACO – Occur within 6 hours of blood transfusion and are the
leading causes of transfusion-related fatalities.
a. There are no specific treatments, best to avoid occurrence
b. Combination of “hit” from the initial trauma and 2nd “hit” to
patient’s physiology from the transfusion
c. TRALI – Transfusion-related lung injury (non-cardiogenic
pulmonary permeability edema)
d. TACO – Transfusion-associated circulatory overload (cardiogenic
pulmonary hydrostatic edema)
 ix. Acute management – Goals
1. Focus on the treatment goal = * Buying time to identify and stop the
bleeding*
2. Initiate massive transfusion early when appropriate
a. YES: Obvious external bleeding with hypotension, tachycardia,
lactic acidosis (no brainer!)
b. MAYBE: Less clear, risk vs benefit
i. The worry is about wasting blood unnecessarily
ii. Check your institutional protocols, can you give unused
products back? Helps weigh activation
c. This is a time-sensitive decision
3. Replace what comes out
a. We bleed whole blood
b. PRBC:FFP:PLT – golden ration = [Link]
c. Consider TXA, cryoprecipitate depending on the situation
d. Normal body temp = 37 degrees (the temp of blood going out)
i. Room temp = 22 degrees
ii. Delta = 15 degrees!!
iii. Hypothermia is a high predictor of death!
e. Keep putting blood in until it stops coming out!
4. Protect vascular tone
a. Give calcium!!
i. It has been chelated out by the citrate in the blood
productions
ii. 1 gram for every 4-6 units of blood
b. Pressors
i. Pressors DO NOT fix bleeding! (not treating the
problem, may mask hypotension)
ii. Use strategically in addition to massive transfusion to
support hemodynamics until hemorrhage and end-
organ perfusion improved
iii. Consider when giving RSI drugs to counteract the
decreased vascular tone, keep hemodynamic balance
5. Manage resus volume
a. Not enough blood = bad AND too much blood = bad
b. Consider permissive hypotension
i. Higher BP = more bleeding
ii. Don’t need to over transfuse just to achieve a certain
blood pressure
iii. Choose the lesser evil in terms of volume and pressure,
this will be a dynamic and ongoing assessment!

b. Head Injuries
i. GCS – scale of 3-15
1. Eye opening response
 a. 4 = Spontaneously
b. 3 = To speech
c. 2 = To pain
d. 1 = No response
2. Best verbal response
a. 5 = Oriented to time, place, person
b. 4 = Confused
c. 3 = Inappropriate words
d. 2 = Incomprehensible sounds
e. 1 = No response
f. T = Intubated, unable to score verbal
3. Best motor response
a. 6 = Obeys commands
b. 5 = Moves to localized pain
c. 4 = Flexion withdrawal from pain
d. 3 = Abnormal flexion (decorticate)
e. 2 = Abnormal extension (decerebrate)
f. 1 = No response
4. Report the score and components: Example: GCS 10 = E3V4M3, this
ensures the treating team all understands the patient’s current level
and can assess for changes
5. Who can this apply to?
a. Patients prior to sedation and paralysis, whenever possible
b. Children 5 and older
c. Younger children might not understand the instructions, should
not be graded down
d. Also consider non-English speaking patients, patients with pre-
existing neurological or intellectual deficits, and hard of hearing
patients, should not be graded down inappropriately
6. Purpose of GCS
a. First appeared in 1974 in reports from neurosurgery professors
at the University of Glasgow
b. Became widespread in 1980s with its inclusion in the first
edition of the Advanced Trauma Life Support (ATLS)
c. Intended for TRAUMA
d. Now generalized across medical complaints (maybe
inappropriately?)
e. Crit Care Resus Pract 2011 article shows some efficacy in
prognosis and deciding treatment in mixed tox poisoning
f. High interobserver reliability
g. Easy, fast, objective, repeatable, no side effects

ii. Concussion
1. CLINICAL diagnosis
2. Very common
 a. Approx 2.5 million people sustain a TBI in the US every year
b. 75-95% are mild
c. Causes – MVC (20-45%), falls (30-38%), occupational (10%),
recreational (10%), assaults (5-7%)
d. Causes vary by age (toddlers and elderly are more likely to fall,
less likely to be engaged in occupational and organized sports
activity)
3. Symptoms are often due to a functional disturbance rather than a
structural injury
4. Typical concussion symptoms, non-red flag
a. Confusion, mild amnesia, nausea, repetitive questioning,
headache, vertigo, mood disturbances, photophobia, sleep
disturbances, difficulty concentrating, saccades with EOM
5. Does not require a head CT if no red flags – Red flags include:
a. Loss of consciousness
b. Persistent vomiting
c. Hemiparesis or focal injury
d. Visual field deficit
e. Pupillary abnormality
f. Seizure
i. Early posttraumatic seizures increase risk of
posttraumatic epilepsy by fourfold
ii. Antiseizure meds does not prevent development of
posttraumatic epilepsy, but may decrease frequency of
seizures and prevent seizure-induced re-injury
g. Review CT head rules below:
6. Canadian CT head Rule – requires head CT for any ONE of the following
a. GCS < 15 two hours after injury
b. Suspected open or depressed skull fracture
c. Any sign of basilar skull fracture
i. Raccoon eyes, battle sign, CSF leak (ears or nose)
d. Two or more episodes of vomiting
e. Sixty-five years old or older
f. Retrograde amnesia for more than 30 min prior to the event
g. Dangerous mechanism
i. Struck pedestrian, ejected from motor vehicle, fall from
> 3 feet or >5 stairs
h. Meet study exclusion criteria
i. Neuro deficit
ii. Seizure
iii. Coagulopathy or anticoagulant use
7. New Orleans Criteria applies to patients with GCS = 15, do a head CT if…
a. Headache, vomiting
b. Age > 60
c. Drug or alcohol intoxication
 d. Persistent anterograde amnesia
e. Seizure
f. Visible trauma above clavicles
8. NEXUS II criteria get CT if
a. Significant skull fracuture
b. Scalp hematoma
c. Neuro deficit
d. GCS <14
e. Abnormal behavior
f. Coagulopathy
g. Persistent vomiting
9. Sports-related sidelines evaluations and scoring tools are less helpful
and not validated if there was no pre-injury assessment done
10. Post-care instructions
a. Don’t send home alone
b. Brain rest
i. Increase sleep hours
ii. Avoid electronics
iii. Avoid complex tasks (work, homework, etc) if
symptoms worsen
iv. Data is mixed, pure rest may prolong symptoms
c. Treat pain and nausea
d. Avoid re-injury
i. Second-impact syndrome is worrisome and can lead to
permanent injury
ii. No return to play/practice/activities until symptom
resolution
iii. Consider a gradual return process, go back to rest if
symptoms occur or worsen
e. Consider outpatient f/u with Neuro or Sports Med concussion
specialist

iii. Epidural Hematoma

1. Bleeding in the potential space between the dura and the skill
a. Lens-shaped bleed
b. Does not cross the suture margins
2. Uncommon but very serious
3. Most often due to MVC, falls, assaults
4. Skull fractures present in 75-95% of cases
5. Caused most often by tear of middle meningeal artery
6. Symptoms
a. Classic “lucid interval” with LOC followed by awakening
followed by repeat LOC (occurs in 47%)
b. Ipsilateral dilated pupil due to uncal herniation with
compression of oculomotor nerve
 c. Cushing reflex (hypertension, bradycardia, resp depression)
d. Can progress to herniation and death
7. Head CT and STAT Neurosurgical consultation
a. Severity can be masked by anemia (lowers density of
hemorrhage on CT), hypotension (reduced rate of arterial
extravasation), scan immediately (hasn’t fully formed yet) – in
these cases, repeat head CT if clinical suspicion persists
b. Rarely need MRI (don’t want to delay), consider if atypical
locations of EDH (vertex) without signs of impending herniation
8. Needs neurosurgical drainage in many cases
9. Medical treatment (often while awaiting neurosurg)
a. Reverse anticoagulation
i. Warfarin – PCC or FFP, Vit K
ii. Xa inhibitors – Andexanet Alfa or 4-factor PCC
iii. Dabigatran – Idarucizumab or 4-factor PCC
iv. Heparin - Protamine
b. Manage pain and nausea
c. Consider anti-seizure medication
d. NO glucocorticoids!
e. Management of increased intracranial pressure
i. Hyperventilation
ii. Head elevation
iii. Osmotic diuresis (mannitol or hypertonic saline)
f. Burr hole if cannot get timely access to neurosurg
10. If rapid surgical evacuation is achieved, good prognosis for outcomes

iv. Subdural Hematoma

1. Bleeding between the dura and the arachnoid membranes
a. Crescent-shaped
b. Can cross suture margins
2. Very common, often less serious
3. Caused by tearing of bridging veins (which are stretched more in brains
with atrophy due to age, chronic alcohol use, etc)
4. Can be acute, subacute, chronic, acute on subacute/chronic
5. Associated skull fracture less common
a. Can be due to minor trauma
b. Higher risk in elderly, atrophy, coagulopathy
6. Symptoms may be mild, subtle, non-focal, or absent
a. May have AMS, speech impairment, headache, nausea, poor
appetite, vomiting, apathy, depression, Parkinsonism, gait
ataxia, somnolence
b. Pupillary changes, focal neuro deficit, paresis, seizures, coma
7. Imaging
a. Have a low threshold for imaging higher risk patients
b. Head CT is the most common
 i. Acute is hyperdense
ii. Chronic is isodense to hypodense
iii. Mixed density with acute on chronic rebleeding
iv. Small symmetric bilateral may be missed!
c. Consider MRI
i. Small, subtle bleeds
ii. Determine age of bleed
iii. Eval for secondary causes (tumor, AVM, etc)
d. N
8. Treatment
a. Reverse anticoagulation
b. Consider neurosurgical evaluation
i. Based on bleed severity, likelihood of subsequent
deterioration, and potential for recovery with surgery
ii. Red flags – dilated pupils, rapid or progressive
deterioration, drop of 2 GCS points, Cushings triad,
midline shift > 5 mm, brainstem compression
c. Pain and nausea management
d. Consider antiseizure medication
e. NO glucocorticoids!
f. Management of increased intracranial pressure if indicated
i. Hyperventilation
ii. Head elevation
iii. Osmotic diuresis (mannitol or hypertonic saline)
g. Serial neuro exams are important to monitor for evolving or
worsening symptoms
i. Re-image if changes in exam
h. Consider burr hole if rapid deterioration and neurosurg not
available
i. Less favorable prognosis, especially with risk factors
i. Older age, lower GCS, coma at presentation,
coagulopathy, other injuries

v. Skull Fractures
1. Most frequent site
a. Parietal > temporal > occipital > frontal
2. Linear is most common, then depressed and basilar skull fractures
3. CSF leak more common in basilar skull fx, particularly depressed
4. Fx over temporal-parietal bone = risk for epidural hematoma
5. Direct pressure if bleeding, but care not to compress/worsen depressed
skull fx
6. Obtain head CT, including bone windows
7. In cases of basilar fx, it is reasonable to obtain CT angio to assess for
vascular injury
 a. Raccoon eyes and battle sign are a LATE finding (hours to days),
may not be present at initial evaluation
b. Assess for hemotympanum (often develops within hours, may
not be immediate)
8. 5-15% of skull injury patients also have a C-spine fracture, consider
imaging
9. Treatment
a. Linear
i. No surgical intervention unless intracranial hemorrhage
ii. Observe 4-6 hours, consider D/C if no risk factors, don’t
d/c home alone
iii. Manage pain and nausea
b. Depressed
i. Prophylactic abx 5-7 days to prevent CNS infection
(scant data)
ii. Antiseizure meds (scant evidence)
iii. Manage pain and nausea
iv. Neurosurg evaluation
c. Basilar
i. Neurosurg consult for all
ii. Admission for all
iii. Maybe prophylactic abx (scant data), higher risk of CNS
infection if CSF leak persists > 7 days
d. Penetrating
i. Of course they will need neurosurg consultation
10. Outcome and prognosis depend on severity of underlying brain injury

c. Facial Injuries
i. Assessment
1. Can have other injuries – lacerations, nerve injury, head and C-spine
injuries, etc
a. Can have aspiration of blood, CSF, teeth, bone fragments, etc
2. Assessment
a. Questions
i. Can you breathe out of both sides of nose
ii. Any trouble speaking (mandibular fx)
iii. Any diplopia (orbital fx)
iv. Is hearing normal
v. Any facial numbness
vi. Do your teeth come together the way they did
yesterday
vii. Any teeth painful or loose
viii. Any bleeding from nose, mouth, ears
ix. Any vertigo
b. Physical exam
 [Link] nerves
[Link] symmetry
[Link] deformity
iv. Increased intercanthal distance (naso-orbito-ethmoid
fx)
v. Focal swelling and bruising
vi. Jaw occlusion
vii. Hemotympanum, CSF leak
viii. Septal hematoma, CSF leak
ix. Eyes – globe rupture, afferent pupillary defect,
hyphema, corneal abrasion, orbital stepoff, visual
acuity, visual fields, lacerations
x. EOM (look for entrapment, enophthalmos)
xi. Dental – fracture, missing or broken teeth
xii. Abnormal mobility, stop-offs
xiii. Crepitance
c. Treatment
i. Airway
ii. Pain and nausea management
iii. Imaging
iv. Consultation
v. Prophylactic abx?

ii. Le Fort Classification/Injuries

1. Type I – Horizontal alveolar ridge
a. Signs
i. Swelling of upper lip
ii. Buccal bruising
iii. Jaw malocclusion
iv. Loosening of teeth
2. Type II – Pyramidal nasofrontal suture
a. Signs
i. Deformity and swelling of midface
ii. Widening or intercanthal space
iii. Mobility of upper jaw and nose
iv. Jaw malocclusion
v. Periorbital edema and ecchymosis
vi. Epistaxis
vii. Bruising and vestibule plate bruising
viii. CSF rhinorrhea
3. Type II – Horizontal craniofacial dislocation
a. Signs
i. Similar to Type II
ii. Lengthening and flattening of face
iii. Orbital hooding
 iv. Enophthalmos
v. Mastoid region bruising
vi. Ear drainage
vii. Hemotympanum

iii. Orbital Blowout

1. Due to assaults, MVC, direct blow (sports, projectile)
2. Consider additional injuries – Intracranial, C-spine, other facial fxs
3. Orbit consists of 5 bones
a. Superior orbit: Thick frontal bone – harder to fx, more likely to
be associated with intracranial injury.
i. Associated injury – supraorbital nerve
b. Lateral wall of orbit: Greater wing of sphenoid bone and
zygoma (relatively thick)
i. Associated injury – lateral canthal ligament
c. Infraorbital rim and floor: Zygoma and (thin) maxillary bone
i. Associated injuries:
ii. inferior oblique and inferior rectus muscle (EOM
entrapment, enophthalmos, orbital dystopia)
iii. maxillary sinus
iv. infraorbital nerve
d. Medial wall: Maxillary and ethmoid bones
i. Injury to medial canthal ligament and lacrimal ducts
e. Extraocular muscles
i. Vertical movement – superior and inferior
ii. Horizontal movement – medial and lateral
iii. Torsion - combination
4. Injuries to extraocular muscles, medial and lateral canthal ligaments,
lacrimal duct system, infraorbital and supraorbital nerves
5. DO NOT PRESS ON THE EYE!
6. Imaging with CT
7. Optho consultation
8. Management of pain and nausea
9. Prophylactic abx? Limited data

iv. Auricular hematoma tx

1. Typically from blunt trauma to the cartilaginous auricle
2. Goal of treatment is prompt drainage and prevention of re-
accumulation of blood
a. Blood eats cartilage
b. Failure to do so results in permanent deformity (cauliflower ear)
c. Can lead to ischemia and/or infection if not treated
3. The protuberance of the ear makes and lack of fat and SQ tissue over
the auricle make it vulnerable to trauma
4. Clinical diagnosis, imaging is not routine
 5. Bleeding begins to organize and clot at approx. 24 hours, becomes more
firm
a. If it is subacute, not soft, consider ENT referral
6. Analgesia options
a. Procedural sedation
b. Auricular block
c. Avoid direct infiltration of local anesthetics into ear, particularly
with epi
7. Evacuation
a. Consider needle aspiration for < 2 cm
i. May have higher recurrence rate, limited evidence
b. I&D for > 2 cm
i. Incision should follow curvature of ear
c. Irrigate
8. After evacuation, compression is very important
9. Home observation for reaccumulation
10. Prophylactic abx – limited blood flow but sparse evidence

v. Retrobulbar hematoma
1. Blunt injury/projectile
2. Exophthalmos
3. Can become vision threatening
4. CT scan
5. Lateral canthotomy
a. Pressure > 40 mmHg
b. Signs of progressing vision loss
c. Don’t wait for optho!!
6. Emergent referral

vi. Globe rupture

1. Obvious penetrating injury
2. Abnormal pupil shape
3. Extrusion of intraocular contents
4. Obvious ocular FB (example: fishhook)
5. Sidel sign for more subtle cases
6. Do NOT put pressure on the eye
7. Cover, emergent referral, keep NPO
a. Pain and nausea management
8. IV Vanco and Ceftazidime or Fluroquinolone
9. Assess for other injuries

d. Environmental Emergencies
i. Hypothermia and hyperthermia
1. Can occur “off season”
 2. Can cause rhabdo, DIC, arrhythmias, seizures, AKI, hepatic injury,
hemodynamic collapse
ii. Hypothermia
1. Classification by core temperature and symptoms
a. Cold stress: 35-37 deg C(95-98.6)
i. Normal mental status
ii. Shivering
iii. Normal functioning
b. Mild: 32-35 deg C (90-95 deg F)
i. Alert but possibly altered
ii. Shivering
iii. Tachycardia, tachypnea, initial hyperventilation
iv. Abnormal function, not able to do ADLs
c. Moderate: 28-32 deg C (82-90 deg F)
i. Decreased LOC
ii. +/- Shivering
iii. Decreased HR and cardiac output, hypoventilation
d. Severe: < 28 deg C (82 deg F)
i. Unconscious
ii. Not shivering
iii. Dilated pupils
2. Cold diuresis, paradoxical undressing
3. DDX: Tox, withdrawal, myxedema coma, adrenal insufficiency, sepsis,
abuse
4. EKG changes
a. Slowed impulse conduction through potassium channels
b. Prolongation of all intervals
c. Osborn waves
d. Shivering can cause artifact
5. Treatment principles
a. Handle gently!
b. Monitor for arrhythmias
c. Core temp monitoring (ETT, rectal, foley)
d. Check glucose, other labs
6. Rewarming – Beware of afterdrop!
a. Remove wet clothing
b. Cover with warm blankets
c. Active external rewarming with forced air
d. Warmed IVF
e. Warmed lavage to stomach, bladder
f. ECMO
g. Peritoneal or pleural warmed irrigation

iii. Heat Stroke

1. Body temperature management
 a. Primarily by evaporation (which is impaired in air humidity >
75%)
b. Radiation, conduction, convection
c. Increased O2 consumption and metabolic rate
d. Heat stroke = Core temp > 40.5 deg C (105 deg F)
2. Exertional vs non-exertional
3. Patients at increased risk
a. Extremes of age
b. Pregnancy
c. Obesity
d. Poor physical condition
e. Lack of acclimatization
f. Social isolation
g. Dehydration
h. Heavy alcohol use
i. Drug and medication use
4. Factors with increased mortality
a. Degree of temperature elevation
b. Duration of exposure prior to initiation of cooling measures
c. Number of organ systems affected
d. Signs of severe – DIC, cardiovascular failure, anuria, ARDS
5. Signs/symptoms
a. Weakness, lethargy, dizziness, N/V
b. Signs may be subtle
c. Pulmonary edema
d. Altered mental status
e. Irritability
6. DDX: Tox, withdrawal, meds, sepsis, thyroid storm, infection, status
epilepticus, pheochromocytoma, DKA, lymphoma, leukemia
7. Treatment
a. Volume repletion
b. Cooling measures
i. Mist bare skin with lukewarm water while fans blow
over the moist skin
ii. Cooling beds/units
iii. Cold water immersion – RISKS
iv. Invasive cooling
c. Treat agitation and possible shivering
d. Stop cooling at 38-39 deg C (100.4-102.2 deg F)

e. Orthopedic Trauma
i. Open Fractures
1. May be under a laceration or blister
2. Good neurovascular assessment
3. Stop the bleeding
 4. Reduce and immobilize
5. Can still develop compartment syndrome!
a. Up to 10 % of patients
b. Wound does not completely relieve pressure
6. Antibiotics and Tetanus prophylaxis
7. Pain medication
8. Ortho referral

ii. Pelvic fractures

1. Pelvic anatomy
a. Sacrum, coccyx, ilium, ischium, pubis
b. Strong ligamentous connections for stability
c. Vasculature – iliac arteries and branches, venous plexus
d. Neurology – lumbosacral plexus arising from L4-S3 nerve roots,
sacral nerves
2. Rare compared to other fractures but has higher mortality
3. Mechanism – MVC, struck pedestrian, falls
4. Associated injuries
a. Hemorrhage – can be life threating
b. Intraabdominal – occurs in 16.5% of pelvic trauma patients
c. Bladder and urethra
d. Neurologic
e. Rupture of aorta
5. Fracture types
a. Lateral compression
b. Anterior-posterior compression
c. Vertical shear
d. Combined forces
e. Open-book
f. Sacral fracture
g. Acetabular fractures
h. Avulsion fractures
6. Assessment
a. Tenderness, swelling, bruising sites
b. Neurologic deficits
c. Vascular deficits
d. Signs of internal bleeding
e. Pelvic rock – only ONCE, if at all
f. Bladder incontinence, blood at urethral meatus
g. Rectal bleeding, loss of tone
h. FAST exam
i. X-rays and/or CT scan if stable
7. Treatment
a. Stabilize
b. Pelvic binder
 c. Look for concominant injuries
d. Fracture pattern does not equal extent of bleeding
e. Posterior pelvic injuries may be missed or underestimated on X-
rays, need CT
iii. Knee dislocation
1. Mechanism of injury
a. High energy (MVC, fall, severe blow)
i. Can result in tibiofemoral dislocation, which is limb
threatening
b. Low energy (twisting, minor fall, minor blow)
2. Consequences of injury
a. Ligament disruption
b. Popliteal artery injury
i. Occurs in up to 40 % of dislocations
ii. Untreated could cause limb ischemia necessitating
amputation
c. Peroneal nerve (sensation to dorsum of foot, controls ankle
dorsiflexion)
i. Occurs in up to 23% of dislocations
d. Muscle and tendon injuries
3. Obvious vs occult
a. MANY dislocations spontaneously reduce prior to medical
evaluation so cannot be completely ruled out just based on
absence of obvious current dislocation
b. May happen with more minor injuries in obese people and
those with prior joint abnormalities
4. Knee examination
a. DP and PT pulses
b. Cap refill
c. Above – hip and femur
d. Below – tib/fib, ankle, and foot
e. Compartments – soft or firm, tender or not, pain with passive
movement
f. Sensation
g. Strength
h. Stability
i. Hyperextension > 30 degrees suggests instability
ii. Posterior, anterior, medial, lateral, rotary stability
i. “Dimple sign”
i. Transverse groove in the skin at the medial joint line
caused by invagination of a portion of the medial
capsule
ii. Indicative of a posterolateral knee dislocation that
cannot be manually reduced
5. Diagnostic evaluation
 a. Ankle-brachial index – take in context of pulses, physical exam
i. >0.9 observe
ii. <0.9, consider additional imaging
b. X-rays
c. CTA or arteriogram
6. Treatment
a. Dislocation reduction if vascular deficit
b. Immobilize
c. Emergent vascular surg consult if concern for impaired flow
d. Pain control
iv. Compartment syndrome
1. Occurs in muscles sectioned by facial membranes
a. Younger patients have more robust facia, are at higher risk
2. Muscles
a. Extremities, back muscles
3. Non-muscular sites
a. Eye, abdominal compartment syndrome
4. Mechanism
a. Chronic repetitive motion
i. Excessive squats, weightlifting exercises
b. Direct blow or crush
c. Fracture
i. Particularly in distal arm and lower leg with both bones
fractures
d. Iatrogenic
i. Massive fluid resuscitation
ii. IV extravasation injury
e. Burns
f. High pressure injection
g. Infection
5. Assessment
a. Pain “out of proportion”
b. Tense, firm compartments
c. Pain exacerbated by passive stretch of the muscle
d. Paresthesia, decreased sensation
e. Weakness
f. Diminished pulses
g. Asymmetric swelling or disproportionate increase in girth
h. Rhabdo
6. Diagnosis
a. Measure compartment pressures
b. Some role for US or CT
c. Diagnostics should not delay treatment
d. Consider the delta between BP and compartment pressures
 i. CS delta pressure = diastolic BP – measured
compartment pressure
ii. If delta < 20-30, indicated need for fasciotomy
7. Treatment
a. Pain control
b. Decrease swelling
c. Normalize extremity perfusion
d. Relieve external causes of compression (cast, eschar, etc)
e. Fasciotomy – mainstay of treatment
f. Amputation for late cases

f. Burns
i. Classification by depth
1. No longer use nomenclature of 1st, 2nd, 3rd degree burns
2. Superficial (epidermal)
a. Dry, red
b. Blanches with pressure
c. Painful
d. Healing time = 3-6 days
3. Superficial partial-thickness
a. Blisters, moist, red, weeping
b. Blanches with pressure
c. Painful to temp, air, touch
d. Healing time = 7-21 days
4. Deep partial-thickness
a. Easily unroofed blisters, wet or waxy dry, variable/patchy color
b. Blanching sluggish
c. Painful to pressure only
d. Healing time = >21 days
e. Usually requires surgical treatment
5. Full thickness
a. Waxy white, leathery gray, charred black
b. Painful to deep pressure only
c. Surgical treatment required
6. Deeper injury
a. Extends into facia, muscle, bone
b. Surgical treatment required
ii. BSA estimation – do not include superficial in BSA assessments
1. Lund-Browder Chart
a. Different for adults and children because kids have
proportionally larger heads and smaller lower extremities
2. Rule of Nines
a. Head = 9%
b. Each arm = 9%
c. Each leg = 18%
 d. Trunk = 18%
iii. Burn fluid resuscitation calculation
1. These are for initial fluid resuscitation
2. Consideration given to age, comorbidities, other associated injuries –
these may affect fluid volume choices
a. Monitor for signs of under and over resuscitation
3. Parkland
a. Total fluid (mL) in 1st 24 hours = 4 x (wt in kg) x % BSA burns
b. Rate for 1st 8 hours (mL/hr) = Total fluid (mL)/16
c. Rate for next 16 hours (mL/hr) = Total fluid (mL)/32
4. Modified Brooke formula
a. Fluid required in initial 24 hours = 2 mL/kg of body weight for
each % of BSA burned
iv. Treatment
1. Immediate cooling
a. Use cool, not cold water, don’t want to create more thermal
injury
b. Keep an eye on core body temp
2. Pain and anxiety management
3. Teatnus immunization update, tetanus IG in patients who never
completed primary immunization
4. Antibiotics
a. Topical for all nonsuperficial burns, if ok with burn center
5. Wound management
a. Escharotomy
b. Remove all debris
c. Irrigate gently
d. Avoid cytotoxic agents (alcohol, betadine, peroxide, hibiclens)
e. Blisters are controversial, never needle aspirate, either unroof
or don’t
f. Dress with non-adherent gauze, non-circumferential
v. Burn transfer criteria
1. Partial thickness burns > 10% BSA
2. Burns involving face, hands, feet, perineum, genitalia, major joints
3. Any full thickness burns
4. Electrical and lightning burns
5. Chemical burns
6. Inhalation injury
7. Burns in patients with pre-existing comorbidities
8. Burn + trauma patients
9. Patients who will require special social, emotional, or rehabilitative
intervention

vi. Inhalation injuries

1. Is a leading cause of morbidity and mortality
2. Can affect the airways as well as systemic toxicity
3. Upper airway – thermal injuries
a. Erythema, ulcerations, edema
b. Aggressive fluid resuscitation can worsen edema
c. Inflammation damages ciliary function, impairs airway clearing,
increasing risk for thick secretions, obstruction, infection,
impaired gas exchange
4. Tracheobronchial injury – smoke and gas
a. Increased work of breathing
b. Neuropeptide-induced bronchoconstriction, increased vascular
permeability, basodilation
c. Exudate and cast formation within the airways, alveolar collapse
d. Ventilation-perfusion mismatch
5. Lung parenchyma injury
a. Typically delayed
b. Atelectasis and alveolar collapse, decreased surfactant, loss of
hypoxic vasoconstriction, massive fibrin deposition in airways
c. Severe ventilation-perfusion mismatch
6. Systemic toxicity
a. Carbon monoxide
i. One of the most frequent causes of immediate death
following inhalation injury
ii. Colorless, odorless gas
iii. Affinity for Hgb 200x higher than that of oxygen,
impairing release of oxygen at tissue level
iv. High index of suspicion for all fires until excluded by
normal carboxyhemoglobin level
v. Cannot rely on pulse oximetry, it cannot differentiate
oxygen and carbon monoxide
b. Hydrogen cyanide
i. Colorless gas with bitter almond odor
ii. Cannot measure cyanide levels easily
iii. Treat on basis of clinical suspicion
iv. The risk of the treatment, hydroxocobalamin, is very
low. The risk of not treating is very high
7. Diagnostics
a. Labs – CBC, lytes, BUN, creat, lactate, tox screen. Consider ABG.
Carboxyhemoglobin, methemoglobin levels
b. CXR – Low sensitivity for inhalation injury, particularly early
i. Opacities on presenting CXR is a poor prognostic
indicator
c. CT chest – not for routine use, consider if associated with
trauma or other concerning etiology
d. Direct airway evaluation with fiberoptic bronchoscopy for signs
of singing, edema, blistering, ulceration, bronchorrhea, charring
 8. Treatment
a. Remove from exposure
b. Err on the side of early intubation, especially prior to transfer
c. Humidified O2
d. Hyperoxia (in carbon monoxide poisoning)
e. Hydroxocobalamin (in suspected hydrogen cyanide poisoning)
f. No benefit for prophylactic abx
i. May kill the “easy” bugs, put patient at risk for more
serious infections
g. Treat ARDS
h. Mucolytics
i. Chest physiotherapy, turn frequently, early ambulation

vii. Electrical injuries

1. Combination of injuries
a. Electrical current sequela
b. Conversion of electrical energy to thermal energy
c. Blunt trauma (thrown from electrical injury site)
2. Up to 40 % are fatal
3. Low voltage
a. Electric cords or outlets
b. Household AC current
c. Causes arrhythmias
d. Prolonged exposure due to hand tetany
4. High voltage
a. Power lines
5. Electrical arc
a. High voltage electric current “jumps” by being conducted by
ionizing gas in the air
b. Generates heat
c. Can occur in proximity to downed power lines
d. Temp can reach more than 50,000 deg C
6. Arrhythmias
a. Typically occur early
b. Most deaths within 1 hour
7. Peripheral and CNS injuries
8. Deep and superficial burns, osteonecrosis, compartment syndrome,
rhabdo, AKI

viii. Lightning injuries

1. There are more than 6,000 lightning strikes every minute around the
world
2. 300 injuries, 100 deaths per yuear in the US
3. More common in young males (occupational or recreational)
4. Direct current injury
5. Strike location
a. Direct hit
b. Contact strike (strikes an object the patient is touching)
c. Side-flash (close proximity to struck object), arc burn
d. Ground strike (hits nearby ground), can result in multiple
victims
6. Current carried rapidly over skin, CNS short-circuited
a. Deep burns less likely
7. Patient may stop breathing, heart briefly in asystole and re-starts
a. Begin rescue breathing immediately, frequent pulse checks
8. Can have blast effect injuries
9. Peripheral and CNS nerve injuries
10. Skin injuries – “feather” pattern
11. Tympanic membrane rupture, cataracts, vitreous hemorrhage, optic
nerve injury
Abdominal and Gastrointestinal Disorders

Esophageal Disorders

a. Dysphagia
• Difficulty swallowing. Signifies an organic pathology in the esophagus.
b. Odynophagia
• Pain with swallowing, typical of inflammatory or infectious pathology
c. Oropharyngeal “transfer” dysphagia
• Occurs within the first 2 seconds of swallowing.
• Patients experience coughing, choking, drooling, repeated swallow attempts.
• Neuromuscular disorders which can cause this including stroke, polymyositis and
dermatomyositis, scleroderma, myasthenia gravis, multiple sclerosis, lead
poisoning, AML, Parkinson Disease
• Inflammatory infectious causes include Pharyngitis, oropharyngeal abscess.
• Infectious neuromuscular causes include poliomyelitis, diphtheria, botulism,
rabies, tetanus.
• Cancer of the tongue, pharynx, or larynx
d. Esophageal “transport” dysphagia
• Upper Esophageal Dysphagia
i. Difficulty swallowing occurs 2-4 seconds after swallowing.
ii. Typically, this is due to an obstructive lesion.
1. Include esophageal webs (Plummer-Vinson syndrome), carcinoma.
2. Extrinsic compression by thyroid, Zenker diverticulum, left atrial
enlargement, aortic aneurysm.
3. Symptoms usually progress from liquid to solids.
• Lower esophageal dysphagia
i. Difficulty swallowing occurs 4-10 seconds after swallowing.
ii. Symptoms are worse with solids.
iii. Report a substernal “stuck” sensation.
iv. Usually due to luminal narrowing
v. Carcinoma is the most common cause.
vi. Achalasia usually occurs with both solids and liquids.
vii. Might regurgitate undigested food.
viii. Esophageal stricture often is a result of reflux or eosinophilic esophagitis.
ix. Schatzki ring is a fibrous structure near the gastroesophageal junction.
x. Diffuse esophageal spasm may appear clinically similar to myocardial
ischemia.
xi. Typically, esophageal is at rest and spontaneous, can be precipitated by
swallowing liquids
e. Esophagitis
• Symptoms can include chest pain, dysphagia, odynophagia or reflux.
 • Causes:
i. GERD (most common)
ii. Infections including candida albicans, viral (herpes, varicella,
cytomegalovirus), bacterial (mycobacterium)
iii. Radiation
iv. Corrosive agents (acids, alkali)
v. Pill esophagitis (antibiotics like doxycycline and tetracycline),
bisphosphonates, anti-inflammatory agents, potassium chloride and iron)
vi. Eosinophilic esophagitis
• Management:
i. Fluconazole IV for esophageal candidiasis
ii. Immunocompromised patients, think Herpes simplex and treat with
acyclovir.
iii. Eosinophilic esophagitis treat with diet, glucocorticoid and PPI
f. Esophageal perforation
• Etiology
i. Swallowed (foreign body or caustic agent)
ii. Instrumentation including surgery, rigid endoscopy, stricture dilation,
intubation.
iii. Trauma, blunt or penetrating
• Mallory-Weiss syndrome
i. Partial thickness tear because of repeated vomiting leading to dysphagia,
odynophagia and upper gi bleeding.
ii. Seen in alcoholics, hiatal hernia, gastritis/esophagitis.
• Boerhaave syndrome
i. Spontaneous esophageal rupture
ii. Can be seen in patients who are vomiting, giving childbirth, weightlifting.
iii. Full thickness, usually located at the posterolateral aspect
iv. Severe chest pain
v. Physical findings include subcutaneous emphysema, Hamman crunch, left
pneumothorax or pleural effusion, mediastinal emphysema, widened
mediastinum
vi. Diagnosis is made via esophagram with water-soluble contrast
vii. Consult surgery emergently
g. Esophageal Foreign Body ingestion
• Most are in children.
i. Cricopharyngeal muscle most common place in kids under 4
ii. Lower esophageal sphincter/diaphragmatic hiatus most common in adults
• Presentation in children under 16 years old
i. Vomiting, gagging, drooling, choking, dysphagia, foreign body sensation,
refusing to eat.
• Presentation in over 16 years old
 i. Anxiety, discomfort, foreign body sensation, substernal chest pain,
inability to handle secretions.
• Order radiographs of the neck and chest
i. If coin is in trachea, it will be oriented in the sagittal plane, and you will
see the edge in PA or AP view
ii. If coin is in esophagus, it will be oriented in coronal plane and PA or AP
view will show flat surface of the coin.
iii. Remember SAFE Side: Airway, Front: Esophagus
iv. Halo sign (a smaller circle inside of a larger circle) suggests a button
battery, which requires immediate endoscopic removal if in esophagus due
to the quick necrosis and perforation that can occur in the esophagus. If it
has passed into the stomach, expectant management is allowed.
v. If a foreign body is not visualized and you know the child swallowed it, an
esophagram with water soluble contrast or endoscopy is indicated.
• Low risk blunt non-magnetic and non-battery objects can be watched in the
esophagus for up to 24 hours.
• Single magnets can be monitored, but multiple magnets should be removed
emergently because they can attract to each other across the bowel leading to
perforation.
• Sharp objects must be removed endoscopically before they pass through the
pylorus due to high risk of perforation.
• Food impaction:
i. Can use glucagon as a measure when awaiting endoscopy
ii. Endoscopic removal is the recommended treatment

GI bleeding

a. Evaluation:
• Is the patient hemodynamically stable vs. unstable
i. If unstable, immediately consult with Gastroenterologist for endoscopy.
• Bloodwork should include: Coagulation profile, Hemoglobin and hematocrit,
platelet count, and type and cross match.
• Obtain a troponin and EKG if at risk of cardiac injury 2/2 bleed or patient with
other complaints.
• Consider holding medications or reversal of coagulation abnormalities
i. This includes Vit K, Fresh frozen plasma or prothrombin complex
concentrate, idarucizumab, Andexanet
• The use of proton pump inhibitors does not reduce mortality but may prevent
rebleeding or prevent the need for endoscopic intervention.
• Octreotide (Somatostatin analog) does not decrease mortality. When combined
with endoscopy it may increase hemostasis and decrease re-bleeding and is
 typically used in variceal bleeding. It can be used if a patient is high-risk and
undifferentiated cause of bleeding.
b. Mortality is reduced by a restrictive transfusion strategy which means to transfuse only if
hemoglobin is < 7 for most patient or 8 if there is pre-existing cardiovascular disease.
c. NG lavage does not have clinical benefit and should not be performed.
d. Signs of an Upper GI source include:
• Melena, History of Coffee Ground emesis, Serum BUN:Cr ratio > 30, Hematocrit
< 20, use of anticoagulants
• Less likely to have an Upper GI if there is blood in the stool or a history of lower
GI bleeding.
e. In the case of ruptured esophageal varices
• Initiate an Octreotide bolus and infusion.
• Place a balloon tamponade device as a temporary measure while awaiting
endoscopy.
• Patient should undergo endoscopic band ligation or sclerotherapy
• The next step if that is unsuccessful is embolization of the gastric vein with
angiography.
f. In the case of bleeding due to peptic ulceration
• This is the most common cause of upper GI bleeding.
• Duodenal ulcers are associated with H. Pylori
• IV proton-pump inhibitors can help decrease the need for intervention while
patient undergoes endoscopy.
• Pantoprazole and esomeprazole are commonly used.
• Consult a gastroenterologist for management if bleeding is significant
• Transarterial angiographic embolization is a treatment option for patients whose
bleeding is unable to be controlled with endoscopy.
g. If a patient has a known abdominal aortic aneurysm, assume bleeding is due to an
aortoenteric fistula and the fistula is typically in the duodenum.
• Remember these patients can have a short-lived “herald bleed”.
• Vascular Surgery should be consulted in these cases.

Appendicitis

a. Appendicitis is the most common indication for emergency surgery.

b. Etiologies include: fecalith, enlarged lymphoid follicles, tumors, parasites, adhesions.
c. Patients present with abdominal pain, nausea, vomiting, anorexia, diarrhea, fever
• Pain typically precedes other symptoms.
d. Physical exam findings include Rovsing sign, Obturator sign, Psoas sign
e. In pregnant patients, the appendix moves laterally and superiorly so they might present
with right upper quadrant or flank pain
f. Old and young patients might have an atypical presentation and be at higher risk for
perforation
g. Diagnosis
 • CT scan with contrast is the diagnostic procedure of choice for men and non-
pregnant women.
• Ultrasonography is useful in pregnant patients and children; however it is operator
dependent and less sensitive.
i. Given the low sensitivity, if there is high suspicion and negative
ultrasound findings, it might be indicated to get a CT scan (for children) or
MRI (for pregnant women) for further evaluation.
• Diagnostic laparoscopy is indicated in equivocal cases of surgical abdominal pain
h. Management
• Surgical consult
• Initiate antibiotics
• Non-surgical management is also an option.
i. Option for uncomplicated cases with no fecalith
ii. Not well studied in children or older patients
iii. Patients should be admitted to the hospital and informed there is a risk of
recurrence.

Obstruction/Volvulus

a. A partial or complete compromise of the bowel lumen

• Closed loop obstruction is a segment of bowel that is blocked proximally and
distally.
i. Includes volvulus, complete colonic obstruction.
b. Small bowel obstruction
• Etiologies include adhesions from prior surgery, hernia, neoplasm, intussusception,
gallstones, bezoars.
c. Large bowel obstruction
• More common in older adults.
• Causes include neoplasm (more commonly left sided tumor), diverticulitis,
volvulus, fecal impaction.
d. Presentation:
• Pain is often non-localized.
• Vomiting
i. Can be feculent in the case of distal ileal and large bowel obstruction
• Abdominal distention and often mild diffuse tenderness.
• Peristalsis is initially increased, leading to increase in bowel sounds.
i. Early on can have passage of gas and stool
ii. Later in obstructive process, bowel loses its ability to contract and patient
will have decreased bowel sounds and stop passing stool and gas.
e. Imaging
• Abdominal radiographs have some utility and can be diagnostic with a 50%
specificity
 i. Typically see air-fluid levels, can see stepladder appearance of dilated
loops.
ii. Cause of obstruction is rarely identified
• CT scan of the abdomen and pelvis
i. Some sources consider the first line of imaging for obstruction
ii. IV contrast can help to identify strangulation
• Bedside Ultrasound has utility in the hands of a skilled sonographer.
f. Management
• Small Bowel Obstruction:
i. NG tube for decompression
ii. Surgery consult for monitoring and management
iii. For those with pneumoperitoneum, peritonitis or sepsis require surgical
intervention
• Large Bowel obstruction
i. NG decompression if patient is vomiting
ii. Surgery consult for monitoring and management
iii. Colonic dilatation > 12 cm or of prolonged duration might require
immediate intervention
g. Volvulus
• Closed-loop obstruction from the twisting of bowel on its mesocolon
• Sigmoid volvulus
i. Is more common in patients who suffer from chronic constipation leading
to elongated sigmoid colon. This includes bedridden elderly patients and
patients with significant neurological or psychiatric disease.
ii. Presents with abdominal pain, distention, nausea, vomiting
iii. On imaging will appear like an inner tube
1. Dilated bowel segment
• Cecal volvulus
i. Can be seen in patients of any age and results from an incomplete
embryologic fixation of the cecum, ascending colon, and terminal ileum to
the posterior abdominal wall.
ii. Typically acute onset of pain and vomiting
iii. Loop is seen in upper or mid abdomen but can be anywhere. Distal large
bowel will be collapsed and small bowel is dilated
• Treatment:
i. NG tube decompression
ii. Surgical consult
1. Sigmoid volvulus typically is a non-surgical reduction with
sigmoidoscopy or barium enema
2. Cecal volvulus requires emergent surgical reduction
Mesenteric ischemia and infarction

a. Patients who are over 50 years old with cardiovascular disease are at higher risk
b. Mortality is 50%
c. Etiologies
• Most common is superior mesenteric artery embolism seen in 50% of cases
i. Predisposing factors include dysrhythmias (atrial fibrillation),
atherosclerosis or valvular heart disease, recent MI with mural thrombosis
• Superior Mesenteric Artery thrombosis (25% of cases)
i. Patients often have a history of intestinal angina or pain that occurs after
meals and spontaneously resolves
ii. Predisposing factors include Smoking, hyperlipidemia, hypertension,
• Non-occlusive etiologies include low-flow states with decreased cardiac output
i. Can be seen in patients with hypotension, CHF, septic shock, and with
vasopressors
• Mesenteric vein thrombosis
i. This is seen in hypercoagulable states and seen in younger patients.
ii. Many will have a prior history of DVT
d. Presentation
• Severe abdominal pain
i. Sudden onset is more likely arterial, gradual onset is more likely venous or
non-occlusive
• Can have tachycardia, fever, diarrhea and vomiting
• Might have a history of intestinal angina with meals
• Pain is diffuse, might have pain out of proportion to exam
e. Diagnosis
• CT angiography is diagnostic imaging of choice.
i. CT with contrast instead of angiography can identify venous thrombosis
• Serum lactate is nearly 100% sensitive when bowel infarction has occurred.
i. However, it is not specific
f. Treatment
• IV fluids and supplemental oxygen
• NG tube to decompress stomach and bowel
• Heparin or LMWH can be helpful especially in the case of venous thrombosis
• Correction of possible causes of low-flow state
• Typically, will be a multi-disciplinary approach.
i. Vascular surgery for evaluation for revascularization
ii. Interventional radiology for angioplasty or intra-arterial thrombolytic
administration
iii. Critical care consultation
• Pressors positive inotropes are preferred and avoid alpha agonists
• Treatments specific to the etiology of ischemia:
i. Non-occlusive will be treated non-operatively as long as there is no
peritonitis or necrotic bowel
 ii. Mesenteric venous thrombosis is treated with anticoagulation with
heparin. Also, can be medical treatment if no peritonitis or necrotic bowel.
iii. Acute Mesenteric arterial occlusion from either embolism or thrombosis is
treated with antithrombotic therapy like heparin, and surgical consult for
likely open or endovascular intervention.
iv. If a patient has peritonitis or necrotic bowel, emergency surgery is
indicated.

Hepatitis

a. Viral Hepatitis
• Hepatitis A
i. Fecal-oral transmission, mild illness
ii. Does not cause chronic liver disease.
• Hepatitis B
i. Typically, percutaneous transmission, can be sexually transmitted
ii. More severe symptoms
iii. Chronic hepatitis is seen, which puts patient at higher risk of
hepatocellular cancer and can continue to transmit the illness
iv. Review the serologic markers
1. HepB Surface antigen is outer protein of the virus, implies active
hepatitis or carrier
2. Antibody to Hep B is a marker of recent infection
• Hepatitis C
i. Transmitted percutaneously, can be sexually transmitted
ii. Typically, less severe than Hepatitis B
iii. 70% develop chronic hepatitis and 20% of those patients develop cirrhosis
iv. Curative therapies are available
• Hepatitis Delta
i. Only occurs in patients with hepatitis B
ii. Superinfection which has a higher mortality rate
• Hepatitis E
i. Like Hepatitis A however higher risk of liver failure
ii. Does not have chronic state
• Prevention
i. Immune globulin to Hepatitis A is available for recent exposure
ii. Hepatitis A vaccine is available and recommended to those who are
planning travel to endemic areas
iii. Immune globulin to Hepatitis B and hepatitis B vaccine are available
• Management
i. Admit patients who have refractory vomiting, prolonged PT, bilirubin >
20, hypoglycemia, immunosuppression, encephalopathy
• Toxic/Drug Induced Hepatitis
 i. Seen with Acetaminophen, some antibiotics, NSAIDs, phenytoin and
valproic acid
ii. Remove the offending agent
iii. Treat acetaminophen toxicity with N-acetylcysteine
iv. Treat valproic acid toxicity with Valproic acid

Biliary disorders

a. Cholelithiasis
• Gallstones are seen more commonly in women, and majority are cholesterol
• Risk factors include: female, obesity, increased parity, older age, rapid weight loss,
• Pigmented stones include
i. Black which is associated with hemolysis (sickle cell disease)
ii. Brown is associated with infection
• Patients can present with biliary colic
i. Right upper quadrant or epigastric pain, radiating to the shoulder
ii. Can have nausea and vomiting
• Ultrasound is preferred for the diagnosis
• Management includes symptomatic treatment and referral to surgeon
i. Definitive treatment is cholecystectomy
b. Cholecystitis
• Acute inflammation of the gallbladder
• Most are caused by obstruction of the cystic duct by a gall stone
i. Obstruction can occur due to tumor, lymphadenopathy, fibrosis, pancreatic
disease
• Patients present with RUQ/epigastric pain, fever, nausea and vomiting
i. Test for Murphys sign
• Lab work may be normal
i. If lipase is elevated, consider pancreatitis due to a common duct stone
• Ultrasound is the preferred and available imaging modality to make the diagnosis
i. Evaluate for a thickened gallbladder wall, presence of gallstone,
pericholecystic fluid, Murphy’s sign
• HIDA scan or Nuclear scintigraphy is the most accurate for diagnosis
i. Indicated in equivocal cases
ii. If the isotope does not pass into the gallbladder within 1 hour, the cystic
duct is presumed to be obstructed.
• Management
i. Consult surgery and plan for admission
ii. Initiate broad spectrum antibiotics, can use piperacillin/tazobactam
iii. Cholecystectomy is definitive therapy
• Acalculous cholecystitis
i. Can be seen in post-partum and perioperative patients, trauma, vascular
patients, diabetes, sepsis
 ii. More likely to have gangrene and perforation
• Ascending cholangitis
i. The stone in the common bile duct can cause an infection that extends into
the liver
ii. Charcot’s triad: fever, abdominal pain, jaundice
iii. Reynold pentad: Charcot’s triad and mental confusion and shock
iv. Requires immediate antibiotic therapy
v. Patients will need emergency surgery either open surgery, percutaneous
drainage
• Emphysematous cholecystitis
i. Infection of the gallbladder with a gas forming bacteria

Pancreatitis

a. There is acute and chronic pancreatitis

• Acute is inflammation of the pancreas
i. Commonly caused by alcohol or a gallstone
ii. Less common causes include trauma, hyperlipidemia, certain medications
including thiazides, furosemide and sulfonamides), surgery, and ERCP.
• Chronic pancreatitis occurs in patients who have had repeated episodes of
pancreatitis
i. Often seen in alcoholism
b. Presentation
• Upper abdominal pain, often left sided or epigastric and radiating to the back, and
vomiting
• Signs of hemorrhagic pancreatitis and retroperitoneal hemorrhage:
i. Grey-Turner sign: blue coloring to the flank
ii. Cullen sign: blue coloring to the umbilicus
c. Diagnosis
• Serum lipase and amylase will be elevated
i. Often these are very elevated when related to a gallstone/biliary etiology
ii. May not be elevated in chronic pancreatitis
• Imaging findings suggestive of pancreatitis include:
i. Abdominal film with ileus and air-trapping in the small bowel adjacent to
the pancreas
ii. Chest film with left pleural effusion and elevated left hemidiaphragm, can
see ARDS in severe cases
iii. CT scan can be normal in mild cases but can help rule out other etiologies
of patient’s pain or causes of pancreatitis. Might see parenchymal
enlargement, surrounding fat stranding.
1. Helpful to evaluate for necrosis, abscess formation, hemorrhage
and pseudocyst
• Diagnosis is made in patients who have two of the following three criteria:
i. Abdominal pain
 ii. Serum lipase > 3 times the normal value
iii. Findings on imaging
d. Management
• Hydration, symptom, and pain control
• Patients can eat if they can tolerate it
• Monitor for complications
• If patient has hypertriglyceridemia, IV insulin therapy or plasmapheresis can be
used
e. Ranson criteria are a way to estimate severity:
• On admission:
i. 1) Age over 55 2) WBC > 16,000 3) Hyperglycemia > 200 mg/dL
ii. 4) AST > 250 U/L 5) Lactate dehydrogenase > 350 IU/L
• 48 hours later:
i. 1) Calcium < 8 mg/dL 2) pO2 < 60 mmHg 3) Hematocrit drop by 10%
ii. 4) Increase in BUN > 5 mg/dL 5) Base deficit > 4 mEq/L
iii. 6) Sequestration > 4 L of fluid
f. The Bedside Index for Severity in Acute Pancreatitis (BISAP)
• BUN 25 mg/dL
• Altered mental status
• Systemic inflammatory response syndrome criteria present
• Over 60 years old
• Pleural effusion present
• Total score of 0–2 indicating lower mortality
g. Complications:
• Pancreatic necrosis
• Fluid collection and pseudocysts
• ARDS
• Acute tubular necrosis
• Disseminated intravascular coagulation
• Schock

Hernias

a. A hernia is a protrusion of a structure from its normal position into another through an
opening
• External hernia: Protrudes to the outside (umbilical hernia)
• Internal hernia: Protrudes within the body (inguinal)
• Incisional hernia: Protrudes from a previous incision
b. Reducible hernias are where the protruding contents can be pushed back through the
opening
c. Incarcerated hernias the contents can not be moved back and are irreducible.
• These are seen when a large size of content has protruded through a small defect
d. Strangulated hernia has vascular compromise of the herniate contents
e. Men are more likely to develop hernias and require repair
• 96% of groin hernias are inguinal, 4% are femoral
 f. Types of hernias
• Direct inguinal hernia:
i. Protrudes through the floor of Hesselbach’s triangle and results from
weakening of the abdominal musculature
• Indirect inguinal hernia:
i. Protrudes through the internal inguinal ring lateral to the inferior epigastric
vessels
ii. Represents a congenital defect and most common in younger patients
• Femoral hernia:
i. Protrudes below the inguinal ligament and the femoral vessels and femoral
canal
ii. More common in women
• Umbilical hernia
i. Common in newborns and most close spontaneously by age 2-3
• Obturator hernia
i. More common in older women, and protrudes into the medial thigh
g. Diagnosis
• Ultrasound can help differentiate inguinal from femoral hernias
i. It is the best initial modality if patient has physical symptoms but no
findings on exam
• CT scan can make the diagnosis.
h. Reduction
• Place the patient in Trendelenburg to aid in manual reduction
• If there is suspicion for strangulation or the hernia is irreducible, then surgery
consult is indicated

Diarrhea

a. Distinguish between acute and chronic diarrhea

• Acute: symptoms less than 2 weeks
i. Suggests viral or bacterial cause
• Chronic: Symptoms present for more than 30 days
i. Suggestive of parasite other disorder
b. Invasive gastroenteritis is associated with a bacterial cause
• Patient often have fever, abdominal pain, blood in the stool
c. If patient does not have fever, abdominal pain or blood in the stool it typically is viral or
pre-formed toxin
• Testing is not typically necessary
d. Viral Diarrhea
• Rotavirus
i. Seen in children 6-24 months old
ii. Onset with vomiting, low grade fever and watery diarrhea for 4-7 days
iii. Babies are vaccinated at 2, 4 and 6 months
 iv. Disease is self-limited
• Norovirus
i. Most common cause of epidemic non-bacterial gastroenteritis
ii. Transmitted fecal-orally or airborne droplets of vomit with viral particles
iii. Can be transmitted on fomites as well
iv. Abrupt onset of nausea, vomiting and diarrhea which lasts for 1-2 days
e. Bacterial Diarrhea
• Invasive bacteria
i. Damage cell membranes and cause blood and mucus in the feces
ii. Campylobacter, Salmonella, Shigella, Vibrio parahaemolyticus and
vulnificus, Yersinia enterocolitica, enteroinvasive e. coli,
enterohemorrhagic e coli O157:H7, Clostridioides difficile
• Enterotoxin-producing bacteria
i. Release a toxin that acts in the small intestine causing profuse watery
diarrhea
ii. Staph aureus, Bacillus cereus, ciguatera and scombroid fish poisoning,
enterotoxigenic e. coli, clostridium perfringens, vibrio cholera
f. Those with severe illnesses such as fever, severe abdominal pain, or more than 6
unformed stools a day, or have severe comorbidities or need for hospitalization should
have stool cultures and testing performed.
g. Recent antibiotic use is seen in cases of c difficile.
h. Traveler’s diarrhea
• Seen in people who travel to resource-limited countries.
• Most cases are from bacterial infection, typically e coli
• Supportive treatment is fine for mild cases
• Patients may need treat with antibiotics, typically azithromycin.
i. E. coli
• Enterotoxigenic E. coli
i. Common cause of traveler’s diarrhea
ii. Watery diarrhea with abdominal cramping
iii. Supportive measures for care and typically self-limited
iv. Can use antibiotics and anti-motility agents
• Shiga toxin-producing e. coli or enterohemorrhagic e. coli
i. O157:H7 is most common serotype
ii. Seen in infected beef, sprouts, unpasteurized milk products
iii. Have watery/bloody diarrhea, cramping and vomiting
iv. Antibiotics do not help and increase risk of hemolytic uremic syndrome
• Shigella
i. Mild watery diarrhea but can develop bloody diarrhea, dehydration,
vomiting, headaches, myalgias
ii. Disease is usually self-limited, lasting 1 week
iii. Relapse can be seen without antibiotic treatment
1. Can use quinolones or ceftriaxone
iv. Complications: Dehydration, arthralgias, Reiter syndrome (urethritis,
polyarthritis, conjunctivitis), hemolytic uremic syndrome, febrile seizures,
pneumonitis
• Salmonella
i. Second most common food borne illness
ii. Contaminated food or drink, usually poultry, beef, unpasteurized milk, egg
iii. Can be a mild gastroenteritis or septicemia
iv. Nausea, vomiting, diarrhea, fever, and crampy abdominal pain
v. Typically self limited
• Campylobacter enteritis
i. The most common cause of diarrhea
ii. Contaminated food or water or contact with infected feces
iii. Avoid antimotility agents
iv. Supportive care
v. If patients have a prolonged symptoms course, antibiotics such as
azithromycin or erythromycin can be given
vi. Complications include Reiter syndrome, Hemolytic uremic syndrome,
Guillan-Barre syndrome.
• Yersinia enterocolitis
i. Fever and diarrhea, can evolve to dysentery
ii. Can get post infectious erythema nodosum, polyarthritis
iii. Typically supportive treatment
iv. Avoid anti-motility agents
v. Can give ceftriaxone if severe disease
• Clostridium Perfringens
i. Diarrhea, abdominal cramping
ii. Self limited for only 10-12 hours
• Staphylococcus Aureus
i. Vomiting with or without diarrhea
ii. Usually resolved in 6-10 hours
• Bacillus cereus
i. 1-6 hours after eating contaminated rice
ii. Resolves in < 10 hours
• Vibrio Cholerae
i. Contaminated seafood or water
ii. Rice-water diarrhea, can lead to severe dehydration
iii. Doxycycline or azithromycin if patient has severe disease
• Vibrio parahaemolyticus
i. Seafood-associated
ii. Can range from mild to severe, can have fever
iii. Typically self-resolving
• Scombroid fish poisoning
i. Seen with Mahi-Mahi, Tuna, Mackerel
ii. Ingest heat stable toxin with histamine-like properties
iii. Signs of histamine intoxication 20-30 minutes after eating
1. Facial flushing
2. Headache
3. Abdominal cramping
4. Nausea, vomiting, diarrhea
 5. Can get bronchospasm and severe hypotension
iv. The fish might have had a metallic, bitter or peppery taste
v. Can treat with H1 and H2 blockers, antiemetics, albuterol and steroids if
there is bronchospasm, and epinephrine if anaphylactoid reaction
• Ciguatera fish poisoning
i. Ingest ciguatoxin typically on grouper, snapper, barracuda,
ii. Impacts sodium channels leading to effect on nervous, cardiac and GI
systems
iii. GI symptoms last 1-2 days
iv. Neurologic symptoms include painful paresthesias, circumoral and throat
paresthesias, weakness, and coma.
v. Patient can experience “hot-cold reversal
vi. Cardiovascular symptoms include symptomatic bradycardia but occur
least frequently
vii. Treatment includes supportive measures
viii. Abstinence from alcohol, seafood, and nuts until all symptoms have
resolved for 3–6 months after exposure.
j. Parasitic infections
• Entamoeba histolytica
i. Transmission usually occurs through ingestion of cysts (
ii. Risk factors include travel to tropical areas with poor sanitation, any
exposure to poor sanitation,
iii. Patient present with chronic amoebic colitis with a gradual onset
iv. Might report foul-smelling feces with bloody mucus
v. Patients can develop Amoebic abscess, especially in the liver
vi. Mild to moderate intestinal illness is treated with metronidazole plus a
luminal agent such as iodoquinol or paromomycin
• Giardiasis
i. Cysts found in soil, food, and water that have been contaminated with
feces containing the parasite by drinking contaminated water
ii. Clinical stem might be a patient returned from a backpacking trip and
presents with abdominal pain and bloating.
iii. Most common symptoms are explosive diarrhea, flatulence, colicky pain,
and greasy, floating, foul-smelling feces.
iv. Diagnose by the presence of trophozoites or cysts
v. All symptomatic patients should be treated.
1. Tinidazole is the drug of choice
2. Nitazoxanide can be giving
3. Metronidazole can be used but is less effective
• Cryptosporidium
i. Most common cause of chronic diarrhea in patients with HIV
ii. Symptoms include profuse watery diarrhea, abdominal cramping,
anorexia,
iii. In immunocompetent patients symptoms are self limited
1. However they may persist for 1–3 weeks and result in significant
dehydration
 2. Can treat with Nitazoxanide
iv. In immunocompromised patients, malabsorption and significant weight
loss occurs
1. Symptoms may persist for months to years
2. Nitazoxanide or paromomycin plus azithromycin may decrease
symptoms in these patients but is not curative- these patients are
resistant to treatment.
• Necator americanus (hookworm)
i. Hookworm larvae penetrate through intact skin on contact with feces-
contaminated soil.
ii. Larvae enter the bloodstream, migrate to the upper intestine where they
attach to the mucosal wall.
iii. Patients have intermittent diarrhea, epigastric discomfort, weakness, low-
grade fever, cough, rash, and weight loss
iv. Diagnosis is made by identifying ova in the stool
v. Treatment is with mebendazole, albendazole, or pyrantel
• Enterobius vermicularis (pinworm)
i. Transmission is via ingestion of E vermicularis eggs
ii. Eggs develop into adult worms in the large bowel
iii. Females migrate to the anus at night to deposit their eggs.
iv. Seen in children who attend schools, daycare centers
v. Patients report itching at the anus worse at night.
vi. Diagnosis is made by seeing adult worms migrating in the perineal area or
eggs on a cellophane tape swab of the anus.
vii. All family members should be treated with a single dose of mebendazole
or pyrantel pamoate that is repeated after two weeks
Cardiovascular I

Matt Hysell MD, Corewell-Lakeland

[Link]@[Link]

I. General (some of the examples will be covered in the second cardiology lecture)
a. Most frequent question type on boards
i. Treatments
ii. Best tests
iii. Most common ___
b. Exceptions to the rule
i. Posterior MI
ii. Sgarbossa criteria
iii. STEMI mimics!!!
c. Common presentations of uncommon things
i. Brugada etc
ii. Wellen’s/DeWinter etc
d. Hard triggers to pull
i. Pericardiocentesis
ii. Thrombolysis in PE
iii. Thrombolytic complications
e. At risk populations
i. Endocarditis
II. STEMI mimics
a. You’re unlikely to be tested on classic STEMI’s
b. Pericarditis
i. Only coves up
ii. Multiple regions of the heart
iii. Essentially no reciprocal change
iv. Is it STE or PR deflection???
v. Often II>III (STEMI usually III>II)
vi. Could be part of a post-interventional Dressler’s state
c. Standard change
i. Note the standard bar
ii. The QRS is also a lot taller
d. LV aneurysm
i. Usually question stem will clarify that symptoms are different from angina
ii. Minimal reciprocal change
e. LBBB
i. Sgarbossa criteria
1. Concordant STE is ischemic!
2. STE greater than 25% of the depth of the QRS is ischemic!
III. Early ischemia patterns
 a. Wellens
i. Type I – biphasic repolarization
ii. Type II – deep TWI
b. DeWinter – J point depression … but otherwise tombstone shaped
IV. Syncope in young people
a. Brugada
i. Sodium channelopathy most common in SE Asia
ii. RSR’ that slopes into STD in V1 and V2
b. Long QT – gotta remember to look at length of repol, not just height/depth
c. HOCM – impressive septal voltage with diffuse TWI
d. WPW – delta waves
i. Afib with WPW
1. Some narrow complex capture beats with delta waves usually sneak in
2. Complexes very erratic, not stereotyped like Afib with LBBB
V. Electrolytes
a. HyperK
i. Classic is peaked T waves leading to widened PR and QRS leading to no PR and
sine wave arrest
ii. But can be any bradycardia
iii. Sine wave can resemble VT but likely slower
b. HypoK
i. Classic is U waves (and remember in real life those count as QT)
ii. Reverse Wellens pattern can be severe hypoK
VI. Dysrhythmia – remember syncope can show seizure activity!!!
a. Heart block – look for lost P waves
i. 3rd degree
1. May have LBBB or bifasc block when not in 3rd degree
2. Stable R-R, unstable “PR” (and may shorten)
nd
ii. 2 degree Mobitz
1. Stable R-R
2. Stable P-P
3. You must recognize P waves superimposed on T waves
nd
iii. 2 degree Wenckebach
1. Unstable R-R
2. Unstable PR
b. Afib – irregularly irregular duh
i. Afib mimics
1. MAT – multi P waves
2. Artifact
c. Digoxin
i. Salvador Dali scooped out T waves
ii. Osborne type waves
iii. Schizophrenic ekgs
1. Accelerated junctional
 2. Tachycardia with blocks
3. Bidirectional VT
d. VT
i. Q or R wave preponderance to chest leads
ii. Late inferior S points
iii. Should be fast on boards
1. Mimics such as sinus with LBBB or hyperK should be less than 150
2. See above for Afib with WPW
3. Reperfusion abnormality also slow and stem should indicate patient
feels improved

V. LVAD

a. Flow rates calculated by device using RPM and Power data

b. normal flow 4-8 L/min (RPM and power vary by device)

c. low flow state

i. Low JVP – probably hypovolemic

ii. normal/elevated JVP

1. VF/VT
2. Suction event (collapsed ventricles, give fluid!)
e. High flow state
i. High power – eval for LVAD thrombosis
ii. Normal power – eval for distributive shock (sepsis, med side effect, etc)
Toxicology In-Service Review

Bram Dolcourt, MD
Assistant Professor of EM
Wayne State University
Disclosures
• No relevant financial disclosures
• No non-FDA approved treatments will be
discussed
• Some treatments discussed may include off
label uses of medications
Questions
• Generally straight forward
• I don’t know the questions
• Review of “Clinical Model of EM Practice”
• These answer are for test purposes
– The test ain’t real life
General
• ABC
• 5W?
• Decontamination
– No lavage unless < 1 hour
• Supportive care
• Antidote?
• Delayed toxicity?
Acetaminophen
• Metabolized to NAPQI via 2E1
• Depletes glutathione
• Centrilobular necrosis (Zone 3)
• Toxic dose:
– Children: 200 mg/kg (single)
– Adults 150 mg/kg (single)
Acetaminophen
• Rumack-Matthew’s Nomogram
Acetaminophen
• N-acetylcysteine
– Oral: 140 mg/kg x 1, 70 mg/kg x 17
– IV: 150 mg/kg over 1 h, 50 mg/kg over 4h, 100
mg/kg over 16 hours
• AST/ALT rises at 24-36 hours
Acetaminophen
• King’s College Transplant Criteria
– pH < 7.3 after resuscitation
– Or
– Cr > 3.5 and
– PT > 100 sec and
– Hepatic encephalopathy grade III or IV
NSAIDs
• Renal failure
– Vasodilation
– IV fluids, dialysis rare
– Papillary necrosis (chronic overuse)
• GI bleeds from COX 1 inhibition
– PPI
NSAIDs
• Acidosis from weak acid metabolites
– Fluids
– Rare dialysis (CHF, volume overload)
• Tocolysis
• Premature ductus arteriosis closure
• Bronchospasm
– Bronchodilators
Aspirin
• Weak acid
• Direct respiratory stimulator
• Classic picture: anion gap acidosis with
respiratory alkalosis +/- tinnitus or hearing
loss
Aspirin
Stage pH Anion gap potassium

1 > 7.4 no nml

2 > 7.4 yes nml

3 < 7.4 Yes low

Aspirin
• Urine alkalinization
– 150 Meq/L of NaHCO3
– Supplement potassium
– Goal: Urine pH > 7.5-8
• Hemodialysis
– Extremus
– Fluid overload/CHF
– ASA level > 100 (potentially lower)
– Refractory to therapy
Aspirin – Reye’s syndrome
• Confusion, lethargy after URI and ASA
• Kids! (6-12, 3-7 days post virus onset)
• Vomiting
• Elevated NH3 key finding
Opiates
• Mu receptor agonism
• Opioid toxidrome
• Decreased respiration
• Miosis
• Decreased temp
• Decreased HR
Opiates
• Respiratory depression/arrest
• Naloxone, 0.4 mg
• Naloxone half-life is shorter than heroin
• Observation period post rescue
• Pulmonary edema after naloxone (48%?)
– PPV
– No lasix
• Right sided endocarditis commonà S.A. or
S.E.
Opiates
• Methadone lengthens QT
– Electrolyte replacement
– Treat torsades
• Mg
• Overdrive pace
• Meperidine metabolite causes seizures
– Avoid naloxone if possible
Opiates
• Tramadol
– Serotonin syndrome
– Seizures
• Admit asymptomatic child who takes
Lomotil
• Fentanyl
– Rigid chest syndrome - intubate
– Myoclonus – wait it out, not seizure
Alcohols
• GABA receptor agonists
• Respiratory depression/Arrest
– Intubate
• Zero order kinetics
– 0.015-0.02 mg/dL/hr metabolism
• Starvation ketoacidosis
– IV fluids/Glucose
Alcohols
• Thiamine for chronic use
– W-K syndrome
• Hypoglycemia 2-10 hours post ingestion
– Worse in kids
Alcohols
• Abstinence syndrome (DTs)
– Altered VS
• Tachy, hypertensive
– Altered sensorium
• confabulation
– Benzos, barbs, propofol
– Seizures
• Tx with benzos, no phenytoin
Toxic Alcohols
• Metabolized by ADH to toxic metabolites
• Methanol à formic acid
• Ethylene glycol à oxalic acid
• Presentation
– Anion gap acidosis
– High Osmlar gap
– “Alcoholic out of money”
– Papiledema/blindness (methanol)
– Renal failure (ethylene glycol)
– Buzzwords: auto repair, moonshiner, industrial worker
• Isopropyl does not cause an acidosis
Toxic Alcohols
• Osm
– 2xNa + BUN/2.8 + glu/18 + EtOH/4.6
– Measure – Cal > 10
• Fomepizole
– 15 mcg/kg load, 10 mg/kg q12 x 4 dose then 15
mg/kg q12
• Ethanol to > 100 mg/dL
– ~10 ml/kg of a 10% solution
Toxic alcohol
• Dialysis
– Methanol
– Ethylene glycol with severe acidosis/renal
failure
• Treat acidosis if pH <7.1
• Cofactors
– Folic acid: methanol
– Pyridoxine: ethylene glycol
Anesthetics
• Local anesthetic toxicity
– 4.5 mg/kg lidocaine
– Metallic taste is early toxicity
– Seizures
• Benzo or barb (thiopental) acceptable
• Intubation with hyperventilation (?)
– CV collapse
• CPR
• Pace
• NaHCO3
• Intralipid (experimental question)
Anesthetic
• Local Anesthetic
– Allerigic reactions
– PABA metabolite
– Esters à PABA
• (1 i)
– Amides do not, possible PABA preservative
• (2 i’s)
• “Cardiac Lidocaine”
Anesthetic
• Malignant hyperthermia
– Muscle Rigidity
– Hypercarbia ß key feature
– Hyperthermia
– Hyperkalemia
– RYR-1 receptor abnormality
– Succinylcholine/halothane
Anesthetic
• Malignant hyperthermia
– Oxygenate
– Dantrolene Sodium
– Active cooling
– Treat hyperkalemia
– (stop using triggering agents)
Antiarrhythmics
• Quinidine/Quinine
• Procainamide
• Lots of others
• Few questions
• Type Ia à TCA like, QRS widening
• Type III à QT prongation
Anticholinergic
• Block acetylcholine
• Antimuscarinic toxidrome
• Dry as a bone
• Blind as bat
• Hot as hell
• Red as a beat
• Mad as a hatter
Anticholinergic
• Tachycarida, urinary retention, absent
bowel sounds
• Confabulation, picking
• Scenario:
– Older patient with confusion, urinary retention
– Younger patient getting high
• Many meds have: antihistamines, TCA,
antipsychotics
Anticholinergics
• Agitated delirum
– Physostigmine preferred?
• Verify QRS is normal prior to use
• Avoid in sick TCAs
– Benzodiazepine
– Treat hyperthermia
– Rhabdo is risk, especially with restraints
Cholinergic
• Increase acetylcholine
• Muscarinic: SLUDGE
• Nicotinic: fasiculations, paralysis, seizures
• OPs, carbamates, -stigmines, donepazil
• Scenario: mass casualty, farmer
– Chemical warfare
Cholinergic
• Atropine until dry
• Oxime (praladoxime)
– Mark 1 kit: 2 mg Atro/600 mg Praladoxime
• Benzodiazepine for severe (unconscious)
• Probably won’t need to dose
• Expect a basic, straight forward question
• Decontamination for mass casualty
Anticoagulant
• FFP/PCC for bleeding
• Vit K for INR > 5
• Scenario: rodentacide
– Some rodentacides aren’t LAAC, don’t expect
these on the in-service
Anticoagulants
• Xa inhibitors
• 4 factor PCC
• Fab probably won’t be a choice
– Idarucizumab for dabigatran
Anticonvulsants
• Phenytoin: ataxia, nystagmus (vertical)
– Cimetadine, Isoniazid, Amiodarone, others
• VPA: sleepiness, high ammoniaàcarnatine
• CBZ: TCA like effect, sedation
– Alkalinization, HD level > 40 mcg/dL
Phenobarbital
• Sedation
• Hypotension
• “Barb blisters”
– Laying down
• Long half life
– Urinary alkalinization
Anticonvulsant Hypersensitivity
syndrome
Antidepressants
• Serotonin syndrome
– AMS, hyperthermia, tachycardia
– Hyperflexia differentiates from NMS
– Sedation with benzo
– Cyproheptadine (likely test answer)
• SSRI
– Relatively safe, possible SSS
Antidepressants
• MAOI à no meperidine
– Phenelzine (nardil)
– Tyramine crisis
• Hunter Sausage, hard cheese, red wine
• Vasodilators
• Phentolamine
• Bupropion
– Seizures, hypertension
– Benzodiazepines
– Decontaminate with WBI
Antidepressants
• TCA
• Amitriptyline, nor, impiramine, des
• Type Ia antidysrrhythmic
• Sodium channel blockade
• Very antimuscaric
• Treat wide QRS with NaHCO3 (> 120ms)
• Goal à Serum pH: 7.45-7.55
Antidepressants
• pH > 7.55 increased mortality
• Lidocaine if refractory
• Can try 3% NaCl (not likely on test)
• ~ 20% who develop wide QRS have Seizure
• No Physostigmine for Antimuscarnic
effects
Antipsychotics
• Typical
– Haloperidol, chlorpromazine
– D2, histamine, alpha-blockade
• Atypical
– Quetiapine, olanzapine, clozaril, risperidone
• Other
– Metoclopramide, promethazine,
prochlorperazine
Antipsychotics
• NMS – Dantrolene (? –
– Rigidity desperation test
answer)
– Hyperthermia
– Elevated CPK
– No hyperflexia
– Benzos
– Bromocriptine
– Cooling
Antipsychotics
• Dystonia
• Occulogyric crisis
• Akesthesia
– Anticholinergic tx
• Clozaril à agranulocyctosis
Carbon Monoxide
• House fire, suicide attempt, broken furnace
• Buzzword: multiple victims
• Hyperbaric Oxygen
– Syncope
– AMS
– CV dysfunction
– Acidosis
– Pulm edema
– CO > 25%
– CO > 15% and pregnant
Carbon Monoxide
• CO half life
– ~ 6 hours @ .21 ATA
– ~ 60 min @ 1 ATA
– ~ 20 min @ 3 ATA
• Give 100% O2
• Stabilize
• HBO
Betablockers
• Decrease CO and BP
• Cool extremities
• Low glucose
• Cardiogenic shock
• Glucagon à increase cAMP
• Vasopressors
• Propranolol also widens QRS (MSA)
– NaHCO3 if QRS > 120 ms
CCB
• Peripheral vasodilation
• Cardiac suppression
• Stops calcium influx and decreases
contractility
• 2 g calcium chloride/6 g calcium gluconate
Digoxin
• Any rhythm except rapid afib
• Indictations for fab
– 10 mg ingestion (4 mg peds)
– Ventricular arrhythmia
– K > 5.0
– Level > 10 ng/ml
• Dose
– 10-20 vials
– (Level x weight)/100
Cardiac Glycosides
• Lily of the valley
• Fox glove
• Red Squill
• ECG based therapy
• 10-20 vials
• No Ca for elevated K (test purposes only)
Caustics
• Strong Acid: coagulative necrosis
• Strong Base: liquifactive necrosis
• Usually have oral burn (2/3+)
• Early endoscopy
• Steroids/antibiotic for circumferential burns
• Acid: Pyloric stricture
• Base: Esophageal Stricture
• 30x increase risk of stomach cancer
• No charcoal or lavage
Cocaine
• Blocks reuptake of epi/norepi/dopamine
• Tachycardia/hypertension
• Psychosis
• Rhabdomyolysis
• TCA effect
– NaHCO3
• Crack lung à bronchospasm, infiltrate
Cocaine
• Benzodiazpeines
• Haldoperidol (?)
• Cooling
• Fluids
Cocaine
• No beta-blockers
• Phentolamine/Nitroprusside for malignant
hypertension
• Cocaine washout à catechol depletion
• Metabolized by plasma
pseudocholinesterase
Cyanide/H2S
• Binds Cytochrome aa3 (oxidase C)
• Blocks electron transport
• Dx: exposure + lactate elevation
• Buzzwords: Jeweler, miner, bitter/burnt
almonds
Cyanide/H2S
• Cyanide antidote kit: amyl nitrite + IV
sodium nitrite + sodium thiosulfate
– Induce methemoglobinemia
– Regenerate Rhodinase
– Skip nitrites if also CO exposure
• Cyanokit: hydroxocobalamin
– Make cyanocobalamin
• H2S is supportive care
– Sewer worker
Hallucinogens
• Serotonin agonists
• Sympathomimetic qualities
• LSD, MDMA, tryptamines, PCP
• Sedation
• Cooling
• Vasodilators
• Rotatory nystagmus à PCP
Heavy metals
• Shock, GI hemorrhage, rice water diarrhea
– Arsenic à British Anti-Lewisite
• Neuropathy, Vomiting, hair loss
– Thalium à Prussian Blue
• Hypokalemia, green vomit
– Barium à replace K, supportive care
• Basophillic stippling, wrist drop, lead lines
– Lead
Hydrocarbons
• Inhaled
– Euphoria, CNS depression
– Hypoxia
– Leukoencephalopathy
– Myocardial sensitization (aromatic, halgenated)
• Ventricular arrhythmias
• Benzos, avoid beta1-stimulation
Hydrocarbons
• Aspirated
• High volatility, low viscosity worst
• Hydrocarbon pneumonitis
• Destroys type II pneumocytes
• Symptoms lag CXR
• If swallowed, don’t give charcoal or lavage
• Some essential oils = seizures
Hydrocarbons
• Methylene chloride à CO
• Carbon tetrachloride à centrilobular necrosis
• NAC
Sulfonylurea
• Potentiate insulin release
• Open K+ ATP channel
• Block with octreotide ~100 mcg or 5-6
mcg/kg div Q6
Inhalational
• Don’t expect much
• Biowarfare Qs
– Phosgene
– Chlorine
• HCO3 neb
• Chemical irritants
• Supportive care
Iron
• Legacy pediatric poisoning
• Severe symptoms when Fe > 450
• N/V/D
• Bloody emesis
• Shock
• Severe Acidosis
Iron
Stage Name Symptoms Time frame

1 GI N/V/D, bloody 0-6

2 Latent Improvement 6-12

3 Metabolic Acidosis, CV 6-48

4 Hepatic Liver dysfunction 12+

GI scarring,
5 Delayed/Recovery Weeks after
obstruction
Iron
• Large volume fluids (GI losses)
• WBI if pills on xray
• No charcoal
• Deferoxamine
– 15 mg/kg/h until urine returns to normal
– 6000 mg/24 hour is max dose
– “Vin rose” urine
Isoniazid
• TB treatment
• Depletes B6
• Need B6 for GABA synthesis
• Refractory seizures
• Pyridoxine: 30-50 mg/kg
• Status epilepticus tx
Methemoglobinemia
• Conversion of Fe2+ in Hgb in Fe3+
• Nitrites
• Aniline dye
• Benzocaine
• Dapsone
• Scenario
– Textile worker
– Toothache, Endoscopy or oral procedure
– Involved with curing meats
– HIV patient
Methemoglobinemia
• Chocolate brown blood
• Persistent low pulse ox
• 1-2 mg methylene blue
• Treat > 20% and symptomatic/co-morbidity
• Treat > 30% and healthy
• Vitamin C for Chronic
Mushrooms
• Amanita phalloides
– Amatoxin kills liver
– Delayed GI symptoms!
– Don’t expect treatment question
• Aminita Muscaria
– Hallucinations
– NOT ANTIMUSCARINIC
– Ibotanic Acid à Mucimal
– Stimulant à Depressant
Strychnine
• Legacy poisoning
• Glycine antagonist in spine
• Confused with tetnus
• Muscle spasm, seizure like effect
• “Risus Sardonicus”
• Clear sensorium
• Benzos, NMB
Stimulants
• Amphetamines
• Release and block reuptake of
epi/norepi/dopamine
• SM toxidrome
– Tachy, hypertensive, hot, big pupils, bowel sounds
• Benzos
• Fluids
• Cooling
• NO URINARY ACIDIFICATION
Theophylline
• Older asthma med
– Bronchodilator
• Adenosine antagonism
• Hypotension, tachycardia in COPD
– Seizure is bad
• 10-20 nml, > 35 bad
• Control seizures, Charcoal, HD
• Propranolol for tach, hypotension
Lithium
• Acute
• Chronic
• Acute on Chronic
• Aggitations à tremor à
clonus/hyperreflexia à fasciulation à
AMS
• Renal elimination à impairment = toxicity
– Handled like sodium
Lithium
• IV fluids
• WBI for SR prep
• No charcoal
• HD for AMS or level > 4.0
• Nephrotic syndrome with chronic use
• If “Kayexalate” is an answer, look for
another before choosing it
Envenomations
• Pit Viper
– Anticoagulant
– Grade envenomation
• Cross joint line?
• Hemorrhagic blister?
– ABC
– Assess coagulation
– If symptomatic à 4-6 vials of Crofab
Envenomations
• Elapid
– Respiratory Depression
– Give snake specific antivenin if bitten
• Sea snakes are Elapids
• Jelly fish
– Vinegar to remove tentacles
– Pain control and antihistamines
– Box Jellyfish antivenom if in Australia
Marine Poisonings
• Ciguatera
– Eating contaminated reef fish (dinoflagellates)
– Hot/cold reversal
– GI effects, ataxia, AMS
– Looks like MS
Marine Poisonings
• Scombroid
– Histadine à histamine
– Peppery taste
– Flushing, urticaria
– Senario: Eating mackerel, tuna, mahi-mahi
– Treat with antihistamines
Marine Poisoning
• Tetrodotoxin
– Pufferfish
– Sodium channel blocker
• Stops nerve conduction
– Peripheral paralysis
– ABC
– Supportive Care
Arthopod
• Hymenoptrae
– Bees, Hornets, Wasps
– Allergic reaction
– Steroids, H1 and H2
• Loxoceles Reclusa
– Necrotic arachnidism
– Slowly developing (days to weeks) sore
– Make sure it isn’t MRSA
– Treatment: Dapsone (?)
Arthropods
• Lactrodectrus Mactans –Black Widow
– Very painful
– “Rigid abdomen”
• Looks like acute api
– Scenario: outhouse, young child
– Pain control
– Antivenin use is rare
Antidotes
• Acetaminophen à NAC
• Benzodiazepine à Flumazenil (avoid)
• Benzocaine à methylene blue
• Betablocker à Glucagon
• CCB à Calcium
• Clonidine à Naloxone (50/50 chance)
• Cyanide à Hydroxocobalamin,
Nitite/thiosulfate
Antidotes
• Digoxin à Fab
• Diphenhydramine à Physostigmine
• Heparin à Protamine
• Iron à Deferoxamine
• Lead à Succimer, EDTA
• Lead, As à BAL
• Methotrexate à Leucovorin
Antidotes
• Nerve agents à Atropine, Pralidoxime
• Opiate à Naloxone
• Pit Viper à Crofab
• Sulfonylurea à Octreotide
• Toxic alcohol à Antizol, EtOH
• Valproic Acid à L-carnatine
• Warfarin, LAAC à FFP, Vit K
Hemodialysis
• Aspirin
• Methanol/ethylene glycol
• CBZ (HP)
• Theophylline (HP)
• Lithium
• Barbs?
Multidose charcoal
• Theoophylline
• Phenobarbital
• Dapsone
• Carbamazpine
• Quinidine
• “These people drink charcoal quickly”
Alkalinzation
Urinary Serum
• Aspirin • TCA
• Phenobarbital • CBZ
• Methotrexate • Type Ia/Ic
• Cocaine
• Chlorpropamide (SU)
Hypotension/Brady
• Alpha agonists
• BB
• CCB
• Digoxin
Hypotension/Tachy
• TCA
• Theophylline
• Antipsychotics
• Antimuscarinics
Toxic Seizures
• Bupropion
• Theophylline
• TCA
• Tramadol (meperidine)
• Isoniazid
• Sympathomimetics
• Late antimuscarinics (unlike Q)
Mammal bites
• Wound care
• 3-6M / year, 85% dog
• Infection
– 10-15% human bite
– Skin flora
– Pasterella (cats and dogs)
– Captnophagus
Dysbarism
• Decombrrssion Sickness
– Type I: Simple: Skin, joints
– Type II: Serious: CNS
• Air Gas Embolism
– Diving
– Iatrogenic
Dysbarism
• DCS: O2 à HBO
• AGE: reposition à O2 à HBO
– May need to look for PFO
Barotrauma
• Rpid Pressure change
– Diving Ascent
– Explosion
• Middle ear/sinuses
– 10-30% of divers
• Lung injury from breath holding
• Supportive
Lightning
• Burn
• Cardiac arrest
• Resp arrest/medullary stunning
– Prolonged CPR/rescue breathing
• Cataracts
• CNS injuries
Lightning
• Rhabdo
• Arrhythmias à ECG
• Blunt trauma
• Admit Severe injuries
Altitude emergencies
• Acute Mountain Sickness
– > 8000 ft
– Lower PaO2
– Don’t feel good
– Flu like
– Dehydration
– EtOH
– Insomnia
– Ibuprofen
Altitude Emergencies
• HACE
– Refractory HA
– Gait disturbance
– Retinal Hemorrhage
– LOC
– Acetazolamide prophylaxis
– Dexamethasone/O2
– Descent
Altitude Emergencies
• HAPE (Pulm edema)
– Cough
– Fever
– SOB at rest
– Pulm Edema
– Rapidly progressive
– Nifedipine/O2
– Descent
Cold Immersion
• Cold water shock
– Involuntary inhalation
– Cardiac Arrest
– Rapid hypothermia
• May be protective
Near Drowning
• Hypoxia
• 3rd leading cause of injury/death
• 90% wet drowning
• 10% maintain laryngospasm
Heat exhaustion
• Overheating, but can still sweat
• Heat cramps mildest
• Thirst
• Rapid pulse
• Temp < 40.6
Heat stroke
• Temp > 40.6 C
• Inability to sweat
• AMS/Coma/Seizure
• Hydration
• Cooling
– Cool/cold immersion most rapid
Frostbite
• 1st Degree: Outer Layer “Frost Nip”
• 2nd Degree: deeper skin, blisters
• 3rd Degree: deeper tissues, prob loss of digit
• Rewarm tissue, don’t allow refreeze
– Warm water bath 40-42
• Surgery for infection only
• Local tPA (?)
Hypothermia
• Temp < 35.0
• Mild: Shiver, HTN, tachy
• Mod: Violent shiver, slow movements, mild
confusion, cold distally
• Severe: Autonomic instability, AMS
Hypothermia
• Risk Factors
– Extremes of age
– Substance abuse
– LSES
– Chronic Medical conditions
Rewarming
• Mild: Passive rewarming
• Moderate: Active external
• Severe: Active internal
Hypothermia
• Complications
– Cold Diuresis: warm fluids
– Rewarming collapse
• Low Cardiac Output
• Hypotension
– Dysryhthmia
• CPR
• Single defib if < 30
Silo Filler
• Fall into grain silo
• Nitrogen dioxide à nitric acid in lungs
• Delayed/diffuse alveolar injury
• Steroids – unlikely to ask treatment
Radiologic
• Hematopoetic
– Anemia
– Leukopenia (first 30 days)
• GI
– Earlier N/V = bad
– < 2 hours = fatal
• CNS
– > 30 gy
– Death
Radiologic
Treatment
• Supportive
• Transfusion
• Burn care
• Sepsis care
• GCSF
• Bone Marrow Transplant
Substance Use Disorders
• Opioid • MAT
• Tobacco • Drug diversion
• Withdrawal
syndromes
– EtOH
– Opioid
• Stimulant Use
Good Luck
Study Guide: Procedural Facts to Know and Pearls

Cardiothoracic Procedures
Pericardiocentesis
-indicated for tamponade
-muffled heart tones, JVD, hypotension, electrical alternans
-bilateral breath sounds
th
-left 5 intercostal space, 3-4 cm lateral to sternum
-enter ABOVE the rib (avoid neurovascular bundle)
-subxyphoid when going blind
-pericardium lies 2-3 cm below skin in average adult
-16-18 gauge needle attached to a large syringe should be used and the chest wall
should be cleaned and draped using accepted sterile techniques.
-The needle should be inserted at the xiphoid process up into the chest at a 45° angle
and directed towards the tip of the left scapula.
-The syringe should be aspirated as the needle is advanced every 1-2mm until fluid is
aspirated. The operator should feel the needle penetrate through the pericardium.
-major complication coronary vessel laceration causing infarction or hemopericardium
-use US when possible
-Best views are based on patient habitus, positioning and which axis of the heart is
optimally viewed. Most typically, the subxiphoid (SX) or parasternal long (PSL) views
are used, but sometimes, an apical-4-chamber (A4C) axis is best.
-Best probe is a low frequency phased array transducer, but curvilinear can also be
used.
Thoracentesis
-immediate needle decompression for tension pneumo
-diagnosis: unilateral diminished or absent breath sounds, hypotension/hypoperfusion,
distended neck veins (may not occur if patient is hypovolvemic)
-late sign: tacheal deviation
-type of obstructive shock since prevents venous return to the right side of the heart
-DO NOT WAIT FOR CXR, STICK THE NEEDLE IN THE CHEST
-14ga IV 2nd intercostal space mid-clavicular line (although evidence suggests lowest failure
rate of needle decompression is at the 4th/5th rib space along the anterior axillary line)
-Always followed by chest tube placement
-diagnostic taps: Exudative vs. Transudative (Light Criteria)
-exudative (if lower than this then transudative)
-fluid/plasma protein >0.5
-fluid LDH/serum LDH >0.6
-fluid LDH > 2/3*serum LDH upper limit of normal
Thoracostomy Tube
-after needle decompression always for tension pneumo
-confirm tube placement with CXR
-4th to 5th intercostal space anterior to mid axillary line
-ABOVE THE RIB
-clamping tube will cause tension pneumo
- >1500 ml of blood out means OR (or >300 ml/hr after)
Thoracotomy
-penetrating trauma with loss of vitals in route or in ED
 -cut pericardium anterior to phrenic nerve
Transcutaneous Pacing
-pads anterior and posterior placement
-initial stabilization
-over-drive pacing
-use if thrombolytics were given
Transvenous Pacing
-unstable bradydysrhythmias
-right IJ then left subclavian (save left IJ for PPM)
-clinical status worsens while placing central line = air embolus
-place patient left lateral decubitus, aspirate RV if necessary, then HBO
-post procedure CXR and feel pulse to confirm capture
Venous Cutdown
-when other access not possible (now will usually use IO)
-go for greater saphenous, ankle 1 cm anterior to medial malleolus
-complication is loss of medial sensation
IO Access
-use in unstable peds without access (also in adults)
-do not place in fractured bone
-can infuse all drugs, fluids and blood for resuscitation
Umbilical Vein Catheterization
-can use up to 1 week after birth
-One vein (two arteries) at 12 o’clock
-advance catheter until get blood return, then place about 1 cm beyond
-Xray shows catheter going toward head, if in liver went too far, pull back

GI Procedures
Paracentesis
-therapeutic for tense ascites causing compartment or respiratory distress
-albumin for removing 5L +
-diagnostic : >250 PMNs is SBP
Balloon Tamponade of UGIB (Blakemore)
-must have endoscopy readily available
-intubate patient and provide adequate sedation
-Confirm with pressure read and xray that gastric balloon is in stomach prior
to full inflation

Neurologic Procedures
LP
-opening pressure only accurate in recumbent patient
-normal pressure <20cm in adults
-CT prior to procedure in altered mental status
Perimortem C-Section
-fundus above the umbilicus assume viability of infant
-must be done within 5 minutes of maternal death
-continue maternal CPR until procedure complete
-midline vertical incision on skin and uterus
Anesthesia
-Esters = one I in name (no I in ester)
-Amides = two I’s in name
-esters and amides don’t cross react (ie patient with allergies)
-pt allergic to lidocaine, answer ok to give ester (look for one i)
-board answer no epi in end artery areas (fingers, nose, ear, penis)
-max dose 4 mg/kg without epi, 7 mg/kg with
-know when to use regional block and which block
-face, (lip), rib, digits
-common to know: mental, infraorbital, inferior alveolar, sup alveolar
ophthalmic, median, ulnar
-RSI avoid (specifically paralytics) if pre-intubation concern for difficult airway

Ophthalmologic Procedures
Lateral Canthotomy
-anything causing increased optic pressure about 40 with vision loss
-think retrobulbar hemorrhage in trauma
-avoid in globe rupture
-visualize lateral canthus tendon by pulling down on inferior lid and
with scissors pointing away from globe dissecting down to inferior
lateral canthus tendon and cut it
-irreversible vision loss if retinal ischemia time >90-120 mins
IOP measurement
-contraindicated with suspected globe rupture
-use topical anesthesia
-normal IOP 10-20, >20 is abnormal
Orthopedic Procedures
Extensor Tendon Repair
-we (EM) don’t repair flexor, need hand referral
-ideal 24 hours within injury
-use non-absorbable suture
Arthrocentesis
-absolute contraindication to tap with overlying infection
-must do if you suspect septic joint
->50,000 WBC is infection
-Pseudogout is positively birefringent (pyrophosphate crystals)
-gout is negative birefringent
-Elbow – go lateral distal to lateral epicondyle
-Shoulder –patient upright, go inferior and lateral to the coracoid and
aim towards glenoid rim
-Knee – many approaches, learn them, easiest joint tap (easiest is superior lateral)
-Ankle – foot plantar flexed, go medial to anterior tibial tendon and
aim to the hollow at anterior edge of medial malleolus, must go
2 to 3 cm deep to penetrate joint

Splints and Casts

-always assess neurovascular before and after placement
-someone returns to ED with increased pain after splint or cast = remove
Compartment Pressure Measurement
-compartment should be at same level of heart for measurement
-pressure >30 mm Hg is abnormal
-treatment is fasciotomy, except for snake bites use HBO

Suprapubic Catheterization
-indications
-men with strictures
-trauma with urethral injury or high riding prostate
-do not attempt to place foley in these patients
-pelvic fractures and suspected urethral injury (blood at meatus)
-do retrograde urethrogram (RUG) first
-needle 2-3 cm superior to pubic symphysis and directed toward pelvis
-aspirate urine then thread foley over guidewire
-US helpful

Random Pearls
Airway
-always revert to basics (jaw thrust/chin lift, BVM, oral/nasal airways)
-blind nasotracheal intubation contra-indicated
-apnea and mid face fractures
-surgical
-precautions with cric: young age, laryngeal fracture, bleeding diathesis, tracheal
disruption
-jet insufflation in peds = oxygenate not ventilate
-obstruction: BLS first Heimlich then magills and finally cric
-Predicting difficult airway
-Mallampati
-1 soft palate, uvula, fauces, pillars
-2 no pillars
-3 no faces, base of uvula
4- only hard palate

Blood Therapy
-O neg for emergent transfusion
-type specific for urgent (10-15 minutes)
 -remember worry about hypothermia and coagulopathy
Know Indications, Technique and Complications of These Diagnostic Procedures
-arthrocentesis
-cystourethrogram
-lumbar puncture
-para/thoracentesis
-tonometry
Testicular Detorsion
-open the book, remember attempt should be >180 degrees
Epistaxis
-anterior pack send out on antibiotics
-don’t cauterize both sides of septum (ie necrosis)
-posterior pack gets admitted
Tooth replacement
-DON’T touch or scrub (will injure the periodontal ligament)
-transport in Hanks solution or milk
-DON’T replace primary teeth
A-line placement
-do allen test prior
Central Lines
-always get CXR and review after, even if unsuccessful
-umbilical vein access up to 5-7 days of age
-IO’s for any age, any med
-don’t line the bone if broken, infected, previous failed attempt in same bone
Inservice Review Prehospital/Disaster
Robert B Dunne MD FACEP
St John Hospital and Medical Center

EMS

Which Federal agency takes the lead in EMS curriculum development

1. Department of Health and Human Services
2. Department of Homeland Security
3. Department of Transportation
4. National Highway Traffic safety Administration
5. Veterans Administration
Answer: 3 The DOT provides the curriculum template. Bledsoe, B Paramedic Care Principles
and Practice, Vol 1, Brady 2000 xix-xxi.

Historical Development
1966 National Highway Safety Act
DOT funding for ambulances
Outlined communication
Provided for training

The components of EMS systems were defined by which federal law.

1. Comprehensive Omnibus Budget Reconciliation Act
2. Emergency Medicine and Treatment of Active Labor Act
3. Emergency Medical Service Systems Act
4. Trauma Care Systems Planning and Development Act
5. McCain – Fiengold Bill
Answer: 3. EMS ACT 1973. Medical Direction of Emergency Medical Services, ACEP, Dallas 2000.
Modern EMS Development
1973 Public Law 93-154 defined 15 elements of EMS

The greatest safety threat to EMS personnel is:

1. Blood body fluid exposure
2. Downed powerlines
3. Lacerations from sharp objects
4. Traffic related accidents
5. Vehicle explosions
Answer: 4. Traffic related incidents cause the largest number of EMS related deaths. Bledsoe, B
Paramedic Care Principles and Practice, Vol 5, Brady 396-399.

EMS medical directors are physicians that provide direct and indirect medical control of patient
care activities in the prehospital setting. Which of the following is not an element of indirect
medical control?
1. Development of EMT patient care guidelines and protocols
 2. Development of emergency medical dispatcher (EMD) patient care guidelines
and protocols
3. On-line radio or telephone communication with the EMTs on the scene or during
transport of a patient
4. Participation in the EMS system quality management and quality assurance
program
5. Participation in the EMT training program
Answer: 3. EMS medical direction consists of direct (on-line) and indirect (off-line) medical
control and oversight..
Blackewell T. EMS: Overview and ground transport. In Rosen P: Emergency medicine concepts
and clinical practice, ed 6, St. Louis, 2006, Mosby. Page

WHAT IS Medical Control

The direction of EMS operations
Medical director of service has final responsibility
Online
Giving orders over radio
Being on scene
Often impractical
Always needs to be available
Physician on scene
Proof of licensure
Radio medical control still responsible
May need to accompany
Should ask what s/he can do
Offline
Developing standing orders
Protocols
Training
Continuous quality improvement

EMT’s are dispatched to a scene. The 911 call by the wife reports her husband acting strangely
and being very ill. On arrival EMT’s find the man belligerent and refusing to go to the hospital.
The appropriate action for the EMTs is.
1. Contact Medical Control with their findings
2. EMT’s should determine the patients competence and transport patient if they
deem him incompetent
3. Have patient sign an AMA form and not transport
4. Not transport and advise the wife to call the police
5. Transport the patient to the hospital.
Answer: 1. This is a case for online medical control to assist the EMTs and protect them medico
legally. Bledsoe, B Paramedic Care Principles and Practice, Vol 2, Brady 2018 122.

Controlling Violent Situations

 • When a psychiatric patient refuses care in the prehospital setting, EMS personnel should
consult with medical direction
• The decision to restrain, treat, or release the patient is a medical direction decision
• Appropriate sedation is safest alternative
• If violent behavior must be contained, “reasonable force” to restrain the patient should
be used as humanely as possible
• In most cases, the restraint duty (if necessary) should be given to law enforcement
personnel

The “Chain of Survival” for cardiac arrest includes all of the following except?
1. Early access
2. Early CPR
3. Early Defibrillation
4. Early Advanced Life Support
5. Early admission to and ICU bed
Answer: 5. AHA 2020 ACLS
Cardiac Care - Chain of Survival, access to specialty care does not mean getting to a bed, just the
hospital having capability

EMTALA

EMTALA provides all of the following guidelines regarding transfers except

1. The patient must be examined prior to transfer
2. The patient must consent to the transfer
3. The transfer must be medically indicated
4. Patients who remain unstable may not be transferred even if the benefits outweigh the
risks
Answer : 4

EMTALA Obligations

If an emergency medical condition exists, the

hospital must:
Provide treatment until the patient is stabilized.
Then transfer the patient to a medical facility that is better able to provide the
necessary treatment.
Requirements of Transferring Hospital
• Provide medical treatment, if possible, to minimize the risk of transfer,
• Obtain patient’s consent for transfer,
• Provide signed certificate of transfer,
• Assure that the transfer takes place with qualified personnel and equipment,
• Send copies of medical records related to the emergency condition.
Obligations of Receiving Hospital
 • Have available space and qualified personnel
• Agree to accept transfer of the patient and to provide appropriate medical
treatment.
• Regional referral centers and hospitals with specialized capabilities cannot refuse
to accept an appropriate transfer if they have the capacity.
Transfer of Non-stabilized Patients
Non-stabilized patients may be transferred
ONLY IF:
• The patient (or someone acting on the patient’s behalf) requests a
transfer in writing after being informed of the risks involved and the
hospital’s duty to treat under EMTALA, or
• A physician certifies that the medical benefits expected from transfer
outweigh the risks involved in the transfer.
Liabilities Under EMTALA
There are 2 courses of action for violations of EMTALA:
• Private civil suits against the hospital (but not the physician).
• HHS penalty fines against hospital, physician, or both.
• Responsibility of the Transferring Physician

Violations of EMTALA can result in:

1. Civil Monetary penalties
2. Terminations or suspensions of Medicare provider agreements
3. Civil action
4. All of the above

Answer: All of the above

EMTALA Applies to:
1. Free standing clinics
2. Hospitals with Medicare participation agreements
3. Nursing Homes
4. All of the Above

Answer: Hospitals that participate in Medicare.

Aeromedical Transport

The most common crew configuration among helicopter aeromedical programs in the United
States is:
1. Nurse/Nurse
2. Nurse/Paramedic
3. Physician/Nurse
4. Physician/Paramedic
5. Respiratory Therapist/Nurse
Answer: 2. All of the providers listed participate in air medical transport and there is wide
variation in crew configuration. The combination of a nurse and paramedic, however, is the
most common.
Stone CK and Thomas SH: Air Medical Transport, in Tintinalli JE, Kelen GD and Stapczynski JS
(eds): Emergency Medicine A Comprehensive Study Guide, ed 5, New York: McGraw-Hill,
2019:11.

Prior to evacuating a critically patient by air you should do all of the following except:
1. Add extra air to the IV bags
2. Be sure all line are secure.
3. Check that the helicopter landing area is clear
4. Replace the air in ET tube cuff with water
5. Understand the radio procedures to contact the air medical service.

Answer: 1. Any air has the potential to expand during air medical transport. Bledsoe, B
Paramedic Care Principles and Practice, Vol 5, Brady 2000 334.
Rodenberg H and Blumen RJ, Air Medical Transport in Emergency Medicine Concepts and
Clinical Practice Vol 3 6th edition Mosby 2006 2994.

Aeromedical Transport
Air ambulance - primary response
Useful in area with long transport times
Controversial
Interfacility transport
Common after initial stabilization
Some fixed wing transport
Aeromedical Transport Problems
Change in air pressure
Gases expand
Potential for hypoxia
Safety issues

Factors in choosing air ambulance transport over ground transport include all of the following
except.
1. Geographic terrain
2. Lack of any advanced ground transport provider
3. Patient insurance status
4. Traffic congestion
5. Transport time to definitive care.
Answer: 3. The T’s Time. Traffic, Terrain, Training are all factors in making a ground vs. air
decision. Bledsoe, B Paramedic Care Principles and Practice, Vol 5, Brady 2000 330.
Rodenberg H and Blumen RJ, Air Medical Transport in Emergency Medicine Concepts and
Clinical Practice Vol 3 6th edition Mosby 2006 2994.
DISASTER MANAGEMENT

All of the following are true about the incident commander (IC) except.
1. Located uphill and upwind of the incident.
2. Organizes the operation of the mass casualty scene
3. Provides medical oversight.
4. Typically chosen from fire or police personnel.
5. Works closely with the EMS branch director.
Answer: 3. The IC does not provide direct medical oversight, but overall command. Medical
Branch Chief oversees medical
Schultz CH, Koenig KL, Noji EK Disaster Preparedness in Rosen’s Emergency Medicine Concepts
and Clinical Practice Vol 3 6th edition Mosby 2006 3010 – 3021.
Sutingco, N The incident command system In Disaster Medicine, Ciottone et al Eds. Mosby 2006
208

What is a…
A. Disaster?
B. Mass Casualty Incident?
Disaster Planning and Response
“Interest in disaster preparedness is proportional to how recent and how severe the last
disaster was”
Disaster - any incident that overwhelms resources
Mass casualty incident - large numbers of casualties from any cause (MCI) not necessarily a
disaster, a facility may be able to handle with the resources they have
Terrorism - MCI, disaster or both, terrorism is intentional

Categorization
PICE - Potential to create injury
Levels based on resources needed
I - Local
II - State
III – National

What is not a component of disaster triage.

1. Blood pressure
2. Mental Status
3. Pulse
4. Respiratory status
Answer: 1. Schultz CH, Koenig KL, Noji EK Disaster Preparedness in Rosen’s Emergency Medicine
Concepts and Clinical Practice Vol 3 6th edition Mosby 2006 3010 – 3021.

What is Triage?
French verb “trier” = to sort
Assign priorities when resources limited
 Do the greatest good for the greatest number
What’s Unique About Disaster Triage?
Number of patients
Infrastructure limitations
Limited providers
Limited equipment
Limited transport capabilities
Hospital resources overwhelmed
Scene hazards
Threats to providers
Decontamination issues
Multiple agencies responding

SALT Triage
Simple
Easy to remember
Groups large numbers of patients together quickly
Applies rapid life-saving interventions early

S.A.L.T. Triage Categories

Immediate
Serious injuries
Immediately life threatening problems
High potential for survival.
 Examples
Tension pneumothorax
Nerve agent exposed patient
severe shortness of breath or seizures
Delayed
Serious injuries
require care but management can be delayed without increasing morbidity or mortality.
Examples
Long bone fractures
neuro-vascular intact
40% BSA exposure to Mustard
Minimal
Injuries- require minor care or no care without adverse affect.
Examples
Abrasions
Minor lacerations
Nerve agent exposure with mild rhinorrhea
Expectant
Important for preservation of resources
DOES NOT MEAN DEAD!
Should receive comfort care or resuscitation when resources are available
Serious injuries
very poor survivability even with maximal care in the hospital or pre-hospital setting.
Examples
90% BSA burn
Multiple trauma with exposed brain matter
Severe traumatic brain injury with herniation
Dead Patients
Tag dead patients to prevent re-triage
Do not move Except to obtain access to live patients
Avoid destruction of evidence

MASS CASUALTY

You are triaging a large number of patients at a Mass Casualty Incident and encounter a patient
who appears apenic and unconscious. Using SALT triage you should:
1. Check for a pulse.
2. Open the airway and assess for breathing.
3. Tag the patient black
4. Tag the patient green
5. Tag the patient red
Answer: 2. Open the airway and check for breathing is a step in the airway assessment for start
triage. If the patient was breathing you would go on to the next step, circulation. If no
breathing, black tag and go on to the next patient. Schultz CH, Koenig KL, Noji EK Disaster
Preparedness in Rosen’s Emergency Medicine Concepts and Clinical Practice Vol 3 6th edition
Mosby 2006 3010 – 3021.

Response personnel arrive to find many unresponsive victims who were all attending a meeting
in a school cafeteria. They should first:
1. Call for the Hazardous Materials Team
2. Evacuate the victims
3. Identify the potential cause of the victims condition.
4. Protect themselves from exposure
5. Treat the victims.
Answer: 4. Schultz CH, Koenig KL, Noji EK Disaster Preparedness in Rosen’s Emergency Medicine
Concepts and Clinical Practice Vol 3 6th edition Mosby 2006 3010 – 3021.
Disaster - Phases
Mitigation - Prevention
Activation - Initial response
Implementation - Rescue, triage, treatment
Recovery - Return to normal operations

The Joint Commission (Former JCAHO) requires hospitals have a written disaster plan, how
often must drills be conducted.
1. One time per year
2. Two times per year
3. Three time per year
4. Recommended but not required.
Answer: 2
Two times per year, actual disasters can substitute.

How long does the Joint commission expect hospitals to be self sufficient in case of a disaster ?
1. 24 hours
2. 48 hours
3. 72 hours
4. 96 hours
5. No need as federal help is immediately available.
Answer 4 – 96 hours per current JC standard
[Link]
[Link]
 GU ITE Review

Acute renal Injury

Pathology Diagnosis, cause Treatment
• oliguric, kidney retains resorptive function and ability to conserve sodium Correct the
• Patients are urine is concentrated (SG >1.020), OSM >500, FENa <1%, low urine Na hypoperfusion
Prerenal <20mEq/L; UA normal or occasional hyaline casts
azotemia- • BUN/Cr >20
60% • Causes: Hypovolemia (= V/D, blood loss, diuretics, insensible losses), shock states (distributive,
cardiac, anaphylaxis), third spacing,

• Obstruction of urine flow Foley, stent,

• Anuria (complete obstruction) polyuria (partial) PCN, relieve
Postrenal • UA normal the
azotemia- • Causes: ureteral (crystals, stones, blood clots, malignancy, retroperitoneal fibrosis), bladder obstruction
15% (BPH, prostate or bladder malignancy, blood clots), neurogenic bladder, urethral stricture,
phimosis
• Pathology of kidney, renal tubule, loose ability to concentrate and reabsorb sodium Remove the
• Urine is dilute (SG <1.010), osm < 300, FENa >2%, High urine Na >40 mEQ/L (= spilling offending
water, Na) agent and
• BUN/Cr <20 treat the
o Acute Tubular Necrosis – 90% underlying
▪ Muddy granular casts cause.
▪ Causes: prolonged hypoperfusion, nephrotoxins
o Acute Insterstitial Nephritis
Renal ▪ Eosinophilia, Granular and white cell casts
Azotemia- ▪ Causes: drugs, (PCN, cephalosporins, sulfa, diuretics), infection, immunologic
25% o Glomerulonephritis
▪ RBCs, RBC casts, proteinuria
▪ Hypertension, edema, CHF, volume overload
▪ Causes: postinfections (post strep) administering abx does not decrease
incidence
o Vascular
▪ Vasoconstriction, TTP, vasculitis
o Thrombosis
▪ Renal artery/vein

Complications:
▪ Hyperkalemia: get an EKG. Most immediate life threatening complication
o Treatment:
▪ Calcium – onset <3 min; gluconate is less toxic than chloride if it extravisates; chloride contains more calcium
than gluconate
▪ Albuterol
▪ Glucose / insulin
▪ Bicarb
▪ Dialysis
▪ Additional electrolyte disturbances: hypocalcemia, hypomagnesemia, AGMA, volume overload

Indications for dialysis

▪ A = acidosis
▪ E = electrolyte abnormalities (including resistant hyperK)
▪ I = ingestion of toxic substance (lithium, methanol, ethylene gycol, metformin
▪ O = overload of fluid
▪ U = uremia (pericarditis, encephalopathy, bleeding

1
Myoglobinuric Renal Failure
▪ Trauma— (=crush injuries, burn, seizure, prolonged exercise), intoxication (= etoh, PCP)
o Rhabdo
▪ Myoglobinemia
• Toxic effect on renal tubules
o ATN
▪ Acute renal injury
▪ Diagnosis: Urine is coca-cola colored, + blood on dipstick, but curiously no RBCs on micro, tubular casts, granular casts
o Serum myoglobin is not reliable, CPK is the most sensitive;
▪ Hypocalcemia, hyperkalemia
▪ Treatment: avoid nephrotoxins, hydrate aggressively, mannitol, Lasix, alkylinize urine with NaHCO3

Other types of Renal Failure

▪ Nephrotic syndrome: high urine protein excretion, peripheral edema, metabolic abnormalities (hypoalbuminemia,
hypercholesterolemia
▪ Minimal Change disease: peds, may be preceded by URI/immunization, treat with steroids
▪ FSGS: can be found in those with sickle cell disease, IVDA, HTN, DM, high frequency of renal failure. Can be treated with
steroids and immunosuppression.
▪ Membranous Nephropathy: caucasions 30-50%, HBV, HCV, syhillis, malaria, SLE, gold penicillamine, 24% associated with
neoplasm; proteinuria, occasional microhematuria, hypercoagulopathy (RV thrombosis), remits spontaneously 25%
▪ Membranoproliferative glomerulonephritis: nephrotic/nephritic features, assoc with infection, autoimmune disease, HCV,
cryoglobulins, low C3, 50% mortality rate or progression to ESRD with 5years of diagnosis
▪ Diabetic nephropathy: leading case of ESRD in US; onset 5-10 years after onset of type 1 DM. treat with TGCP, ACEI
▪ Misc: lymphoma, myeloma, HIV, HBV, HCV, syphilis, leprosy, malaria, SLE, amyloidosis, sickle cell, preeclampsia

Dialysis related problems

▪ Vascular access hemorrhage
o Minor bleeding from puncture: non occlusive pressure; reassess for thrill
o Significant bleeding from aneurysm/pseudo aneurysm: direct pressure, vascular consult
▪ Vascular access thrombosis
o Most common problem: loss of thrill, unable to access during dialysis session; vascular consult.
▪ Vascular access infections
• Vascular access infection
o Often Staph; more common in artificial than native grafts
o Signs of infection (redness, warmth, induration) may be absent; may only have fever
o Tx= blood cultures, antibiotics (Vanco); may not require removal of device
• Peritoneal dialysis
o Peritonitis: cloudy dialysate effluent, abdominal pain, fever; fluid WBC > 100 with > 50% PMNs or positive Gram
stain ; intraperitoneal abx.
• Disequilibrium syndrome
o Rapid solute shifts during hemodialysis; most often during first session
o Headache, nausea, malaise, disorientation, confusion, seizure, coma, death
o Tx= supportive; r/o other causes of ∆MS
• Cardiac arrest: beware of hyperkalemia and acute pericardial tamponade

Urinary tract infections

• Cystitis: dysuria, urgency, frequency, hematuria, suprapubic discomfort, significant bacteriuria
• Causes: SEEK PP: Staph saprophyticus (2nd), E. coli (1st), Enterobacter, Klebsiella, Proteus, Pseudomonas
• Uncomplicated UTI: most UTIs; nonpregnant, healthy women with no neurologic or structural dysfunction
o Treatment: 3-6 days (Bactrim, quinolone, nitrofurantoin)
• Complicated UTI: associated with any neurologic, structural, or comorbid condition that increases risk for acquiring
infection and reduces efficacy of standard tx regimens.
o Factors that predispose
▪ Structural (calculi, catheters, stents, prostatic infection, urinary diversion procedures)
▪ Metabolic or hormonal (diabetes, pregnancy)
▪ Vesicoureteral reflux, immunocompromise, recent urinary tract instrumentation
▪ Male gender, extremes of age, unusual pathogens, recent antibiotic use or failed treatment for UTI,
symptoms longer than 7 days
o Treatment: 7-10 days
• Pyelonephritis: fever, flank pain, vomiting, malaise, CVA tenderness, significant bacteriuria

2
 o Consider hospitalization: Severe illness/sepsis; extremes of age; uncertain diagnosis; h/o stones, obstruction,
instrumentation; underlying anatomic urinary tract abnormality; comorbidities; failed outpatient; persistent vomiting;
immunocompromised; poor access to followup
• Culture all except uncomplicated cystitis

Nephrolithiasis
• Composition
o 80% contain calcium (2/3 calcium oxalate, 1/3 calcium phosphate); associated with dehydration, hyperoxaluria,
hypercalciuria (hyperthyroidism, hyperparathyroidism, neoplasm, sarcoidosis, multiple myeloma, distal RTA), PUD
(ingest large amts of calcium)
o 15% struvite (magnesium-ammonium-phosphate); caused by chronic UTI from urea-splitting organisms (Proteus)
o 6-10% uric acid; gout, myeloproliferative disease, leukemia, high protein diet
o 1-3% cysteine; familial
o Presentation
o Unilateral colicky pain in flank, back, lower quadrant
o Radiation to groin, labia, testicles
o Dysuria, frequency, hematuria
o Nausea, vomiting
o Severe discomfort, diaphoresis, restlessness
o Diagnosis
o Only 80% have hematuria
o 90% seen on KUB; can be used to follow progression/passage
o CT is test of choice
o IVP can show delayed nephrogram, hydronephrosis, hydroureter, extravasation
o Ultrasound in pregnant patients and kids
o Image: first episode, unclear diagnosis, coexistent UTI, elderly
• Most common sites of stone impaction
o Ureteropelvic junction
o Pelvic brim (where ureter crosses iliac vessels)
o Ureterovesical junction (most narrow point in ureter)
o Likelihood of spontaneous passage: <5mm pass 90%, 5-8 mm pass 15%, >8mm pass 5%
o Coexistent UTI is a urologic emergency!!
o Beware of AAA, iliac aneurysms, renal vein thrombosis
o Admit: High-grade obstruction, intractable pain or vomiting, associated UTI, solitary or transplanted kidney, unclear
diagnosis, extravasation of dye, renal failure, stone > 5mm (relative)

o Bladder calculi: elderly men; complication of other urologic disease, assoc w urinary stasis, infection of residual bladder
urine with urea-splitting organisms. Pain on voiding, hematuria, sudden interruption of urinary stream

Acute urinary retention

• Presentation
• hesitancy, diminished stream quality, dribbling, nocturia, sensation of incomplete bladder emptying often precede
retention
• Causes
• Obstructive: BPH is the most common. prostate carcinoma, prostatitis, urethral stricture, posterior urethral valves,
phimosis, paraphimosis, balanitis, meatal stenosis, calculi, blood clots, circumcision, urethral foreign body,
constricting penile ring, clogged Foley
• Infectious: UTI, herpes
• Neurogenic: spinal cord injury, herniated lumbosacral disk (cauda equina), CNS tumors, stroke, diabetes, MS,
encephalitis, tabes dorsalis, syringomyelia, herpes simplex, herpes zoster, alcohol withdrawal, postop
• Pharmacologic: anticholinergics, antihistamines, antidepressants, antispasmodics, narcotics, sympathomimetics,
antipsychotics, antiparkinsonian
• Treatment
• Pass a Foley, coude, suprapubic catheter
• Beware of postobstructive diuresis, especially if chronic urinary retention

Male GU disorders
• Infectious:
• Orchitis
• Usually direct extension of epididymitis; viral orchitis is caused by mumps
3
 • Testicular pain and swelling; with mumps, symptoms evolve several days after onset of parotitis.
• Epididymitis
• Gradual onset unilateral pain and swelling; associated fever and dysuria
• Exam: tenderness and swelling of epididymis (located posteriorly); elevation of testicle relieves pain
(Prehn’s sign)
• Etiology: Age <35-Chlamydia, gonorrhea; age >35- gram negatives (E. coli, Pseudomonas)
• Tx= <35 years- ceftriaxone IM and doxy x 10 days; >35 years- quinolone 10-14 days
• 3-11% pts on amiodarone develp epididymitis
• Acute bacterial prostatitis
• Frequency, urgency, dysuria, obstructive voiding symptoms, perineal discomfort, fever, myalgias, malaise,
low back or rectal pain
• Usually gram negatives (80% E. coli)
• Tender, swollen prostate is warm and firm
• Do not massage the prostate because it can precipitate bacteremia
• Treatment with quinolone or Bactrim for 30 days
• If urinary drainage needed, suprapubic catheter (not foley)
• Penile ulcers (infectious, immunologic)
• HSV, syphilis, chancroid, granuloma inguinale, lymphogranuloma venereum
• Behcet’s syndrome * autoimunie: Vasculitis with chronic oral ulcerations, relapsing iridocyclitis, genital
ulcers; may also have polyarthritis and erythema nodosum; tx=steroids
• Fournier’s gangrene
• Necrotizing infection of subq tissue of perineum
• Bacteroides fragilis, E. coli
• Acute onset, toxic; painful, erythematous edematous scrotum, +/- crepitus/gangrene
• Risk: diabetes, chronic steroids, alcoholic, local trauma
• Abx, urology consult, debridement, hyperbaric oxygen
• Balanoposthitis
• Inflammation of glans penis (balanitis) and the foreskin (posthitis)
• If recurrent, think diabetes, can be caused by candida
• Retraction of foreskin reveals foul, purulent material; glans is red, swollen, tender to palpation
• Topical antifungal, circumcision, good hygiene, consider anti-strep abx, r/o diabetes
• Structural
• Phimosis
• Inability to retract foreskin behind glans; usually secondary to chronic infection of foreskin; usually
uncircumcised men
• Tx= dorsal slit if difficulty voiding; circumcision
• Paraphimosis
• Inability to pull retracted foreskin back over glans
• Infection, trauma, hair tourniquet, sexual activity
• Distal venous congestion can lead to arterial compromise, necrosis, gangrene
• Tx= manual reduction, ice, dorsal slit, circumcision
• Penile fracture
• Tear of tunica albuginea (usually during erection)
• Retrograde urethrogram to r/o urethral injury
• Priapism
• Low-flow: decreased venous outflow→venous stasis, ischemia of corpus cavernosae but spares glans and
corpus spongiosum→rigid, painful penile shaft and soft glans
• Causes: sickle cell, leukemia, intracavernosal injections for ED, trazodone, marijuana, idiopathic
▪ Treatment: Terbutaline sub q, analgesia, pseudoephedrine injection, corporeal aspiration, shunt
surgery
▪ High-flow: rare; not a true emergency; increased arterial blood flow to corpus cavernosae→increased
venous blood flow→partially rigid, painless penile shaft and hard glans
▪ Causes: groin/straddle injury (arterial-cavernosal shunt), high spinal cord injury/lesion
▪ Obtain a penile blood gas to tell the difference
▪ Testicular torsion
▪ Presentation: Acute onset severe unilateral testicular pain or lower abdominal pain; +/- recent history of
strenuous physical activity or h/o of testicular pain with resolution Bimodal peaks: first few days of life
and ages 12-18

4
 ▪ Patient stands during exam: testicle is swollen, firm, high-riding testicle with transverse lie; contralateral
testicle also transverse lie b/c bell-clapper deformity; +/- reactive hydrocele; loss of cremasteric reflex most
reliable sign; no urinary sx;
▪ Predisposition: bell-clapper deformity
▪ Increased mobility; testicle lacks normal attachment at vaginalis
▪ Immediate urology consult!! Then attempt manual detorsion (opening a book), Doppler
ultrasound
▪ Salvage rate 100% at 6 hrs but approaches 0% at 24 hours
▪ Torsion of appendices epididymis and testis
▪ Unilateral pain, more gradual in onset, not as severe, localized to involved appendix early; late, generalized
scrotal swelling and tenderness
▪ Blue dot sign: visualization of necrotic appendix testis through scrotal wall on superior aspect of testicle on
transillumination
▪ Self-resolving, benign processes. Rest, scrotal elevation, analgesia
▪ Hydrocele: fluid collection in tunica vaginalis; transilluminates, not firm or hard
▪ Varicocele: “bag of worms,” 85-95% on left
▪ Testicular tumor: painless, unilateral scrotal mass palpated discretely from the testis; firm and hard
Pediatric UTI
▪ Boys
▪ <1 year, uncircumcised
▪ <6 months, circumcised
▪ Girls
▪ < 3 years
▪ infants are more likely to have GBS
▪ >1 year most likely infection is [Link]

Hematuria
• Trauma: bladder injury, ureter injury, retroperitoneal injury
• Anemia, thrombocytopenia, renal insufficiency: HUS
• Flank pain: nephrolithiasis
• Urine + for heme and – for RBCs: rhabdomyolysis
• Dysuria, frequency: UTI
• Hearing loss: Alport syndrome
• Hemoptysis: Goodpasture syndrome
• Immigrant: Schistosomiasis
• Nephrotic syndrome, flank pain: renal vein thrombosis
• Proteinuria, RBC casts: glomerulonephritis
• Recent URI: glomerulonephritis, IgA nephropathy
• Gross hematuria: imaging is recommended for age >40

THE DAY BEFORE YOUR ITE, REVIEW THESE QUESTIONS

What should you do when torsion is suspected? Call urology

Treatment of prostatitis in >35 Bactrim/fluoroquinolone
<35, ceftriaxone, doxy
Best indication that a kidney stone will pass on it’s own? <5mm
Patient who presents with maculopapular rash on palms, soles, Secondary syphilis, PCN, RMSF
lymphadenopathy, 6 weeks after painless penile lesion
Dispo for patients with gonococcal conjunctivitis Admit
16 year old male presents with testicular pain, cremasterics in Epididymitis, sti treatment
tact, elevation results in relief of symptoms
Gram stain appearance of gonorrhea Gram negative, intracellular diploccocci
Cloudy peritoneal dialysate Send fluid for analysis; >50% neutrophils are indicative, staph
epi, staph aureus. Can rapidly exchange luid to decrease the
number of inflammatory cells. Add heparin to decrease fiblin
clot formation. INTRAPERITONEAL administration of abx.
Treat with first gen cephalosporins. You don’t have to exchange
the catheter

5
Rhabdo AKI, elevated CPK, hypocalcemia, hyperkalemia, maintain UOP
of 200/300cc/hr
65 year old male presents with symptoms of renal colic, blood in Do an Abdominal US to rule out AAA
urine
Get a urine culture on Pregnant females an those with complicated UTIs
Sexual trauma that leads to priapism results in injury to which Corpus cavernosum—terbutaline
part of the penis
10-20% of those with kidney stones have a normal UA
Fournier’s Clinda, vanc, ertapenem. OR [Link] predominates but mixed
organisms are also there
Paraphimosis Foreskin retracted around the glans, true emergency. Sugar for
reduction, dorsal slit, surgical consult.
Glomerulonephritis RBCs, casts
HUS 5-year old child, Ecoli HO15787
hemolytic anemia,
renal failure
thrombocytopenia
plasmapheresis and dialysis
HSP Rash on pressure dependent areas
Abdominal pain (common to have intussusception)
Normal platelets
Blood in urine and stool
NSAIDS and steroids
TTP Fever
Anemia
Thrombocytopenia
Renal insufficiency
Neurological issues
Plasmapheresis.

6
 Trauma 2 Supplemental Study Guide

▫ Thoracic Injuries
▪ Tension pneumothorax
• Dx: absent breath sounds/JVD/tracheal deviation/shock, EFAST
o do NOT wait for CXR
• Tx: Needle decompression in mid axillary line, finger thoracostomy
o Always followed by chest tube/percutaneous catheter
▪ Hemothorax
• Blood in pleural space, potential hemorrhagic shock
• Dx: Decreased breath sounds, EFAST, blunted costophrenic angle on XR
• Tx: Stable = consider percutaneous pigtail catheter. Unstable = chest tube.
o 1500ml blood or more that 200ml/hr or unstable = thoracotomy
▪ Thoracic fractures
• Rib fractures
o Flail chest is >= 3 ribs fractured in two places, treat with PPV +/- surgery
o Lower rib fractures need to rule out intraabdominal injury
o Higher morbidity in elderly
o Tx: pulmonary toilet, IS device, pain control
• Clavicles most commonly fractured in middle third, sling and d/c unless tenting or
vascular injury
• Sternal fx usually unrestrained steering wheel, CT diagnosis, rarely cardiac
contusion = EKG changes and need echo
▪ Pulmonary contusion = opacity on CXR, hypoxia (often delayed), supportive care
▪ Tamponade
• If from blunt trauma almost always fatal injury
• Dx: FAST (heart first). Becks triad = hypotension, muffled sounds, JVD. Also pulsus
paradoxus, electrical alternans.
• Tx: fluids/blood and thoracotomy if able, otherwise pericardiocentesis then OR
▫ Abdominal Injuries
▪ Most common injuries: Blunt trauma = spleen, Penetrating trauma = liver
▪ GSW: high incidence of peritoneal cavity penetration and intraperitoneal injury; most
require laparotomy
▪ Stab wounds: lower incidence of intraperitoneal injuries (1/3); local exploration and
observation or diagnostic laparoscopy
▪ Solitary lap belt or abdominal seatbelt sign: jejunal, mesenteric, retroperitoneal injuries
(also Chance vertebral fx). CT can be negative early on.
▪ Ultrasound
• Advantages: noninvasive, detects intra-abdominal/pericardial/pleural fluid, rapid,
safe, portable, doesn’t interfere with resuscitation, no contrast, specific
• Disadvantages: can miss bowel and retroperitoneal injuries, cannot differentiate
fluids, impaired in obese, operator-dependent
• Unstable pt + positive US = laparotomy
 • Stable patient + positive US = CT
• Unstable patient + negative US = repeat US or laparotomy
• Stable patient + negative US = observation or CT
▪ CT
• Study of choice for hemodynamically STABLE patients with blunt trauma, GU
trauma, suspected retroperitoneal injuries
• Advantages: noninvasive, gives information on specific organ injury, diagnose
retroperitoneal and pelvic organs
• Disadvantages: contrast, radiation, more time, expert interpretation, can miss
diaphragm/pancreas/bladder/bowel injuries
▪ DPL (diagnostic peritoneal lavage)
• No longer performed
▫ Neck and Back Injuries
▪ Neck injuries
• Most common cause of death for penetrating neck trauma is hemorrhage
• Historically all injuries that penetrate platysma explored surgically; no longer true
• ‘Hard signs’ suggesting deep injury:
o Neuro deficit
o Dyspnea
o Dysphagia
o Hemoptysis/hematemesis
o Subcutaneous air
o Expanding hematoma (carotid most commonly injured artery)
o Bruit
• Zone I: base of neck to cricoid cartilage
o Structures at risk: subclavian vessels, brachiocephalic veins, common
carotid arteries, aortic arch, jugular veins, trachea, esophagus, lung apices,
cervical spine, spinal cord, and cervical nerve roots
o Angiography needed to determine integrity of thoracic outlet vessels
▪ Positive angio may necessitate thoracotomy
• Zone II: cricoid cartilage to angle of mandible
o Structures at risk: carotid and vertebral arteries, jugular veins, pharynx,
larynx, trachea, esophagus, cervical spine and spinal cord
o Most common location for penetrating trauma
o Easily accessible surgically
o Some recommend CT angiography or carotid duplex ultrasonography
• Zone III: angle of mandible to base of skull
o Structures at risk: salivary and parotid glands, vertebral bodies, carotid
arteries, jugular veins, and major nerves (including cranial nerves IX-XII)
o Difficult to expose surgically
o Angiography to assess internal carotid and intracerebral circulation
▫ Unstable spinal fractures
• Maintain spinal precautions and suspect cord injury if any neuro deficits
• Spinal cord ends at L2 in adults (lower in kids)
 • Know NEXUS and CCR criteria
• CT is recommended, still tested on XRs (need C1-C7 vertebrae on lateral). Nearly all
will get MRI.
• Jefferson fracture: C1 ring blowout. Axial load injury. Seen on open-mouth
odontoid view XR.
• Odontoid fractures: swelling anterior to C2 on lateral film. Abnormalities on open-
mouth odontoid:
o Type I: tip of the dens
o Type II: through base of dens
o Type III: involves vertebral body of C2 = unstable
• Hangman’s fracture: bipeduncular fracture of C2; extension injury
• Facet dislocations
o Unilateral (flexion-rotation) or bilateral (flexion)
o Anterior displacement of superior vertebral body relative to the adjoining
inferior vertebral body
• Flexion teardrop fracture: significant disruption of posterior ligaments and anterior
cord syndrome
• Fracture-dislocations: extreme flexion or severe blunt trauma to spine- disruption
of posterior elements (pedicles, facets, laminae)
o Often complete neuro deficit
▪ Stable spinal fractures
• Clay shoveler’s fracture: flexion avulsion fx of spinous process of C6-T3 (C7 most
common). Flexion injury or direct blow to spinous process
• Chance fracture: transverse fx through vertebral body from flexion about axis
anterior to vertebral column
o MVCs when only lap belt worn
o Associated with retroperitoneal and abdominal visceral injuries
• Vertebral body compression fractures
▫ Spinal Cord Injuries
▪ Maintain MAP >85
▪ Anterior cord syndrome
• Flexion injury
• Loss of function of anterior two thirds of cord
• Complete loss of motor function, pain, and temperature below level of injury
• Preservation of posterior column functions of vibration and position
▪ Central cord syndrome
• Hyperextension injury in patients with degenerative spurring or congenital
narrowing
• Weakness greater in the arms than legs
• Good prognosis
▪ Brown-Sequard syndrome
• Penetrating injury hemisects cord
 • Ipsilateral motor paralysis, loss of proprioception and vibration with contralateral
loss of pain and temperature
• Good prognosis
▪ Cauda equina syndrome
• Injury to lumbar, sacral, coccygeal nerve roots causing peripheral nerve injury
• Motor/sensory loss in lower extremities, bladder dysfunction (most consistent),
bowel dysfunction, saddle anesthesia, decreased rectal tone, weakness in
dorsiflexion of great toe
▪ Neurogenic shock (NOT spinal shock)
• Loss of neurologic function and accompanying autonomic tone
• Flaccid paralysis, loss of reflexes, loss of urinary and rectal tone, bradycardia (may
need atropine or pacemaker), hypotension (IVF, may need norepi or
phenylephrine), priapism
• Rule out hemorrhage first, fluids/blood/pressors to maintain MAP
▪ SCIWORA
• Spinal Cord Injury Without Radiographic Abnormalities
• Kids more susceptible because greater elasticity of cervical structures
• Brief episode of upper extremity weakness or paresthesias with delayed
development of neuro deficits. Obtain MRI.
▫ Renal/GU
▪ Renal injury
• Flank ecchymosis, lateral abdominal tenderness or mass, hematuria, fracture of
lower posterior ribs or lumbar vertebrae
• Deceleration injury can cause pedicle injury—can cause uncontrolled hemorrhage,
renal ischemia, exsanguination
• Dx: CT, IVP
▪ Urethral injury
• Most common mechanism: straddle injury
• Perineal pain, inability to void, gross hematuria, blood at urethral meatus, perineal
swelling/ecchymosis, absent/high-riding/boggy prostate
• Dx: retrograde urethrogram
• Do not place foley catheter
▪ Bladder injury
• Extraperitoneal: assoc with pelvic fx, nonsurgical tx; foley for 1-2 weeks
• Intraperitoneal: surgical tx; full bladder ruptures with urine spillage into
peritoneum
• Dx: CT cystography, retrograde cystography (need contrast in bladder)
▪ Asymptomatic microscopic hematuria
• Not good predictor of GU tract injury; amount of blood does not correlate with
severity of injury
• No tx; close follow-up and repeat UA
▪ Penile fracture
• Sudden tear in tunica albuginea with rupture of corpora cavernosum
 • Snapping noise and immediate detumescence
▪ Testicular disruption
• Fall or kick to scrotum; swollen, ecchymotic scrotum, absent testis
▫ Pregnant Patients
▪ Most common cause of non-obstetric maternal death during pregnancy
• MVC, interpersonal violence, falls
▪ Fetal survival depends on maternal survival; management should be directed at
resuscitation of mother
• Most common cause of fetal death: maternal death; abruption is second
▪ Normal physiologic changes of pregnancy can delay recognition (increased HR, decreased
BP, increased plasma volume, physiologic anemia, increased WBC, hyperventilation,
uterine flow comprises 20% cardiac output)
▪ Position patients on left side; inclined 15° = offload IVC
▪ >20 weeks should undergo continuous cardiotocographic monitoring
▪ Uterine rupture
• Free intraperitoneal air, extended fetal extremities, abnormal fetal position
▪ Placental abruption
• Vaginal bleeding, abdominal pain, uterine tenderness, expanding fundal height,
maternal shock, fetal distress, DIC
• Detected 50% by US
▪ Chest tubes: never below 4th ICS
▪ Rhogam: mini dose (50 mcg) if < 12 weeks; standard dose (300 mcg) if > 12 weeks
▪ Resuscitative hysterotomy (perimortem c-section)
• >24wks/fundus at or above umbilicus
• Within 5 mins of maternal death
• Fetal prognosis improves with advanced gestational age; maternal improvement
may be from relief of aortocaval compression by fetus
Neurology:

Supplemental Study Guide Tips:

In addition to your lecture content, please provide us with a bulleted supplemental handout that can be
used by learners as a quick study guide review and reference. This handout will be for high yield board
style information, however, please have these be a broader review of your topic than can be provided in
your lecture session. Refer to the high yield board review books mentioned previously as guides for this
type of information. See below for an example of study guide format/content.

Acute Ischemic Stroke

Common ss: abrupt onset of hemiparesis, monocular visual loss, ataxia, vertigo, aphasia, or sudden
depressed LOC

Transient Ischemic Stroke (TIA):

Transient neuro deficit that resolves within 24 hours
80% resolve within 60 min
*Distinguish CVA from mimics (seizures, tumors, toxic-metabolic disturbances, positional vertigo,
hypoglycemia, etc)

Localization:
MCA:
Contralateral: Hemiparesis, Hemianopsia, Sensory loss
Ipsilateral: Gaze pref
Dominant Hemisphere: Aphasia
Non-Dominant Hemisphere: Hemi-neglect & cortical sensory deficits

Imaging Finding:
Hyperdense MCA sign

ACA:
Disinhibition, primitive reflexes, CL hemiparesis (legs >arms), urinary incontinence
PCA:
CL hemianopsia, cortical blindness, AMS, impaired memory

Vertebrobasilar:
Vertigo, nystagmus, ataxia
Crossed findings (ipsilateral CN deficits & CL long track signs)

Lacunar Infarcts:
Pure motor, pure sensory, ataxia/hemiparesis
TPA Inclusion Criteria
SBP < 185 mmHg, DBP < 110 mmHg (can treat BP to reach acceptable range for TPA)
If no TPA - permissive BP is acceptable up to 220/120 (unless aortic dissection, MI, end organ
dysfunction)

Vertigo:
Central: persistent/constant, non remitting, not affected by position
Peripheral: Not constant, is positional

Bell’s Palsy:

CN VII Palsy
Clinical Dx: Forehead is not spared (inability to raise eyebrow), inability to close eyelid, droop of mouth,
Evaluate for Ramsay Hunt Syndrome
Tx:
Steroids (within 72 hours)
Antivirals (No data to support benefit when combined with steroids)
ABX: Doxycycline if suspect Lyme

Consider Tick borne Lyme ds if bilateral facial palsy

Intracranial Hemorrhage
Most common Cause -> HTN
Post hemorrhagic hydrocephalus
Uncal Herniation:
Ipsilateral blown pupil, CL hemiparesis, depressed LOC
Caudate hemorrhage most likely to rupture into ventricles
TX:
Intubation for airway protection
Keep HTN <160 SBP
Consider SIADH, Cerebral salt wasting
Seizure prophylaxis
Fix underlying coagulopathy
ICP Management
Consider EVD if hydrocephalus present
Consider hyperventilating to keep PaCO2 ~ 30 mmHg
Subarachnoid Hemorrhage
Aneurysmal rupture → ~80-85% SAH
Increased with patients with PCKD
RF:
Advanced age, smoking, HTN, cocaine use, ETOH abuse, connective tissue ds, SSC, 1st degree
relatives w/ aneurysms, arterial dissection, cerebral AVM, septic aneurysm, pituitary apoplexy,

Sensitivity of CT head < 6 hours ~ 98.5%

Tx:
Vasospasm: Nimodipine 60 mg PO Q 4 hours x 21 days
Endovascular coiling

Temporal Arteritis
Elevated ESR/ CRP (higher sensitivity and specificity)
Confirm with Bx
Tx with Steroids

Guillain-Barre Syndrome (GBS)

Progressive ascending weakness & cranial neuropathies
Weakness ~follows sensory disturbances
Minimal sensory deficits
Areflexia
~follows infectious process/immunization
1-4 weeks prior to onset of weakness
URI, diarrheal illness
C. jejuni, CMV, EBV, M. pneumoniae, dT, OPV, VZV

Workup:
CSF: Albuminocytological Dissociation
Elevated protein without pleocytosis
Protein >45; Low WBC <10
*HIV pts can have pleocytosis
Nerve conduction: EMG
Negative Inspiratory Force (intubate if < 30 mmHg)
Forced Vital Capacity: (intubate if < 15 mL/kg)
Treatment:
IVIG
5 day infusion of 0.4 g/kg per day
Preferred over plasma exchange
Plasmapheresis
5 exchanges (40-50 mL/kg)
No role for Steroids

Transverse Myelitis:
Motor: Paraparesis or Quadriparesis
Sensory: ~Spinal cord level
Early loss of bladder/bowel control
No Cranial Nerve pathology

Dx:
MRI: Usually focal area of increased T2 signal w/ or w/o gad

LP: ~CSF pleocytosis &/or inceased IgG index

Myasthenia Gravis:
Autoimmune disorder defined by humoral mediated immune attack on Ach receptors on skeletal muscle

Clinical Features:
Bulbar weakness
Ophthalmoparesis and Ptosis
Respiratory muscle weakness
Distinguish from Lambert-Eaton myasthenic
Lambert-eaton (autoAB against presynaptic membrane)
Assoc. With cancer (~SCLC)
Weakness ~ improves with exercise
MG → weakness is fatigable with repetitive testing

Diagnosis:
Clinical
Preserved DTRs
Fatigable weakness
Ice test
Apply ice for 2-5 min
Tensilon test (Ach Esterase inhibitor) - Edrophonium
Can help distinguish MG crisis from cholinergic crisis
Should increase muscle strength in MG (2/2 increased Ach)
EMG
Treatment:
AchE inhibitor (Mestinon/Pyridostigmine)
Immunosuppression
High dose Methylprednisolone
IVIG
Plasmapheresis
Thymectomy
Consider elective intubation if respiratory depression, decreased ventilatory drive, abnormal NIF/FVC
VC < 15 mL/kg
NIF (normal is -80 to -100); >); if > +20 → intubate
Remove exacerbating medications
ABX: Aminoglycosides, Fluoroquinolones, Tetracyclines, Macrolides, Quinolones
Quinidine
Anticholingerics
Steroids
Muscle Relaxants
Magnesium

Seizure:
Single seizure >5 min or >2 within 5 min period without return of normalcy
Workup:
Check VS, glucose, Lytes (Na, Mg, Ca), urine/serum tox, TCA, Cocaine, Isoniazid, anti-seizure levels,
Imaging (CT head*)
Tx:
Benzo
Lorazepam
Diazepam
Phenytoin/Fosphenytoin
Phenobarbital: Be aware of respiratory depression
Keppra
Propofol
Consider intubation for airway protection

Complications of seizures:
Lactic acidosis
Hypoxia
Hyperthermia
Rhabdomyolysis
Cerebral edema
Hypotension
Shoulder dislocation
~Posterior Dislocation
Aspiration PNA

Multiple Sclerosis
Pathophysiology:
Ds process consists of loss of myelin, disappearance of oligodendrocytes, proliferation of astrocytes
Changes → plaque formation w/ plaques throughout CNS
S/S:
Optic Neuritis
Visual changes + pain with EOM
RAPD
Red cap test
Myelitis
Sensory or motor ss below affected spinal level
Other
Cognitive dysfunction, mental/physical fatigue

Diagnosis
MRI: Plaques
LP
Elevated IgG AB levels ~75-85% pts
Oligoclonal bands

Bacterial Meningitis
Newborns:
Group B Strep, [Link], Listeria Monocytogenes
Infants and Children:
Strep. Pneumoniae, N. Meningitidis, H. Influenzae type b
Adolescents and young adults:
Strep. Pneumoniae, N. Meningitidis
Older Adults:
Strep. Pneumoniae, N. Meningitidis, Listeria Monocytogenes
Workup:

CSF: Elevated opening pressure (~>25 mmHg)

10-10,000 WBC/mm3; >80% PMN
Elevated protein (>45 mg/dL)
Low glucose
Glucose-CSF:serum ratio <0.5
+Organism on gram stain
Abx:
Neonates:
Amp/Cefotaxime or Gent; consider Acyclovir; add vanco if [Link]/MRSA suspicion
>1 month old:
Ceftriaxone & Vanco
Adult <50:
Ceftriaxone & Vanco
Adult > 50 & Immunocompromised:
Ceftriaxone & Vanco & Amp (for Listeria)
Prophylaxis:
Rifampin, Cipro: household members, school/daycare contacts in previous 7 days
Ceftriaxone
Abx for Healthcare providers if +mouth-to-mouth resus, intubation, suctioning of secretions
No prophylaxis when exposed to pneumococcal meningitis
 Pediatric Supplemental Study Guide

1. ABDOMINAL DISORDERS
a. Pyloric Stenosis
i. General
1. Narrowing of the pyloric canal due to muscle hypertrophy
2. Usual onset of symptoms is during the third to fifth week of life
ii. Presentation
1. Initially presents with occasional vomiting after meals and then progresses
to vomiting after each meal; can result in classic “projectile” vomiting
2. Palpable “olive” in RUQ;
iii. Diagnosis
1. Metabolic alkalosis: hypochloremic, hypokalemic early in course; if the
patient is markedly dehydrated, then acidosis occurs
2. Ultrasound: Normal pyloric thickness <2 mm; with pyloric stenosis, the wall
thickness is ≥4 mm and the canal length is elongated to ≥14 mm.
3. Upper GI: shows the “string sign” – contrast going through the stenotic and
elongated channel
iv. Treatment
1. Surgical treatment – incision of the pylorus (pyloromyotomy)
b. Intussusception
i. General
1. Prolapse of one part of the intestine into the lumen of an immediately
adjacent distal part; most common location is the ileo-cecal junction
2. Age: most common between 3 months and 5 years of age
ii. Presentation
1. Classic triad: seen in 20% to 40% of patients
a. Intermittent colicky abdominal pain: 50% to 90% of cases
b. Vomiting: 60% to 90%
c. “Currant jelly” stools: 21% to 60%
2. Colicky pain
3. Mental status changes
iii. Diagnosis
1. Abdominal films
2. Ultrasound: classic finding is “target” or “donut” sign, which is a single
hypoechoic ring with a hyperechoic center
3. Enema
a. Barium or air
iv. Treatment
1. Call pediatric surgeon before performing definitive treatment
c. Malrotation with Midgut Volvulus
i. General
1. Abnormal fixation of the bowel mesentery (Ladd bands), which can lead to
twisting of loop of bowel around mesenteric attachments
2. Age: usually occurs in the first months of life, but can occur anytime;
3. 75% of malrotations develop volvulus, most within the first month of life
ii. Diagnosis
 1. Abdominal films: classic “double bubble sign” – overall there is a paucity of
gas, with two air bubbles – one is the duodenum and one in the stomach
2. Upper GI: this is still the gold standard; the small intestine is rotated to the
right side of the abdomen, with narrowing of contrast at the site of
obstruction; “cork-screw” or “apple core” sign is seen, which is the spiraling
of the small intestine around the superior mesenteric artery
3. Ultrasound: may show distended, fluid-filled duodenum and dilated loops of
small bowel to the right of the spinal column
iii. Treatment
1. Place NG tube.
2. Start antibiotics: ampicillin, gentamicin, and metronidazole or clindamycin
3. Contact pediatric surgeon immediately.
d. Appendicitis
i. General
1. Most common surgical cause of abdominal pain in children
2. Male to female ratio is 2:1
ii. Diagnosis
1. Laboratory data: >96% of patients have an elevated WBC count or a left-
shifted differential with >75% neutrophils; also elevated CRP
2. Abdominal films: fecalith is seen in only 10% of patients
3. Ultrasound: the inflamed appendix is not compressible and measures >6 mm
in diameter; fecalith may be present; peri-appendiceal fluid collection may be
evidence of early perforation
4. Helical CT
iii. Treatment: IV rehydration, initiate antibiotics if perforation is suspected;
appendectomy
1. Consider triple antibiotics (ampicillin, gentamicin, and metronidazole or
clindamycin) or cefoxitin, consider meropenem if perforation
e. Gastroenteritis/Enterocolitis
i. General
1. Etiology: viral 60%; bacterial 20%; parasitic 5%; remainder idiopathic
ii. Diagnosis
1. Complete blood count (CBC): Shigella gives a normal or low WBC count but a
marked left shift
2. Stool studies: fecal leukocytes, culture, Rotazyme, ova, and parasites
iii. Treatment
1. Oral rehydration therapy, with quick return to formula or breast milk; BRAT
(bananas, rice, applesauce, toast) diet is no longer recommended. Consider
NG tube placement for oral rehydration.
2. Selected antimicrobial therapy
3. AAP does not recommend antidiarrheals
f. Meckel’s Diverticulum
i. General
1. Most common congenital abnormality of the small intestine
2. Remnant of the omphalomesenteric duct that connected the embryo’s guy to
the yolk sac
3. Rule of 2’s: found in 2% of population, 45% of the symptomatic patients are
younger than 2 years of age, 2 cm wide, 2 cm long, and 2 feet from the
ileocecal valve.
ii. Presentation
 1. Isolated rectal bleeding is common in patients younger than 5 years of age;
classic presentation is painless GI bleeding
iii. Diagnosis
1. Meckel’s scan:
2. Arteriography can detect the site of active bleeding.
iv. Treatment
1. Diverticulotomy
g. Hirschsprung’s Disease/Aganglionic Megacolon
i. General
1. The absence of intramural ganglion cells in the rectum,
ii. Presentation
1. Suspect the diagnosis if there is no passage of meconium stool in the
newborn within the first 24 to 48 hours
2. Abdominal distension & Chronic constipation
3. Toxic megacolon
iii. Diagnosis
1. Abdominal films: may show signs of obstruction
2. Barium enema: cone-shaped transition zone with dilated segment of
proximal colon
3. Rectal manometry: shows paradoxic contraction of the internal anal
sphincter
4. Rectal biopsy: definitive diagnosis; reveals the lack of ganglion cells in the
rectal submucosa
iv. Treatment
1. Surgical repair: decompressing colostomy followed by closure at 1 year of
age versus a one-step repair

2. RENAL/GENITOURINARY DISORDERS
a. Hemolytic Uremic Syndrome (HUS)
i. General
1. Most common in infants and children younger than 5 years of age. Most
commonly associated with vertoxin-producing E. coli O157:H7 (up to 10%)
ii. Presentation
1. Severe abdominal cramping
2. Watery diarrhea followed by grossly bloody stool
3. Emesis and symptoms of upper respiratory infection (URI) may be also
present; this stage is followed by acute renal failure, petechiae, GI bleeding,
and CNS symptoms such as irritability, seizures, hemiparesis, or coma.
4. Hypertension is seen in 40% to 50% of patients.
iii. Diagnosis
1. CBC shows microangiopathic hemolytic anemia and thrombocytopenia
(platelet count < 50,000mm3).
iv. Treatment
1. Early peritoneal dialysis for severely affected patients, rehydration,
treatment of hyperkalemia, transfusion of packed red blood cells, platelet
transfusion for active bleeding or counts below 20,000/mm3
2. HTN can be treated with nifedipine, labetolol, captopril, or hydralazine

3. CARDIOVASCULAR DISORDERS
a. Congenital Heart Disease (CHD)
i. General
 1. 8 to 100 cases per 1000 live births
2. Patent ductus arterious (PDA) dependent lesions: usually have a sudden
onset and present in the first week of life with cyanosis and shock when the
ductus closes
ii. Causes of cyanotic congenital heart disease
1. Tetralogy of Fallot (6%-10%)
2. Transposition of the great arteries (3%-5%)
3. Tricuspid atresia (1%-2%)
4. Truncus arterious (1%)
5. Total anomalous pulmonary venous return (1%)
6. Pulmonary atresia (<1%)
7. Hypoplastic left heart (<1%)
iii. Presentation
1. Difficulty feeding, sweating with feeds, failure to thrive, tachypnea
2. Sudden onset of lethargy, pallor, or central cyanosis
a. Central cyanosis: tongue, conjunctivae, and body are cyanotic
b. Peripheral cyanosis: tongue and conjunctivae are pink
3. Hepatomegaly may be seen.
4. Weakened/absent femoral pulses – coarctation; check four extremity blood
pressures and simultaneous pre- and post-ductal saturations
5. Hyperoxia test: 100% for 10 minutes, then ABG, PaO2 <150 mm Hg or O2
saturations <75% suggest cyanotic CHD; expect at least a 10% increase in the
O2 saturation if a pulmonary process is present
iv. Treatment
1. ABC’s: it may not be necessary to intubate, because the patient should not be
brought up to 100% oxygen saturation; however, the use of PGE1 may be
required intubation because of the risk of apnea.
2. If you suspect a ductal-dependent lesion, start PGE1 infusion (prostaglandin
E1): 0.05 to 0.1 μg/kg/min IV; usually see improvement in 15 minutes; side
effects are apnea, tachycardia, fevers, and hypotension
3. If the patient has congestive heart failure, administer furosemide, 1 mg/kg

4. ENDOCRINE/METABOLIC DISORDERS
a. Congenital Adrenal Hyperplasia
i. General
1. Deficiency in one of five enzymes involved in the production of cortisol
2. Most common is 21-hydroxylase deficiency
ii. Presentation
1. Vomiting and dehydration
2. Females may have enlarged clitoris and fusion of labial folds
3. Some children have hyperpigmentation due to increased melanin production
that is concurrent with increased ACTH level
4. Hyponatremia, hyperkalemia, hypoglycemia
iii. Treatment
1. Replace cortisol with hydrocortisone, 25 mg IV, then 25-50 mg/m2/day
divided every 6 to 8 hours
2. Usually hyperkalemia responds to fluid replacement; however, severe
hyperkalemia should be treated
3. Monitor glucose; these patients may be hypoglycemic

5. NEUROLOGIC DISORDERS
 a. Febrile Seizures
i. General
1. Incidence, 2% to 5%
2. Risk increases to 10% to 30% with parent or sibling with history of febrile
seizures
3. Recurrence rate of 25% to 30%
ii. Simple Febrile Seizure
1. Brief duration of <15 minutes
2. Occurs only once in a 24-hour period
3. Generalized seizure without focal findings
4. No evidence of CNS infection
5. Age range: 6 months to 5 years
iii. Complex Febrile Seizure
1. Seizure duration > 15 minutes
2. Focal seizure
3. More than 1 seizure in a 24-hour period
iv. Risk Factors for Recurrence
1. Age <12 months with initial seizure
2. Lower temperature with initial seizure (<39oC)
3. Complex seizure
4. Parent or sibling with history of febrile seizure
v. Diagnosis
1. No need for routine CT or MRI in cases of simple febrile seizures
2. Fever evaluation based on patient age
b. Infant Botulism
i. Presentation
1. Ptosis
2. Constipation
3. Loss of development milestones
4. “Floppy child”
ii. Treatment
1. Supportive
2. Trial of antitoxin, but this is usually not effective because of minimal amounts
of circulating toxin
3. Antibiotics also are not effective, but if they are used, avoid aminoglycosides.

6. ORTHOPEDICS
a. Physeal Injuries
i. Salter-Harris classification
ii. Distal radius is the most common site of injury (30%-60%)
iii. Ligaments tend to be stronger than physis: physeal separation/fracture is most
common than sprain
b. Elbow Fractures
i. Supracondylar most common (60%)
ii. Posterior fat pad/large anterior fat pad alone is highly predictive of elbow fracture.
iii. Remember sequence of ossification centers:
1. CRITOE: Capitellium, Radial head, Internal epicondyle, Trochlea, Olecranon,
External epicondyle
c. Slipped Capital Femoral Epiphysis
i. General
1. Medial slip of the femoral epiphysis; associated with obesity and puberty
 2. Peak incidence is 12 to 16 years of age in boys and 10 to 14 year in girls
ii. Diagnosis
1. Obtain AP and frog leg views of the hip: medial slip of the femoral epiphysis
is seen on AP hip film; in the PA view, a line across the lateral (superior)
aspect of the femoral neck should transect the lateral portion of the femoral
epiphysis (Klein’s line)
iii. Treatment
1. Operative reduction and fixation to avoid avascular necrosis
d. Legg-Calve-Perthes Disease
i. General
1. Avascular necrosis of the femoral head
2. Age presentation of Legg-Calve-Perthes disease is younger than for SCFE
ii. Presentation
1. Limp and pain for weeks to months; pain is referred to the groin and knee
iii. Diagnosis
1. Radiograph of the hip shows widening of the cartilage space and smaller
femoral head; MRI and bone scan can also be helpful for diagnosis
iv. Treatment
1. Orthopedic consultation for traction and future therapy, including surgery
e. Osgood-Schlatter Disease
i. Seen in early adolescence, boys are more commonly affected
ii. Repetitive injury from inflammation of the tibial tubercle apophysis; partial or
complete avulsion of the tibial tubercle can occur
iii. Symptoms include localized swelling, pain, and tenderness over the tibial tubercle.
iv. Treatment: rest, NSAIDs, knee immobilization; avulsion may require surgery
f. Transient Synovitis of the Hip
i. Presentation
1. Preceding viral syndrome (URI)
2. Pain on palpation of the anterior hip
3. Decreased range of hip motion
ii. Diagnosis
1. Diagnosis of exclusion
2. WBC count and ESR/CRP are usually normal; if elevated, consider join
aspiration to rule out septic arthritis
3. Hip radiographs may show a mild hip effusion
iii. Treatment
1. NSAIDs and close follow-up

7. EARS, NOSE, AND THROAT

a. Epiglottitis
i. General
1. Etiology
a. H. influenza type B incidence is decreasing due to vaccine
b. Reported cases of S. pneumonia, S. aureus, and group A β-hemolytic
streptococci
ii. Presentation
1. Several hours of fever and sore throat with rapids progression
2. Dysphagia
3. Severe stridor is usually absent
4. Tripod/sniffing position
iii. Diagnosis
 1. Lateral neck radiograph
a. Classic “thumb” sign
2. Confirmed by direct visualization in the operating room
iv. Treatment
1. Keep patient in position of comfort
2. Third-generation cephalosporin are antibiotics of choice
3. Steroids are not indicated
b. Croup (Laryngotracheobronchitis)
i. General
1. Parainfluenza type 1 is the most common cause; also RSV, adenovirus,
influenza A
2. 6 months to 6 years; peak incidence at 2 years
ii. Presentation
1. Hoarse voice and barking cough
2. Stridor: in severe cases can be inspiratory and expiratory
iii. Diagnosis
1. Radiographic confirmation (rarely needed, consider to exclude other causes)
a. Lateral neck film findings
i. Subglottic narrowing
ii. Normal epiglottis
b. Frontal (AP) neck film findings
i. Classic “steeple sign” in the subglottic region
iv. Treatment
1. Cool mist humidification is without proven benefit but has little downside
2. Racemic epinephrine via nebulizer is indicated in moderate/severe croup
3. Dexamthasone should be administered to all patients with croup
c. Bacterial Tracheitis
i. General
1. Etiology: S. aureus is the most common; also S. pneumonia, group A β-
hemolytic streptococci, H. influenza, M. catarrhalis, mixed flora with
anaerobes
ii. Presentation
1. Stridor
2. Dysphagia
3. No improvement or deterioration with standard croup interventions
iii. Diagnosis
1. Clinical suspicion: child appears toxic
2. Radiographs: subglottic narrowing similar to croup
iv. Treatment
1. Emergent intubation is usually necessary
2. IV antibiotics: nafcillin + ceftriaxone
8. Gingivostomatitis
i. General
1. Etiology: herpes simplex virus (HSV), Coxsackie virus, Candida albicans
a. Vesicles and ulcerations are more common in viral causes
b. Involvement of the anterior portion of the mouth and lip is more
common with HSV
c. Only soft palate/tonsillar pillar involvement suggests Coxsackie virus
ii. Treatment
1. Supportive with appropriate pain control
2. Nystatin suspension or fluconazole if treatment Candida
9. RESPIRATORY DISORDERS
a. Pneumonia
i. Treatment
1. Age less than 3 months: admission with IV ampicillin and cefotaxime
2. 3 months to 4 years: amoxicillin, or cefuroxime, amoxicillin/clavulanate,
macrolide, trimethoprim-sulfamethoxazole, IV medication include
cefuroxime, cefotaxime, and ceftriaxone
3. Children ≥5 years of age: macrolide (azithromycin, erythromycin,
clarithromycin) to cover for Mycoplasma pneumonia; consider doxycycline if
>8 years of age
ii. Chlamydial pneumonia
1. Young infants, usually afebrile
2. Classic cough is staccato like and may be associated with post-tussive emesis
3. Up to half of patients have concurrent or had previous eye infection with
Chlamydia.
4. Treatment is with oral erythromycin or sulfonamide.
iii. Pertussis
1. General
a. Bordetella pertussis: gram-negative organism
b. Transmitted by respiratory droplets
c. Stages: catarrhal, paroxysmal, convalescent
2. Diagnosis
a. WBC count >15,000 with lymphocytosis
b. Fluorescent antibody staining
c. Nasopharyngeal culture
3. Treatment
a. Erythromycin
b. May use TMP/SMX, if erythromycin is not tolerated
c. Antibiotics therapy does not shorten the paroxysmal stage
d. Treat household contacts with a 14-day course of erythromycin.

10. RHEUMATOLOGIC DISORDERS

a. Kawasaki Disease
i. General
1. Also called mucocutaneous lymph node syndrome
2. A generalized vasculitis of unclear etiology, which involves the coronary
arteries and the small- to medium sized arteries
3. One of the most common childhood vasculitis
4. Most common causes of acquired heart disease in the United States
ii. Presentation
1. Fever for at least 5 days plus at least four of the following
a. Bilateral non-exudative conjunctivitis
b. Changes of the lips and oral mucosa (fissured lips, strawberry tongue)
c. Changes in the extremities (erythema of the palms and soles, edema,
periungal desquamation)
d. Polymorphous rash
e. Cervical adenopathy (1.5 cm in diameter or greater)
iii. Complications
1. Coronary artery aneurysms
 2. MI, CHF, peripheral artery occlusion, hydrops of gallbladder, arthritis, aseptic
meningitis
iv. Diagnosis
1. Criteria above; ESR/CRP and WBC count are usually elevated, sterile pyuria,
elevated liver enzymes, thrombocytosis after 1 week; check ECG and
echocardiogram
v. Treatment
1. ASA
2. Single infusion of IVIG
b. Henoch-Schönlein Purpura
i. General
1. IgA-mediated vasculitis involving the small vessel of the skin, GI and renal
tracts, and musculoskeletal system
2. Most common acute vasculitis in children
ii. Presentation: “ARENA”
1. A = Abdominal pain (bloody stools, intussusception)
2. R = Rash, purpuric, classically “palpable purpura”
3. E = Edema
4. N = Nephritis
5. A = Arthralgias
iii. Diagnostics
1. No pathognomonic tests
2. Positive anti-streptolysin-O (ASO) or group A β-hemolytic streptococcal
(GABHS) throat cultures is common
3. Elevated BUN/Cr or significant hematuria à glomerulonephritis
iv. Treatment
1. Arrthralgias can be treated with NSAIDs
2. Renal/GI or joint involvement sometimes treated with steroids and IVIG

11. SKIN AND SOFT TISSUE INFECTIONS

a. Impetigo
i. Superficial bacterial infection of the skin due to S. aureus and group A streptococci;
ii. The hallmark is honey-crusted lesions, the characteristics site being between the
upper lip and nose
iii. Glomerulonephritis is rare
iv. Topical antibiotics (mupironcin) or an oral course of either cephalexin, penicillin, or
erythromycin; combination therapy is not necessary
b. Erythema Infectiosum (Fifth Disease)
i. General
1. Caused by Parvovirus B19
2. Usually respiratory transmission; also maternal-fetal
ii. Presentation
1. Classic rash
a. Slapped cheeks on face
b. Lacy rash on arms, trunk
iii. Complications: aplastic crisis in hemolytic disease (sickle cell), fetal hydrops in
pregnancy
iv. Treatment: supportive, isolate pregnant women
c. Roseola (exanthema Subitum)
i. General
1. Caused by human herpes virus 6
 ii. Presentation
1. High fever for 3 to 5 days
2. Febrile seizures are possible
3. Maculopapular rash develops after defervescence
iii. Treatment
1. Antipyretics
d. Varicella
i. General
1. Macules, papules, and vesicles that develop and spread over 24 hours
2. Rash start on trunk, then to face and extremities
3. Highly contagious until crusted
ii. Complication
1. Cellulitis
2. Pneumonia
3. Encephalitis: seizures, coma (early)
a. Cerebellitis: benign ataxia (late)
b. Reye syndrome (especially in association with aspirin use)
iii. Treatment
1. Antipruritic
2. Antipyretics: use acetaminophen
3. Consider acyclovir
4. Varicella zoster immune globulin (VZIG) for children at high risk for
development of severe disease
e. Scarlet Fever
i. Commonly associated with group A β-hemolytic streptococci
ii. Presentation
1. Sand paper rash first noted in skin folds such as the axillae, groin, and
antecubital area (Pastia’s lines)
2. Circumoral pallor
iii. Treatment
1. Penicillin VK or erythromycin
f. Staphylococcal Scaled Skin Syndrome
i. Presentation
1. Generalized skin erythema followed by bullae formation and skin
desquamation
2. The skin by be rubbed off in layers with lateral pressure – Nikolsky’s sign
3. Mucous membranes are not involved
ii. Treatment
1. Admitted for IV cefazolin or nafcilllin
g. Candida
i. Oral candidiasis
1. Causes inflammation of the tongue, palate, and buccal mucosa
2. White plaques cannot be wiped off the mucous membrane
3. Treat with oral nystatin suspension
ii. Cutaneous candidiasis
1. Erupts in moist, warm areas of the body, axillae, neck folds, and diaper area
2. Satellite lesions are common along the edge of the eruption
3. Treatment is with topical antifungal agents (nystatin, clotrimazole)
h. Herpangina
i. Vesicular stomatitis in the posterior pharynx
ii. High fever and sore throat, with drooling
 iii. Symptomatic therapy
i. Hand-foot-mouth disease
i. Coxsackie virus
ii. Vesicular rash in mouth, hands, and feet (palms and soles are included)
iii. Treatment is symptomatic
j. Tinea Capitus
i. Trichophyton tonsurans transmitted from person to person via fomites
ii. Presentation
1. Alopecia
2. “Black dot” appearance on scalp
3. Kerion (swollen boggy abscess of scalp)
iii. Diagnosis
1. Clinical or, if unclear, may send culture of scraping from hair roots
iv. Treatment: must be oral
1. Griseofulvin
2. Selenium sulfide shampoo
3. Prednisone may be added in the treatment of a severe kerion

12. PYSCHIATRIC DISORDERS

a. Abuse
i. General
1. Child abuse is broadly defined as maltreatment of a child by parents,
guardians, or other caregivers.
2. May take the form of physical, sexual, or emotional abuse
ii. Physical abuse
1. Red flags
a. Child claims to have been injured
b. No history at all is offered
c. History of inflicted injury
d. History of changes over time or different caretakers give different
histories
e. Serious injury is blamed on another child
f. Child is developmentally incapable of acting as described
g. History provided is inconsistent with injuries suffered
h. Delay in seeking medical care
2. Clinical indicators
a. A lack of physical findings does not exclude abuse.
b. Lethargy, poor feeding, colic, bulging fontanelle, apnea, seizures
c. Retinal hemorrhages beyond the neonatal period
d. Injury does not match history
e. Multiple injuries of various types and ages
f. Pathognomonic injuries: loop marks, cigarette burns, immersion
burns, fractures of posterior ribs, metaphyseal or “bucket handle”
fractures, spiral femur fractures in non-weight bearing infants, retinal
hemorrhages
3. Characteristics fractures of abuse
a. High specificity
i. Fractures or metaphyseal corner (“bucket handle”), posterior
rib, sternum, long-bone shaft in non-weight-bearing age
b. Medium specificity
 i. Complex skull fractures, vertebral body fractures, multiple
fractures of different ages
c. Low specificity
i. Long-bone shaft fracture in weight-bearing age, linear skull
fracture
4. Shaken baby syndrome
a. Subdural hematoma
b. Retinal hemorrhage
c. Long-bone fracture
d. Minimal signs of external physical abuse
5. Management of suspected physical abuse
a. Laboratory studies
i. Platelet count, PT, PTT, if contusions or hematomas are present
ii. Other labs as indicated
b. Radiographic studies
i. Complete skeletal survey indicated for children <2 years of age
with evidence of abuse
ii. Other x-ray films as clinically indicated
c. Call the Child Protection Team

13. SUDDEN INFANT DEATH SYNDROME/BRIEF RESOLVED UNEXPLAINED EVENT (BRUE)

a. Definitions
i. SIDS: sudden death of an infant younger than 1 year of age, which remains
unexplained after a thorough case investigation
ii. Apnea: absence of respiration for 20 seconds or any length of time if associated with
a decrease in heart rate, hypotonia, or change in color (pallor or cyanosis)
iii. Brief resolved unexplained event (BRUE) characterized by one or more of the
following: (1) central cyanosis or pallor, (2) absent, decreased, or irregular
breathing, (3) marked change in tone, (4) altered level of responsiveness
1. <1 year of age; brief < 1 minutes
2. Unknown association with SIDS
3. Differential: seizure, gastroesophageal reflux, bronchiolitis, pertussis,
choking, URI, head injury, breath holding
b. Evaluation
i. CBC
ii. Electrolytes
iii. Blood, urine, stool, and CSF cultures and respiratory syncytial virus testing in infants
born prematurely and patients with congenital heart disease
iv. Consider a lumbar puncture if <2 months of age
v. Pertussis and Chlamydia culture should be obtained if clinically suspected
vi. Chest radiograph and, if upper airway obstruction is suspected, anteroposterior and
lateral soft-tissue radiographs of the neck
vii. ECG
viii. Toxicology screen
ix. Head CT should be obtained in patients with an altered level of consciousness,
abnormal muscle tone, focal neurologic findings, or retinal hemorrhages.
c. Disposition
i. Children who meet the criteria for a low risk BRUE may potentially be discharged
with close follow-up
Cardiovascular 2 Study Guide

Pericarditis
• Most commonly idiopathic
o Can be infectious (Viral, bacterial), malignancies, autoimmune, medications,
radiation, acute or recent MI (Dressler syndrome)
• Chest pain is typically increased in the supine position and relieved by sitting up and
leaning forward, but opposite is occasionally present.
• Pericardial friction rub is pathognomonic, although uncommon
• ECG is normal sinus rhythm or sinus tachycardia (ventricular dysrhythmia is uncommon).
o Stage I ECG changes: Diffuse, nonanatomic ST segment elevation with upward
concavity.
o PR segment depression in multiple leads is common in viral pericarditis.
• Echocardiography is most sensitive and most specific for detecting associated pericardial
effusion.
• Laboratory abnormalities
o WBC, ESR, CRP often increased.
o Cardiac enzymes often minimally elevated.
• Indications for admission are intractable pain or underlying precipitant requiring
admission (MI, uremia, bacterial infection).
• Treatment includes anti-inflammatory agents (aspirin, ibuprofen, indomethacin,
colchicine). Steroids should be avoided since found to be an independent risk factor for
recurrence.

Myocarditis
• Viral infection most common cause.
• Presenting symptoms determined by degree of cardiac involvement: nonspecific
symptoms of fatigue and dyspnea, CHF, dysrhythmias, sudden cardiac death.
o History of a preceding or concurrent viral illness is common.
o Often presents in association with acute pericarditis.
• Cardiac biomarkers characteristically have a slow rise and fall over a period of days.
• Additional diagnostic tests can include cardiac MRI and endomyocardial biopsy.
• Immunosuppressive agents and NSAIDS are contraindicated in early myocarditis.
• Manage CHF with standard treatment
o Digoxin should be avoided
• Manage dysrhythmias with standard antidysrhythmic agents and electrical therapies.

Endocarditis
• Patients with congenital / acquired valvular disease or prosthetic valves are most
commonly affected.
• Most commonly caused by bacteria, however can also be caused by fungi, rickettsiae,
and viruses.
• Left-sided endocarditis leads to systemic vascular involvement
• Right-sided endocarditis leads to pulmonary vascular involvement

Adapted form Carol River’s Textbook, Eleventh Edition

Cardiovascular 2 Study Guide

• Presenting symptoms are nonspecific including fever, chills, sweating, malaise, fatigue,
weight loss, chest pain, cough, neurologic symptoms/focal deficits.
• Physical exam findings:
o Most common is fever
o Heart murmur
o CHF
o Signs of metastatic infection (e.g. meningitis, pneumonia)
o Ophthalmologic signs
▪ Conjunctival hemorrhages
▪ Roth spots
o Cutaneous signs
▪ Splinter hemorrhages
▪ Osler nodes
▪ Janeway lesions
▪ Petechiae
o Neurologic findings
▪ Focal motor deficits
▪ Altered level of consciousness
• Diagnostic Evaluation
o WBC, ESR, CRP elevated
o Chest radiograph may reveal septic emboli in patients with right sided
endocarditis.
o Blood cultures are the most useful test for making the diatnosis
o Echocardiography is useful if positive for vegetations, but a negative examination
does not exclude the diagnosis.
• Empiric antibiotic regimens
o In patients with native valves with acute endocarditis:
▪ Vancomycin IV plus cefazolin or ceftriaxone
o In patients with native valves with subacute endocarditis:
▪ Vancomycin IV plus ampicillin-sulbactam
o In patients with prosthetic valves:
▪ Vancomycin plus cefepime plus gentamicin

Aortic Stenosis
• Etiology
o Congenital bicuspid most common cause in ages less than 65 years.
o Calcific aortic stenosis most common cause in ages greater than 65 years.
o Rheumatic heart disease also a common cause.
• Clinical presentation
o Symptoms appear late in the disease process:
▪ Exertional syncope
▪ Angina
▪ Dyspnea on exertion

Adapted form Carol River’s Textbook, Eleventh Edition

Cardiovascular 2 Study Guide

▪ Heart failure
o Physical exam findings
▪ Systolic crescendo-decrescendo murmur, diminished carotid pulse,
narrow pulse pressure, left chest heave, ejection click, S4 gallop.
o Diagnostic evaluation
▪ ECG: LVH, LBBB
▪ Chest radiograph: LV enlargement, dilation of ascending aorta, CHF, aortic
valve calcification.
o Management
▪ Administer CHF medication that decrease preload or afterload with
caution.
▪ Phenylephrine is first line vasopressor.
▪ Valve replacement, valvuloplasty

Mitral Valve Prolapse

• Epidemiology and etiology
o Most common valvular heart disease; female-to-male ration of 2:1
o Autosomal dominant congenital disorder or part of a connective tissue disorder
(Ehlers-Danlos syndrome, Marfan syndrome)
• Clinical presentation
o Typical patients: young woman with palpitations; young female athlete with
syncope during exertion reporting chest pain and palpitations; older man with
syncopal episode at home
• Physical exam findings
o Characteristic murmur late systolic best heard at the apex. A systolic click may
also be heard.
• Diagnostic evaluation
o ECG: most often normal. Findings may include flattened or inverted T waves in
inferior leads and prolongation of the QT interval.
o Echocardiograpy is confirmatory
▪ Mitral valve displacement >2mm above the mitral annulus in long-axis
view.

Acute mitral valve regurgitation

• Etiology
o Rupture of chordae tendieae, papillary muscle, valve leaflet
o Acute MI, infectious endocarditis, trauma
• Clinical presentation
o Symptoms are those of fulminant CHF/pulmonary edema
o Physical exam findings
▪ Loud apical systolic mumur radiation to axilla
▪ Findings consistent with acute pulmonary edema
• Diagnostic evaluation

Adapted form Carol River’s Textbook, Eleventh Edition

Cardiovascular 2 Study Guide

o ECG: no left atrial enlargement, no LVH, sinus tachycardia

o Chest radiograph
▪ Severe pulmonary edema
• Management
o Treatment of pulmonary edema
o May need intra-aortic balloon pump to augment cardiac output
o Consultation of cardiothoracic surgeon

Thoracic Aortic Dissection

• Epidemiology
o Men are affected more commonly than women (ratio 3:1)
o Risk factors
▪ Hypertension history
▪ Connective tissue disorders
▪ Pregnancy in third trimester
▪ Congenital heart disease
▪ Turner syndrome
▪ Cocaine and methamphetamine use
• Pathophysiology
o Start with an intimal tear that allows blood to leak into the media
o Propagation depends on dP/dt (rate of change in pressure/time)
o Mortality rate is 90% if untreated
• Classification system
o DeBakey classification
o Stanford classification
• Clinical presentation
o Pain is the most common presenting symptom
▪ Anterior chest pain +- radiation into neck, jaw, arms typical of ascending
dissections
▪ Pain in neck and jaw typical of arch dissections
▪ Interscapular back pain (+-radiation into the abdomen of lumbar area) is
typical of descending (distal) dissections.
o Based on the location of dissection patients may also present with:
▪ Acute stroke, visual changes
▪ Acute paraplegia, spinal cord deficits
▪ A cool, pulseless extremity
▪ Pulmonary edema
▪ Abdominal pain (mesenteric ischemia)
▪ Flank pain (impaired renal blood flow)
▪ Syncope
▪ Acute MI
▪ Aortic regurgitation
o A significant number of patients present with only ischemic or neurologic
complications of a painless aortic dissection.

Adapted form Carol River’s Textbook, Eleventh Edition

Cardiovascular 2 Study Guide

o Difference in extremity blood pressure of 20mmHg is classic.

o Diastolic murmur of aortic insufficiency
o Signs of cardiac tamponade
• Diagnostic evaluation
o Chest radiograph: a normal chest radiograph does not exclude the diagnosis.
▪ Mediastinal widening>8cm
▪ Loss of space between the aorta and pulmonary artery
▪ “eggshell” or “calcium” sign
▪ A blurred aortic knob of on with a localized hump
▪ A “double density” appearance of the aorta
▪ On the right side of the radiograph
• Deviation of the trachea / nasogastric tub
• Shift and elevation of right mainstem bronchus
• Deviation of right paraspinous line
▪ On the left side of the radiograph
• Pleuro-apical cap
• Depressed left mainstem bronchus
• Pleural effusion
o ECG
▪ Abnormal in most patients with aortic dissection
▪ Can show changes consistent with acute ischemia or Varying degress of
AV block
o Transesophageal echocardiography
▪ Contraindicated in patients with esophageal disease.
o CT aortography
▪ Diagnostic gold standard
▪ May miss a dissection flap if moving rapidly.
o MRI
▪ Sensitivity and specificity 100%
▪ Time consuming and some units cannot accommodate monitoring and
life support equipment .
• Management
o Blood products on standby
o Consultation with thoracic surgeon
o Control of blood pressure, heart rate, dP/dT
▪ IV Beta Blocker administered first and titrated to a heart rate of 60-80
beats per minute.
▪ Nitroprusside titrated to systolic blood pressure of 100-110 mmHg.
o Long term management
▪ Dissections involving the ascending aorta are treated surgically.
▪ Dissections involving only the descending aorta are treated medically.

Adapted form Carol River’s Textbook, Eleventh Edition

Cardiovascular 2 Study Guide

Abdominal Aortic Aneurysm (AAA)

• Vast majority are infrarenal in location
• Risk factors
o Advanced age
o Male sex
o Family history if first-degree relative
o Smoking history
o Hypertensive history
o History of CAD or peripheral vascular disease
o Hyperlipidemia
• Clinical Presentation
o Sudden onset of severe abdominal, back, or flank pain
o Frequently associated with a syncopal episode from sudden hemorrhage
• Physical exam findings are variable.
o Pulsatile mass is present in epigastric area in 77% of patients with a ruptured
AAA.
o Most intact aneurysms are not tender.
o Bruits may be heard.
o Signs of distal extremity ischemia
• Diagnosis and management
o Two large-bore IV lines
o Blood products on standby
o Immediate surgical consultation
o Hemodynamically unstable patients:
▪ Prompt surgical repair
▪ “Permissive hypotension” with the goal to prevent further tearing before
surgical repair.
o Hemodynamically stable patients
▪ Ultrasonography
▪ CT with contrast
▪ MRI

Hypertensive emergency
• Definition
o Patients with elevated diastolic blood pressure (>140 mmHg) and evidence of
acute end-organ dysfunction or damage
o The heart, brain, and kidneys most often affected.
• Clinical presentation
o Hypertensive encephalopathy
o Acute intracranial events (hemorrhagic stroke, thrombotic stroke, subarachnoid
hemorrhage)
o Aortic dissection
o Acute pulmonary edema

Adapted form Carol River’s Textbook, Eleventh Edition

Cardiovascular 2 Study Guide

o Acute myocardial ischemia or injury

o Eclampsia
o Acute hypertensive renal insufficiency
o Catecholamine-induced hypertensive crises
▪ Pheochromocytoma
▪ Concomitant use of MAOI’s and sympathomimetic agents.
▪ Acute cocaine intoxication
▪ Acute clonidine withdrawal
• Management
o The exact extent of blood pressure reduction is determined by the clinical
situation.
o A reasonable target is to reduce the blood pressure by 20%-30% of pretreatment
levels over the first hour of therapy.

Hypertensive urgency
• A diastolic blood pressure of 115mmHg without evidence of end-organ dysfunction or
damage
• Patients are asymptomatic and usually present to the ED for an unrelated problem.
• Management
o Goal of therapy is to lower the blood pressure gradually over a period of 24-48
hours with oral medications.

DVT
• Clinical Presentation
o Acute DVT:
1. The physical manifestations of DVT are determined by the degree of
thrombosis present (partial versus totally occluding), its location, and
the extent of collaterals at the level of the occlusion. Physical findings
may be minimal or absent and cannot be relied on by themselves to
make or exclude the diagnosis.
2. Commons signs and symptoms
a. Unilateral pain, swelling, edema (most reliable sign), and
tenderness.
b. Presence of a palpable cord (most often detected in the
popliteal fossa), superficial venous dilatation,
discoloration, and Homans sign (the least reliable finding)
c. Unilateral swelling is the most specific physical finding
(especially if the measured difference is > 3 cm).
o Massive DVT: an ischemic form of venous occlusion due to massive iliofemoral
thrombosis that also involves most of the venous collateral system.
o These patients require catheter-directed thrombolysis or surgical
thrombectomy to prevent gangrene.
o Phlegmasia cerulea dolens (painful blue inflammation)
▪ Occurs in <1% of patients with symptomatic venous thrombosis

Adapted form Carol River’s Textbook, Eleventh Edition

Cardiovascular 2 Study Guide

▪ The leg is tensely swollen, painful, cyanotic; petechiae and skin

bullae may also be present.
▪ Occasionally results in venous gangrene (irreversible ischemia)
o Phlegmasia alba dolens (painful milk / white leg)
▪ Due to massive iliofemoral thrombosis associated with arterial
spasm.
▪ The entire leg is swollen but not tense, and the pulse may be
diminished.
▪ The skin is doughy and white; petechiae are often present.
▪ This is a temporary condition; as the arterial spasm resolves, the
leg takes on the cyanotic appearance of phlegmasia cerulea
dolens.
• Prevalence of DVT is directly correlated with the number of risk factors present; the
greater the number of risk factors, the greater the risk of DVT.
• Patients can be stratified into high- and low-risk groups based on the number of risk
factors they possess.
• Predicting Pretest Probability for DVT: The Well’s Clinical Criteria
• Diagnostic Evaluation
o Duplex venous ultrasonography (B-mode, ie, two-dimensional
o Contrast venography
o MRI
o D-dimer assay
• Pharmacologic Therapy
o Anticoagulation: DOAC, VKA, Unfractionated heparin, LMWH
o Thrombolytic Therapy
o Inferior vena caval interruption with a Greenfield filter
• Admission Criteria
o Extensive iliofemoral DVT with circulatory compromise
o Increased risk of bleeding requiring close monitoring of therapy
o Limited cardiorespiratory reserve
o Risk of poor compliance with home therapy
o Contraindications to LMWH necessitating IV heparin therapy

Pulmonary embolism
• Risk factors (most common)
o Current DVT
o Obesity
o Prior DVT of PE
o Immobility (including travel) or prolonged bed rest
o Recent trauma or surgery
o Carcinoma
• Dyspnea, pleuritis chest pain, or tachypnea is present in 95% of patients.
• Chest radiograph useful in excluding other disease processes.

Adapted form Carol River’s Textbook, Eleventh Edition

Cardiovascular 2 Study Guide

o Hampton hump
o Westermark’s sign
• ECG
o Sinus tachycardia most common finding
o Transient nonspecific ST-T wave changes
o Evidence of right heart strain
• D-dimer should be used only as a screening tool in low pretest probability patients.
• VQ scan scans are interpreted as normal; indeterminate; or low, intermediate, or high
probability of pulmonary embolism based on the number and size of V/Q mismatched
present.
• A negative CT angiography in a patient with high pretest probability for pulmonary
embolism requires pulmonary angiography.
• Pulmonary angiography is the gold standard for diagnosing pulmonary embolism.
Although test is invasive with complications associated with mortality (0.1%-0.5%) and
morbidity (1%-5%).
• Management
o Three anticoagulation treatment approaches
▪ Direct oral anticoagulation
▪ IV unfractionated heparin
▪ SC low-molecular-weight heparin (LMWH)
o Thrombolytic (fibrinolytic) therapy indications
▪ Hemodynamic instability in patients with confirmed pulmonary embolism
▪ Hemodynamic instability in patients with a high clinical index of suspicion
▪ Right ventricular dysfunction on echo in hemodynamically stable patients
with confirmed pulmonary embolism.
o Pulmonary embolectomy reserved for patients in whom thrombolytic therapy is
unsuccessful or contraindicated.
▪ Operative mortality is 25%

Peripheral Vascular Disease / Acute Limb Ischemia

• Pathophysiology
o Peripheral arteriovascular disease
▪ Atherosclerosis and thrombosis are responsible for most cases of the
disease.
• History
o Pain
o Change in sensation
• Physical examination
o Palpation of pulse volume in pairs
o Capillary refill
o Ankle-brachial index (ABI)
▪ Comparing the systolic blood pressure at the level of the ankle with the
brachial systolic pressure

Adapted form Carol River’s Textbook, Eleventh Edition

Cardiovascular 2 Study Guide

• Diagnostic testing
o Doppler ultrasonography
o Contrast angiography
o Computed tomography angiography (CTA)
o MRI with angiography
• Management
o Noninvasive therapy
▪ Acute anticoagulation with heparin
▪ Fibrinolytic therapy
• Direct administration into the clot
o Invasive therapy
▪ Fogarty catheter thrombectomy
▪ Peripheral percutaneous transluminal angioplasty
▪ Grafting

Adapted form Carol River’s Textbook, Eleventh Edition

 Pulmonary Study Guide

I. Pneumonia
a. “Typical” Pneumonia Patterns by Organism
i. Streptococcus pneumoniae (Gram + diplococci)
- Lobar consolidation
- Rusty colored sputum, rigors
- MOST COMMON OVERALL, and most common cause of pneumonia
associated effusions
ii. Hemophilus influenzae (Gram – rods)
- Lobar or patchy infiltrate
- COPD patients and smokers are typical patients
iii. Staph aureus (Gram + cocci in clusters)
- Pleural Effusion, abscesses, empyema
- Post viral complication, IVDU
iv. Klebsiella pneumoniae
- Lobar (RUL preference), Bulging minor fissure
- Currant jelly sputum- although rarely seen
- Alcoholics, COPD, Diabetics
v. Pseudomonas aerogenesis (Gram – rods)
- Patchy and multilobe pneumonia, can form abscesses
- Cystic fibrosis patients, Immunocompromised, hospital acquired
vi. Anaerobes
- Patchy infiltrates, lower lobes (R>L)
- MOST COMMON cause of lung abscesses
- Alcoholics and those with poor dentition, complication of aspiration
events
b. Atypical pneumonia
i. Mycoplasma pneumoniae
- Patchy infiltrates, XRAY looks worse than patient→ “walking
pneumonia”
- Most common in teenagers/young adults
- Look for extrapulmonary findings/associations: GBS, encephalitis,
hemolysis, erythema multiforme
ii. Chlamydia pneumoniae
- Patchy infiltrates
- Noted in non-toxic appearing infants (3-20 weeks of age)
- Staccato cough
iii. Legionella pneumophilia
- Unilateral lobar infiltrates
- Seen in older, comorbidity laden men; Range of mild to very severe
illness
- RELATIVE BRADYCARDIA., GI SYMPTOMS, LOW SODIUM, LFTS abnormal
 - Comes from contaminated water sources, air conditioning units, seen in
outbreaks
c. Atypical Pneumonias
i. Fungi: Geography dependent
- Chest Xray→ Bilateral hilar adenopathy associated with diffuse patchy
infiltrates
- Southwest US (Coccidiomycosis), Miss River Valley (Histoplasmosis),
Southeast US (Blastomycosis)
ii. Q Fever (Coxiella burnetti): Seen in vets, farmers, those exposed to
sheep, goats, cattle
- Chest Xray is variable
- Associated with endocarditis
iii. Psittacosis (Chlamydia psittaci); Seen in bird handlers
- Highly variable Chest Xray
- Associated with low WBC count, relative bradycardia
d. Aspiration pneumonia
i. Risk factors: Seizures, alcoholics, obtunded patients, those with
swallowing/gag impairment
ii. Severity of symptoms: Large volume aspiration, low pH, bacteria/foot in
aspiration (anaerobes)
iii. Clinical features: Immediate symptoms can occur with normal initial
Chest Xray; Hypoxia, wheezing and rales
iv. Chest Xray: often findings on lower lobes, R/L, May take 6-24 hours to be
seen
v. Treatment: Supportive care, Antibiotics ONLY if developing fever, do not
routinely give prophetically
e. Pneumonia Mimics
i. Multiple cannonball infiltrates: metastatic disease, septic emboli from
right sided heart lesions
ii. Hampton’s Hump: Wedge shaped deformity, uncommonly seen opacity
near the pleural edge from Pulmonary Embolism related ischemia
f. Typical treatment recommendations (forever evolving and somewhat complex)
i. Community acquired pneumonia adults
- Inpatient ceftriaxone/Unasyn + Zithromax or Doxycycline
- Pseudomonas coverage if h/o Pseudomonas and MRSA coverage if h/o
MRSA for all admitted non-severe pneumonia patients if had within
past 1 years
- If hospitalized and received IV antibiotics within last 90 days AND
severe pneumonia (shock w/ vasopressor OR intubated) provide
pseudomonas coverage and MRSA coverage
- Outpatient: No Comorbidities: Amoxicillin or Doxycycline (Zithromax
only if local resistance patterns are low)
- Outpatient Comorbidities (DM, Chronic renal, COPD, Asthma): 3 rd gen
cephalosporin + Doxy or Augmentin
 g. Pulmonary Manifestations in HIV/AIDS
i. CD4>200:
- Increased risk of CAP (Pneumococcus most common); May have
somewhat atypical chest XRAY appearance
- Increased risk of TB: Atypical TB findings may be present
ii. CD4 <200 (As above CAP/TB + PCP pneumonia)
- PCP (caused by Pneumocystis jirovecii now classified as a fungus)
- Bilateral Batwing infiltrates classic appearance (can be more lobar or
normal as well)
- Often subacute and gradual presentations
- Hypoxemia + LDH elevation is classically found
- Treatment: Bactrim (1st line) + steroids if pO2<70 mmHg (Pentamidine
or Dapsone are 2nd line treatments)
iii. CD4<50
- CMV: often disseminated
- Fungi: Cryptococcosis, histoplasmosis, aspergillosis, candidiasis
- Mycobacterium avium complex
- Non-Hodgkin’s lymphoma can be present, Kaposi’s sarcoma (may mimic
pneumonia)
II. Hemoptysis
a. Etiology:
i. Most common cause is acute bronchitis (pneumonia) although this is
often small volume in amount
ii. Other causes: Bronchiectasis, neoplastic, TB (these can be massive
bleeds), Cardiovascular (CHF), PE, vasculitis, necrotizing pneumonia
b. Classification:
i. Massive is >600 mL in 24 hours or 50 mL with single episode
ii. Death by asphyxiation is most common cause (not hemorrhage)
iii. Bronchial artery damage leads to most large bleeds (5% of pulmonary
blood supply but under arterial pressure as opposed to low pressure
pulmonary artery)
c. Treatment for massive bleed:
i. Oxygen and intubation if needed, Nebulized TXA may help
ii. Keep bleeding side down, Selective mainstem intubation to non-bleeding
lung
iii. Correct coagulopathies along with Interventional Radiology consultation
(bronchial artery embolization), Pulmonary and Vascular surgery
consultants all should be involved
III. Asthma
a. Asthma affects specific populations disproportionately
i. Increased rates with poverty and lack of access, overuse of albuterol w/o
preventative therapies (steroids), African Americans and Latinos
ii. Severe disease/Death Risk Factors:
 -h/o severe disease intubation, ICU admits, Frequent ED visits, Recent
steroid use, comorbid disease, illicit drug use
b. Pathophysiology: it is a chronic disease leading to reduced airway diameter
i. Bronchial constriction, edema, mucous plugging (reversible)
ii. Bronchial muscle hypertrophy, airway remodeling (less reversible)
iii. Precipitants triggering this cascade of events: URI (most common),
smoke, chemicals, cold, exercise, GERD, Beta blockers, NSAIDS
c. Clinical Features: Decreased expiratory flow (pCO2 may rise with normal
oxygenation), Air trapping and barotrauma, rising intrathoracic pressures
(hypotension)
- Wheezing may be absent in SEVEVE disease
- Accessory muscle usage may be better indicator of moderate/severe
disease
d. Testing for Asthma:
i. ABG/VBGs of limited value although pCO2 may become elevated late,
normal despite profound tachypnea
ii. Chest XRAY: 1o for barotrauma: pneumothorax/pneumomediastinum; do
not need to be routinely obtained
e. Treatments:
i. Selective Beta2-agonists (albuterol) relaxes smooth muscles via
increasing cAMP
- MDIs as good as nebulizers if tolerated
- IM Epi/Terbutaline ONLY in severe disease in which aerosolized beta-
agonist cannot be inhaled due to air trapping
ii. Anticholinergics (ipratropium/Atrovent)
-Decreases secretions, dilates bronchial smooth muscles (decreases
cGMP)
- Administered with albuterol in initial stages with benefit
iii. Steroids: either oral or IV/IM (not inhaled for acute exacerbations)
- Decreases inflammation (takes hours)
- May upregulate beta-receptors (more immediate benefit)
iv. Magnesium: Smooth muscle relaxant benefits bronchiole dilation;
evidence with severe disease toward improved outcomes
f. Mechanical Ventilation in Asthmatics/Cardiac arrest
i. Barotrauma and air trapping are inevitable upon intubating asthmatics as
lack of patients forced ventilation; avoid if possible
ii. Allow permissive hypercapnia (60-80 mmHg pCO2), Decrease resp rate,
increase inspiratory flow rate, decrease I:E ration
iii. If arrest occurs: Disconnect ventilator, compress chest, bilateral chest
tubes, fluid bolus
IV. COPD
a. Pathophysiology: Non fully reversible and progressive
- Chronic inflammation and alveolar destruction
 - Leads to pulmonary vascular bed destruction, thickened vessel walls→
pulmonary HTN→ Right sided heart failure
- Hypoxemia and hypercapnia are the norm, Polycythemia common to
compensate for hypoxia
- Classically COPD patients are divided into Chronic Bronchitis (Blue
bloater- high BMI, chronic sputum cough, crackles/wheeze, less
dyspnea) and Emphysema (Pink puffer- low BMI, hyperinflation,
wheeze, alveoli destruction, dyspnea and pursed lips)
b. Acute exacerbations are defined by increased dyspnea, sputum volume and
degree of purulence increased
- Etiology: Viruses, Bacteria, Environmental exposures
- Pneumothorax is not uncommon; confirm that this is not a bleb prior to
chest tube insertion
c. Treatment:
i. Beta agonist and Anticholinergics (Albuterol and ipratropium) initially
ii. Parenterally or oral steroids: Decrease inflammation
iii. Antibiotics: Only indicated in cases with increased sputum volume and
purulence (no lobar consolidation is needed)
iv. Non-Invasive Ventilation with BIPAP is highly effective in prevention of
need for intubation
- Introducing early in exacerbations most effective
- Hypotension and patients with impending respiratory arrest are not
appropriate for positive pressure ventilation
v. Long term treatment cannot reverse disease however can reduce
mortality and slow progression: Smoking cessation and home oxygen if Ox
sats are less than 88%
V. Pneumothorax
a. Who is at greatest risk?
i. Primary: Idiopathic primarily in tall thin men; Spontaneous or provoked
with Valsalva maneuver or high negative pressures/glottic closure
generated during smoking (Muller maneuver)
ii. Secondary: COPD and asthma patients, neoplasm, Marfan’s, Ehlers-
Danlos, Cystic fibrosis, Pneumonia Catamenial (menstruation associated
b. Chest Xray
i. Upright PA film with expiratory views best identifies pneumothorax
ii. Deep sulcus sign may be only finding on supine Xray
iii. CT scan with greater sensitivity, can help differentiate Blebs from true
pneumothorax in patients with COPD
c. Ultrasound is very effective at pneumothorax identification, much better than
supine Xray in trauma patients that can’t be upright
- Loss of lung sliding, Absence of z-lines/comet tail artifacts are evident
- 100% specificity if the point sign (junction b/w sliding lung and absent
sliding) is found although not always identified
 d. Treatment options: Observation and high flow Ox for small pneumothorax,
Catheter aspiration, Heimlich valve, standard chest tubes
e. Tension Pneumothorax: Need for emergent Needle thoracostomy/Chest tube
thoracostomy:
- Pleural defect creates a one-way valve leading to positive pressure in
pleural space and enlarging pneumothorax
- Mediastinal shift from increased pressure → impedes venal cava blood
flow return→ hypotension and cardiac arrest occur
VI. Pulmonary Embolism
a. Understanding Virchow’s Triad provides insight into why clots occur
i. Stasis: Central line catheters, Immobilized individuals, long distance
travelers, post-operative casts
ii. Endothelial damage: trauma, postoperative, smokers
iii. Hypercoagulable state: Cancer, increased estrogen (pregnancy,
contraception), Lupus/Phospholipid syndrome, HIV, others
b. Presentation
i. While classically tachycardia, tachypnea, pleuritic chest pain, and hypoxia
are found, low grade fever: many of these are found in less than 50% of
individuals; Dyspnea is most common complaint
ii. Syncope, Seizure like activity; PE may have these atypical presentations
iii. EKG: sinus tach (most common, around 50%), RBBB, right axis deviation,
S1Q3T3 (10-20%), non specific ST and T wave changes (50%)
iv. Chest Xray: Elevated hemidiaphragm, Hampton’s Hump (wedge shaped
infarction), Westermark sign(decreased vascularity distal to PE site)
c. Laboratory Workup
i. Clinical gestalt or Wells Criteria to determine pretest clinical probability,
D-Dimer/PERC utilized for low pretest probability patients, advanced
imaging if d-dimer elevated OR if high pre-test probability w/o need for
d-dimer
ii. Troponins and BNP may be used to determine cardiac strain if PE present
d. Treatment
i. Heparin traditionally utilized for admitted patients although oral
anticoagulants can be used. Heparin has advantage of being able to be
stopped if thrombolytics are used
ii. Oral anticoagulants used with outpatient treatment for patients
considered to be at low risk of mortality (simplified PESI score, Hestia
criteria frequent used)
iii. IV and catheter directed thrombolysis usage is evolving, used for
persistent hypotension and increasingly for those demonstrating right
heart strain on US, CT, and suggested by laboratory studies.
VII. Tracheostomy Complications:
a. Obstruction: From mucous plugging, acts as a ball/valve or profound obstruction
i. Removal and cleaning of inner cannula, Saline spray to assist in loosening
plugging followed by aggressive suctioning can treat most obstructions
 ii. If plugging remains the outer cannula may be removed. Cleaned, and
potentially replaced if needed
iii. No replacement of recently placed Tracheostomy tubes as stoma will
close quickly- see ENT surgical assistance
b. Infection
i. Infection of skin site, trachea, and bronchioles are common
ii. Often colonization does take place, Infection should it be leading to
significant recurrent purulent drainage should be treated
c. Tracheostomy tube dislodgement
i. If suction catheter cannot be passed the tracheostomy may not be fully in
the trachea
ii. This may be visualized on XRAY
iii. Removal and replacement if long term tracheostomy in place should be
done
d. Tracheostomy bleeding
i. Small amount of bleeding right at the stoma may be treated with silver
nitrate
ii. Large amount of bleeding is Tracheoinnominate artery fistula until
proven otherwise; May be precipitated by a small sentinel bleed
iii. Risk factors: newly placed tube (< 3 weeks), cuff pressure 25mmHg,
chronic steroids, Placement of tracheostomy below the 3rd tracheal ring
iv. Treat with a) hyperinflating the cuff, if fails b) Intubate patient with
balloon below bleeding, then manual pressure with finger in stoma and
pressure against manubrium (Utley maneuver)
e. For all tracheostomy tube placements, be set up for intubation. With patients
who have a tracheostomy due to malignancy, upper airway stenosis, etc.,
exercise extreme caution as rescue intubation may not be possible
VIII. Pleural Effusions
a. Transudative: from Increased hydrostatic pressure/loss of oncotic pressure
i. Etiology: CHF, Cirrhosis, Nephrotic syndrome
ii. Fluid analysis: <3 mg/dL, Pleural/serum albumin: <0.5; LDH <200
b. Exudative: Neoplastic, Inflammatory, Infectious Etiology
i. Etiology: Lung CA, Lupus (SLE), RA, Pneumonia, TB, abscesses
ii. Fluid analysis: >3 mg/dL, Pleural/serum albumin:>0.5; LDH >200
c. Pneumonias commonly associated with effusions: Strep pneumoniae, [Link],
Staph, Legionella, TB
d. Location of effusion may be helpful in non-infectious sources
i. L>R: Aortic dissection, Boearhaave’s (esophageal rupture)
ii. R>L: CHF, Pancreatitis, Hepatitis
IX. Acute Respiratory Distress Syndrome
a. Pathophysiology: Acute diffuse, inflammatory changes in the lungs from capillary
endothelial injury and diffuse alveolar damage; Alveolar edema results
- Impaired gas exchange, poor lung compliance, pulmonary HTN occur
 b. Defined by: PaO2 of <300 mmHg (Berlin definition) + acute onset + Bilateral lung
infiltrates on chest XRAY (and not due to cardiac origin)
i. PaO2 of 200-300 mmHg → mild
ii. PaO2 of 100-200 mmHg → moderate
iii. PaO2 of <100 mmHg → severe
c. Common Causes: Sepsis (most common), trauma, aspiration, near drowning, Tox
(ASA, opiates, hydrocarbons), Pancreatitis, CNS events
d. Treatment of ARDS focuses on maintaining oxygen saturations by minimizing
excessive pressure put on lungs + treating underlying cause
i. Low tidal volume (6 mL/kg)
ii. Prone position may improve oxygenation
X. Tuberculosis
a. Transmission: Occurs via respiratory droplets from infected (symptomatic and
asymptomatic) host
i. Skin test conversion 6-8 weeks later
ii. Patient rarely initially symptomatic if immunocompetent
b. Primary TB: in first 1-2 month may develop a focal lobar pneumonia, hilar
adenopathy, pleural effusion
- Uncommon to occur in immunocompetent patients
c. Latent TB: For those who are exposed and no or minimal initial symptoms occur,
encased and asymptomatic infection in the upper lung lobes with hilar lymph
node enlargement may develop (Ghon complex),
- For many people this will never progress. Test positive for skin
test/QuantiFERON gold during this time period
- XRAY shows enlarged hilum + 1-1.5 cm lesion in the lung parenchyma
d. Reactivation TB
i. Cavitary lesions/non cavitary lesions in posterior upper lobe of lungs
(high oxygen areas) most common
ii. 5% of immunocompetent progress to full blown TB cavitary lesions in first
2 years, 5% after 2 years
- Risk factors: advanced age, steroid use, HIV
iii. For HIV infected individuals: 10% per year will develop reactivation TB
e. Miliary TB: Hematogenous spread (uncommon)
- Very ill patients, during primary or reactivation stage
- Often immunocompromised
- Diffuse pellet size (1-3 mm) lesions throughout the lung fields
f. Testing: PPD skin
i. >15 mm health immunocompetent no risk factors
ii. >10: Recent at risk immigrant, health care workers, children, prisoners, IV
drug users, DM, CKD on dialysis
iii. >5: HIV infected, Recent exposure, Fibrotic Chest Xray changes,
Transplant and prolonged steroid patients (>1 month)
 - Interferon-Gama-Release Assays (QuantiFERON gold) are blood test
back in 16-24 hours, do not distinguish from active and latent disease
(no impact if have perceived Calmette-Guerin immunization however)
g. Treatment:
i. For Active TB: Typically includes 8 weeks of “intensive phase” then 18-31
weeks of “continuation phase”
- Intensive phase → INH, Rifampin, pyrazinamide, ethambutol
- Continuation → INH/Rifampin
ii. Paradoxical Reaction or Immune Reconstitution syndrome can occur
- Most common in HIV patients with CD4<50
- Result of improved immune system leading to dramatic inflammatory
response-> Fever, worsening respiratory status/infiltrates,
lymphadenopathy
iii. TB Meds have well known side effects to be aware of:
1. Hepatitis: Isoniazid, (5-33%) Rifampin, Pyrazinamide
2. Peripheral Neuropathy: Isoniazid
3. Ethambutol: optic neuritis
4. Pyrazinamide: Gout
5. Streptomycin: Ototoxicity
6. Rifampin: Reddish-orange urine, feces, saliva, sweat, tears
iv. Treatment for Latent TB: reduces risk of conversion to active disease by
70%
- Recommendations are frequently updated
- Currently 3-9 months of INH and/or Rifampin at varying frequency of
administration
 OB/GYN High Yield In-Service Review
First Trimester Bleeding

Multiple Possible etiologies

• Management
o As always, ABCs
o Rule out ectopic pregnancy, miscarriage
o Pelvic Exam, U/S
o Type and screen
• Treatment
o Treat cause
▪ Ectopic, spontaneous abortion, G/C, cervicitis, trauma, CA fibroids
o Rhogam if patient Rh- to prevent isoimmunization against future pregnancy
o Ob/gyn consult for close follow up
Spontaneous Abortions
• Defined as pelvic pain/bleed before 20 weeks
o Threatened
▪ Os closed
▪ Ob/gyn follow up
o Inevitable
▪ Os open – but no tissue present
▪ Sometimes D&C necessary
o Incomplete
▪ Os open -fetal tissue present
o Complete
▪ Os closed – all tissue passed
o Septic Miscarriage
▪ Os open – uterine tenderness, +/- tissue, fever, leukocytosis
o Missed miscarriage
▪ Os closed
▪ No products, no progress in pregnancy and no fetal heartbeat on US
▪ Will need D&C
• Rhogam as need for all!
Rh Isoimmunization
• Administer when Rh(-) pregnant patients experience miscarriage, trauma, placenta previa, or
any mixing of maternal-fetal blood
• Treatment
o <12 weeks → 50 mcg Rhogam
o >12 weeks → 300 mcg Rhogam
Ectopic Pregnancy
• Presents around 5-8 weeks
• Risk factors include previous ectopic, Hx of PID, IUD, tubal ligation
• Symptoms
o Unilateral adnexal tenderness +/- bleeding
 o Referred shoulder pain (blood in peritoneum)
• Investigation
o bHCG, U/S
o Consider an ectopic if
▪ bHCG > 6000-6500 + abdominal U/S with empty uterus
▪ bHCG> 1200-1500 + vaginal US with empty uterus
o If bHCG <1200 → repeat bHCG in 48 hours
• Treatment
o Unstable → OR
o If pregnancy <4 cm, bHCG<5000 and patient stable → consider methotrexate with OB
consult
• Consider heterotopic pregnancy (IUP + ectopic) in IVF patients

Physiologic changes of pregnancy

Gestational Diabetes
• Poor glucose control = increased risk of macrosomia and associated complications
• Insulin requirements increased through pregnancy
• DKA more quickly and at increased glucose levels than in nonpregnant patients
• Tight glycemic control needed but avoid hypoglycemia
Late term complications – Preeclampsia/Eclampsia
• SBP > 140 or DBP > 90 and proteinuria
o >0.3gm in 24 hrs, persistent 1+ proteinuria, spot protein/Cr ratio ≥ 0.3
• Eclampsia = seizures in patient with preeclampsia
o Severe Symptoms/signs -headache, blurry vision, RUQ/epigastric pain, abnormal
LFTs/platelets
▪ <100,000 platelets
 ▪ LFTs 2x normal
o SBP ≥ 160 or DBP ≥ 110 (2 occasions)
o Pulmonary edema
• Management
o Rule out HELLP
o Aggressive BP control (e.g. labetalol 20 mg)
o IV magnesium load (4-6 g over 15 min) and infusion
o Transfer to high-risk obstetric care
• Both can occur up to 4 weeks postpartum
HELLP
• Variant of preeclampsia
• Can occur pre, peri, or postpartum
• Consider in patients > 20 weeks EGA or 7 days postpartum with abdominal pain or headache
• Signs
o Hemolytic anemia (increased LDH), elevated Liver enzymes, low platelets, +/-
hypertension, +/- proteinuria
• Management
o Emergent ob/gyn consult
o Treat hypertension (e.g. IV labetalol)
o Correct coagulopathies (FFP, platelets, pRBC)
o IV Mg
o Emergency delivery often required
▪ <34 weeks gestation, consider steroids for neonate’s lungs

Prepartum Complications

Placenta Previa
• Placenta over internal cervical os
• Bright Red PAINLESS bleeding in second trimester or later
o Bleeding can be brief or copious
o Can have a sentinel bleed before hemorrhage
• Diagnose by U/S - NO transvaginal
• Risk Factors
o Prior c-sections, fibroids, AMA, previous previa
• DO NOT PERFORM a pelvic exam if this diagnosis is being considered
• May require C-section for delivery
• RhoGAM if Rh negative
Placental Abruption
• Bleeding between placenta and uterus
• Can cause
o DIC, fetal distress/death, maternal death
• Risk factors
o AMA, oligohydramnios, HTN, cocaine use, smoking, previous abruption
• “Concealed” = no blood seen per vagina
o Signs of preterm labor
• “Revealed” = bleeding noted per vagina
• Can be caused by minor trauma
• Diagnosis
 o Do not rely solely on u/s to diagnose (has low sensitivity
o History of trauma
o Physical exam (pain on abdominal exam)
• Management
o ABCs, RhoGAM PRN, may require urgent delivery, observe and fetal monitoring for 4
hours post trauma

Uterine Rupture
• Common causes = VBAC or trauma
• Symptoms/signs
o Increased pain, decreased contractions, fetal distress, change in fetal station
• Increased risk with just lap belt alone
• Management
o ABCs, ATLS in trauma, emergency C-section

Peripartum Complications

Preterm Labor
• Labor < 37 weeks estimated gestational age
• Management
o Consult OB/GYN
o Consider transfer to OB/GYN center if not active labor
o Consider tocolytics
▪ But not in placental abruption
o Consider steroids for lung maturation
▪ Between 24-36 weeks
Premature Rupture of Membranes
• Amniotic sac breaks before onset of labor
o Often laughing or cough
o Vs urine incontinence
• Increased risk of infection in mother and baby
• Management
o Consult OB/GYN
o Can confirm rupture with nitrazine or ferning test
o Minimize number of digital exams
o Use sterile gloves
o Consider Abx
Prolapsed Cord
• Obstetrical emergency
• Umbilical cord ahead of presenting part of baby
o High risk of cord compression
• Cord Compression → life threatening to infant
• Suspect cord compression in fetal bradycardia
• Management of visualized or felt cord prolapse
o Manually elevate fetal presenting part off the cord
o Do not remove your hand until after delivery
o Do not try to reduce the cord
Nuchal Cord
 • Potential obstetrical emergency
o Can cause fetal asphyxia if not recognized and treated
• Options if nuchal card preventing delivery
o Attempt to reduce over fetal head
o If all else fails double clamp and cut if
▪ Too tight to reduction
▪ Not enough time for reduction
Shoulder Dystocia
• Failure of baby’s anterior shoulder to pass below pubic symphysis
• Symptoms/signs
o Protracted labor, turtle sign, facial flushing
• Management
o Mother
▪ McRoberts maneuver (sometimes all fours)
▪ Place legs in hyperflexion, place foley
▪ Apply suprapubic (not fundal) pressure
o Baby
▪ Corkscrew maneuver
▪ Rotate baby’s posterior shoulder into the anterior plane
o If conservative maneuvers fail
▪ Fracture baby’s clavicle
▪ Episiotomy
Uterine Inversion
• Occurs if excessive traction on umbilical cord during placental delivery
• Symptoms/signs
o Acute abdominal pain, low BP, hemorrhage, shock
• Management
o ABCs
o Manual compression and restoration of uterus
o Start oxytocin only after restoration completed
• Do not confuse with uterine prolapse
o Old ladies
▪ Vaginal pessary, pelvic floor exercises, surgery
Endometritis
• Usually caused by normal vaginal/cervical flora that ascend into upper reproductive tract
• Risk factors
o Premature rupture of membranes
o C-section/instrumentation
• Signs/symptoms
o Postpartum fever, tender uterus, foul-smelling lochia
• Diagnosis is clinical
• Treatment
o Admission
o IV abx
▪ Gentamicin plus clinda/Zosyn
▪ < 48 hr = staph/strep
▪ > 48 hr = atypical bacteria
Postpartum Hemorrhage
 • Need high index of suspicion
o Hematologic changes of pregnancy can mask early signs of hemorrhage
▪ Might only see mild increased pulse rate
▪ Can lose 30% total blood volume before see BP drop
o Hemorrhage may be contained in uterus/pelvis
• Management
o ABCs, consult ob/gyn, pRBC as needed
o Uterine atony
▪ Massage and oxytocin
o Placenta accreta
▪ Remove all placental remnants
o Uterine inversion - reduce
o Repair all minor lacerations
Postpartum – Sheehan Syndrome
• Panhypopituitarism
• Occurs during or after childbirth
o Increased risk if traumatic birth
• Ischemic necrosis of pituitary caused by blood loss and hypovolemic shock
• Signs/Symptoms
o Inability to breastfeed, fatigue, lack of menstruation, loss of pubic and axillary hair, low
BP
• Diagnosis
o Obtain brain imaging
o Check chemistry,TSH
• Treatment
o Lifelong hormone therapy

Non-Pregnant Pelvic Discomfort

Vaginitis (Bacterial or Yeast)

• Abnormal discharge can be from vagina, cervix, upper reproductive tract (PID)
• Causes
o Infectious, irritants, atrophy (postmenopausal), foreign body
• Bacterial Vaginosis
o Thin discharge, fishy odor, clue cells on microscopy, can be sexual transmitted
o Treat with metronidazole or clindamycin
• Candida vaginitis
o Cottage cheese discharge, inflammation, discomfort/itching, may present with dysuria
o Oral fluconazole (not if pregnant) or clotrimazole vaginally
o Higher suspicion in diabetics
PID, Fitz-Hugh Curtis, Tuboavarian Abscess
• Usually ascends from cervicitis
• Risk factors
o Multiple sex partners or unprotected sex, adolescence, IUD (recently placed), recent
menses (eliminates normal cervical-uterine barrier), smoking, previous PID
• Chlamydia and Gonorrhea most common cause
• Classic presentation
o Bilateral lower abd pain for days, discharge, fever, CMT
 • Antibiotic covering G&C
o Ceftriaxone 500 mg IM, doxy BID x 14 days, metronidazole 500 mg x 14 days
o Admit if pregnant, toxic appearing, or complications (FHC syndrome or TOA)
• Fitz-Hugh-Curtis syndrome
o Bacterial perihepatitis
o Patients with RUQ pain and appears unwell
o “Violin Strings” adhesions around liver
• Tubo-ovarian abscess
o May cause unilateral pain
o U/S to rule out
o Start antibiotics and consult ob/gyn for possible surgical drainage
• Long term complications
o Ectopic pregnancy, infertility, and chronic pain
HPV
• Fleshy growths or cauliflower-like projections which later coalesce
• Can become cancerous
• Clinical diagnosis
o ob/gyn or primary care can test for HPV stains on pap smear and do a dilute acetic acid
test (warts turn grey vs white)
• Treatment
o Guided by ob/gyn or dermatology consultants
o Medical therapies
▪ Podofilox or imiquimod
o Surgical therapies
▪ Cryo/laser/excision
Bartholin’s Cyst
• Painful, fluctuant mass near posterior fornix of the introitus
• If patient > 40 years, follow up with gyn to evaluate for malignancy
• Treatment
o Consider concomitant STIs
o I&D → small incision on vaginal mucosal side of mass
o Insert Word catheter
▪ Creates a fistula from cyst to vestibule, allows drainage
▪ 6-8 weeks
▪ Gyn follow up
Endometriosis – (lower yield)
• Endometrial tissue found outside uterus, adheres to other structures
• Presents with
o Recurrent pelvic pain with menses
o Infertility
• Treatment → depends on patient’s reproductive wishes
o NSAIDs, hormonal therapy, surgery
Ovarian Cysts and Tumors
• Symptoms/signs
o Usually unilateral pelvic pain
o Cyst rupture
▪ Causes sudden onset pain
▪ Can cause significant bleeding and peritonitis
 • Tests
o Rule out pregnancy
o Pelvic U/S
▪ Look for mass and/or cyst
▪ Look for torsion
• Increased risk if cyst > 5 cm
• Management
o ABCs - rare but can cause hemodynamic instability
o May need gyn consult
o May require surgery
o Repeat imagining usually recommended
Ovarian Torsion
• More likely if > 5 cm cyst of mass
• Ovary has dual arterial supply → might not see complete ischemia in torsion
o Therefore, somewhat difficult to diagnosis
• Keep high index of suspicion
o Torsion can be intermittent
▪ Pain might come and go
▪ Exam may be normal between episodes
• Management
o Rule out ectopic
o Consult ob/gyn
Fibroids
• Benign mass
• African American women increased risk
• Symptoms/signs
o Mass effect, torsions, heavy menses, pelvic pain
• Can cause infertility
• Tend to shrink after menopause
• Treatment
o Conservative
o Myomectomy vs hysterectomy
Abnormal Uterine Bleeding
• Always rule out pregnancy with bHCG
o FYI tampon holds ~ 5 cc of blood
▪ Usual cycle 10 - 35 cc
• Refer to ob/gyn or consider consult
o For patients > 35 years with AUB
o For high risk patients < 35 years (obese, chronic, anovulation)
• Treatment
o ABCs, resuscitation
o Mild
▪ NSAIDs
o Estrogens, medroxyprogesterone (often in consult with ob/gyn
o TXA
▪ Sometimes prescribed monthly if bleeding recurrence
• 1.3 g TID x 5 days
Mastitis
 • Pathogens = staph aureus or strp
• 2-6 weeks postpartum
• Symptoms/signs
o Breast tenderness, redness, edema, malaise, fever
• Rule out other diagnosis (blocked duct, cancer, abscess)
o U/S to rule out abscess
• Treatment
o Abx - cephalexin, dicloxacillin, or clindamycin
o Alternate hot and cold compress
o NSAIDs
o Continue breastfeeding and/or pumping
Breast Masses
• 1 in 8 women will have breast cancer in their lifetime
• General signs/symptoms
o Mass
o Abnormal nipple discharge
o Scaly, red, itchy nipple and areola (paget’s disease)
o Palpable axillary nodes
• Signs/symptoms of inflammatory breast cancer
o May resemble cellulitis and/or abscess
o Peau d’orange skin
o Nipple retraction
o Warm, tender breast
• Boards focus on red flag signs/symptoms
o Correct answer is usually
▪ Imaging (mammogram +/- ultrasound)
▪ Urgent surgery referral