Grand Rounds Recap 4.26.23
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Ultrasound in early Pregnancy w/ Dr. Frederick
1st trimester pregnancy accounts for 10% of all ED visits from women of reproductive age
28% present on weekends
37% present after hours
Despite the fact that a lot of these patients present after hours, radiology is rarely available 24/7
TVUS diagnoses nearly 50% of early pregnancies after an inconclusive transabdominal US
ED-performed TVUS has not been shown to increase ED length of stay
Patients have not been shown to refuse a second TVUS after ED-performed study
Steps:
Get set up
Scan transabdominally first (you do not have to wait for the b-hcg to result)
Do the TVUS at the same time as the pelvic exam
Anatomy:
Version: the relationship between the uterus and the vagina in the sagittal plane
Flexion: the relationship between the uterine body and the cervix in the sagittal plane
Start by getting a true sagittal plane
Identify the fundus, follow the endometrial stripe (trilaminar endometrium) along its entire course down to the cervix
Include maternal bladder
Scan through the adnexa bilaterally, best evaluated in the sagittal plane. You can use the iliac vessels as your landmark to locate the ovaries (which have been described to look like chocolate chip cookies)
Scan through in two orthogonal planes
Always perform a comprehensive exam, even if you see an IUP right away
Identifying the IUP
Gestational sac
thick-walled anechoic structure
seen at about 5 weeks or b-hcg of 1000
Yolk sac
thick, hyperechoic structure, round like a cheerio
seen at about 6 weeks or b-hcg of 2500
Fetal pole
seen at about 6.5 weeks or b-hcg 5000
Amion
thin walled structure within the gestational sac (not always seen)
Fetal HR
seen at about 7 weeks or b-hcg of 7000
120-160 bpm
Use M mode (never use doppler as this can harm the fetus)
Positioning
IUP ideally positioned in the upper ⅔ of the uterus, adjacent to and touching the endometrial canal
Endomyometrial mantle (measured at the thinnest point from the inner border of the gestational sac to the outer border of the uterus, measured in two planes)
8mm to be adequate
<5mm is very concerning for ectopic
5-8mm requires OB/GYN consult
Interstitial Pregnancy
Pregnancy that implants on the portion of the fallopian tube adjacent to the uterus
Angular Pregnancies
Pregnancy that implants just medial to the utero-tubal junction on the lateral angle of the uterus
Dating of Pregnancies
most accurate in 1st trimester
most accurate measure is crown rump length
ED assessment is often earliest ultrasound
dating in the ED can assist with the scheduling of prenatal care and testing
early dating is critical in establishing EDD for patients with indications for late preterm or early-term deliveries
Late preterm infants have 3-5x higher mortality when compared with term infants
Early Dating (1st trimester)
Ultrasound machine will calculate for you (freeze a still image, hit the “calc” button, and these two are programmed in)
Mean Sac Diameter
measure length, width, and height of gestational sac
average of these measurements + 30 = gestational age in days
used at 5-7 weeks gestation
Crown Rump Length
can be used as soon as fetal pole is seen (6-13 weeks)
find the longest midsagittal embryo length in the horizontal plane (not flexed or extended)
measure from head to rump (excluding limbs or yolk sac)
measure 3 times and average
Ectopic Pregnancy
1-2% of all pregnancies
#1 cause of first trimester maternal death
10% of total maternal mortality
Concerning if: failure to diagnose an IUP, extrauterine mass, pelvic free fluid
Heterotopic Pregnancy
simultaneous IUP and ectopic pregnancy
58-73% are missed on ultrasound
expectant management or surgery
Cervical Ectopic
gestational sac implanted in the cervix
often confused for miscarriage in process
Cesarean Scar Ectopic
eccentrically located in the lower anterior myometrium
Corpus luteum cyst
created from follicle after release of egg
can be confused with ectopic pregnancy
thick walled, cystic structure in the ovary
look for characteristic “ring of fire” on color doppler
Free fluid
most often posterior to the uterus
quantify by dividing the posterior uterus into thirds
the TIE Fighter sign can be seen and represents the uterus suspended in free fluid by the ovarian ligaments
If a RUQ view is done in the ED, patients with diagnosis of ruptured ectopic were found to have their diagnosis made 2.2 hours earlier and went to OR 3.5 hours earlier
Free fluid in the RUQ has been shown to have a LR of 112 of requiring operative management
Risk Factors for Ectopic Pregnancy
prior ectopic pregnancy
surgery
infection
assisted reproductive technologies
IUD
However, 50% of patients with ectopic pregnancy have no risk factors
High and Lows w/ Dr. Comiskey
Hyperammonemia
10% of of patient presenting with hepatic encephalopathy do not have elevated ammonias
Most commonly seen in adults is secondary to liver dysfunction with cirrhosis or portal venous system shunting. Other causes include infections, certain drugs and hematologic disorders
In the pediatric population, more commonly seen are the urea cycle disorders
Cerebral edema occurs due to edema of the astrocytes within the brain, which are the primary ammonia scavengers within the CNS
Significant edema can lead to herniation and brain death
Treatment is aimed at reducing the production and absorption of ammonia, and common agents are lactulose and rifaximin, although these do not confer mortality benefit. Once ammonia levels are high enough, usually 2-3x the upper limit of normal, dialysis will be initiated.
For cerebral edema, hypertonic saline is the preferred solution over mannitol
Propofol is the preferred sedating agent due to its hyperosmolar state and anti-epileptic properties. Avoid Depakote in these patients if they begin seizing, as that will only worsen their disease process
Essential Thrombocytosis
most commonly seen in females, with average age of onset between 50-60 years
differential diagnosis also includes clonal neoplasms, spurious lab values, and reactive thrombocytosis
about half of patients diagnosed with essential thrombocytosis are found to have a JAK2 mutation
patients are at risk for thrombosis, but also develop an acquired vWD because there are so many platelets that they become dysfunctional which increases risk for bleeding
Treatment is aimed at preventing complications, mostly from thrombotic and hemorrhagic events
Low risk = <60 yrs old and no prior thrombotic events
aspirin, close monitoring
High risk = > 60 yrs old with prior history of thrombosis
antiplatelet, cytoreduction
Hydroxyurea is the first line cytoreductive therapy, with one study demonstrating patients on hydroxyurea experiencing a 3.6% incidence of thrombosis compared to 24% of patient on placebo over a 6 month period
Hyperviscosity syndrome
most commonly seen with hypergammaglobulinemia due to their large structures, with 30% of patients with Waldenstrom macroglobulinemia developing HVS in their lifetime
caused by increased thickness of the blood
presents with visual disturbances, neurologic complications and bleeding
treatment is aimed at reducing complications. Methods include hydration, emergency plasmapheresis if indicated, and treatment of the underlying pathology, usually with chemotherapy
Severe Iron Deficiency Anemia
often related to poor nutrition in the pediatric population
complication is high output cardiac failure
feared and rare complication of chronic anemia is high output heart failure, the least common form of heart failure
defined low SVR and oxygen a-v gradient with high cardiac output; which differs from low output heart failure since there is usually an associated increase in SVR with circulating vasoconstrictors
activation of the RAAS system and increased ADH in attempt to increase intravascular volume, but eventually leads to cardiac remodeling and hypertrophy
treatment is aimed at correcting the underlying cause of heart failure, in this case correction of the anemia with a blood transfusion, but must be a slow infusion over 3-4hr per unit and IV iron sucrose
reduction of extravascular volume with diuretics, fluid and salt restriction
vasopressors may be used to increase SVR
HIV/AIDS
Labs prior to initiation of HAART therapy
CMP, CBC, b-hcg, STI testing, and screening for AIDS-defining illness
HAART should be started on patients once the diagnosis is confirmed regardless of their CD4 count
If patients are able to increase their CD4 >500, they are anticipated to have a normal life expectancy
Left untreated, HIV patients are anticipated to live ~10yrs and if they are transition to AIDS, life expectancy falls to <2 yrs
Undetectable = untransmittable
R3 Small Groups: Commercial In-Flight Emergencies w/ Dr. Smith
Quick Facts regarding In-Flight Emergencies:
2.75 billion passengers annually
1 medical emergency per 604 flights
Most common complaints:
Syncope/presyncope: 37.4%
Respiratory symptoms: 12.1%
Nausea and vomiting: 9.5%
Diversion occurs 7.3% of in-flight emergencies
Deaths occurred 0.3% of in flight emergencies
31% EMS was not requested, of those where EMS was requests, only 37% were transported
60% of OB cases were miscarriages prior to 24 weeks gestation
Most commonly used medications are: oxygen, IVF, and ASA
Your Team
Flight attendants should have some basic medical training, can help you locate supplies, and can help with communication with the pilot
Medical Ground Support:
Usually by radio or telephone in the cockpit
May be able to speak directly with them or all information may have to be relayed
All conversations are recorded
Typically EMS fellowship trained EM physicians - two groups in the US. One through UPMC, one through Phoenix
Ground control has the ability to supercede decisions made by in flight responders
If multiple people respond, introduce yourselves and assign roles
Special Circumstances:
Diversion:
Decision made by pilot, +/- medical ground support
Cost estimated 10,000 to 500,000 dollars
Death on Board:
Can presume death and stop resuscitation
Don’t declare deaths. Legal implications vary from country to country.
Pilot will decide when/how/who to inform on the ground
DNRs:
Airlines can refuse to honor DNR and can still request medical assistance
Individually decide whether or not to honor it versus resuscitate
Airline can ask for someone different (aka ignore you)
If there is concern for a communicable disease, make pilot and team aware if other passengers need to be evaluated or quarantined
Legal:
US: the Aviation Medical Assistance Act passed April 24, 1998 which states individual not liable for damages in any action brought in Federal or State court from the acts or omissions in providing or attempting to provide assistance in the case of in-flight emergencies (unless the individual is guilty of gross negligence or willful misconduct)
International: depends on the country, but most countries have something similar.
No known cases of an individual medical provider being successfully sued anywhere in the world for an in-flight emergency. Airline companies have been sued. Generally accepted (and some airlines spell it out) that they are assuming the liability even for you helping
Documentation:
To protect yourself (and the airline), will/should make documentation of what happened. Each airline generally has their own protocol.
Recommend keeping a copy of the records for yourself
FAA Regulation Medical Kit
Sphygmomanometer
Stethoscope
Airways, oropharyngeal: 1 pediatric, 1 small adult, and 1 large adult or equivalent
Self-inflating manual resuscitation device with 1 pediatric mask, 1 small adult mask, and 1 large adult or equivalent mask
Cardiopulmonary resuscitation masks: 1 pediatric, 1 small adult, and 1 large adult or equivalent
V. administration set: 1 tubing with 2 Y-site connectors, 2 alcohol-soaked sponges, 1 standard roll of 1-inch-wide adhesive tape, 1 pair of tape scissors, and 1 tourniquet
Protective nonpermeable gloves or equivalent, 1 pair
Needles: 2 18 gauge, 2 20 gauge, and 2 22 gauge; or 6 needles in sizes necessary to administer required medications
Syringes: 1 5 cc and 2 10 cc; or 4 syringes in sizes necessary to administer required medications
Analgesic, nonnarcotic, 325-mg tablets, 4
Antihistamine, 25-mg tablets, 4
Antihistamine injection, 50-mg single-dose ampule or equivalent, 2
Atropine injection, 0.5-mg single-dose 5-mL ampule or equivalent, 2
Aspirin, 325-mg tablets, 4
Bronchodilator, metered-dose inhaler or equivalent
50% Dextrose injection, single-dose 50-mL ampule or equivalent
Epinephrine injection, 1:1000 (1 mg/mL) single-dose 1-mL ampule or equivalent, 2
Epinephrine injection, 1:10,000 (0.1 mg/mL) single-dose 2*-mL ampule or equivalent, 2
Lidocaine injection, 20-mg/mL single-dose 5-mL ampule or equivalent, 2
Nitroglycerin, 0.4-mg tablets, 10
9% Sodium chloride injection, 500 mL
Basic instructions for use of the drugs in the kit
AED
Of note, there is no requirement for airlines to carry a glucometer or some other common medical equipment. Some airlines may carry more than what is required.
The AirRx app contains information regarding common medications and equipment available, top diagnoses, medicolegal information and more, and is available to download for free.
High Altitude illnesses w/ Dr. Kletsel
Physiology
High-altitude environment leads to hypoxemia
o Concentration of oxygen in inspired air (FiO2) stays constant at 21% regardless of altitude
o However, as barometric pressure decreases with altitude, the partial pressure of oxygen decreases as well
o This leads to reduced arterial partial pressure of oxygen (PaO2) in those residing at higher altitudes
· Physiology of acclimatization
o Body tries to adapt to the hypoxemia of a high-altitude environment if given time
o Respiratory
Will increase RR to compensate for low PaO2
Yet, this is limited by respiratory alkalosis, which serves as a brake on the respiratory system
Eventually kidneys will act to excrete bicarbonate, to lower the pH
Now RR can increase further
But, need 4-7 days for kidneys to begin to excrete bicarbonate
o Cardiovascular
Increase in HR to maintain adequate CO
Global pulmonary vasoconstriction in response to hypoxemia
Increase in cerebral blood flow to deliver more oxygen-deprived blood to the CNS
o Circulatory
Increase EPO production to increase RBC mass over days to weeks
Increase 2-3 DPGA production to shift oxygen-dissociation curve to the right and allow easier oxygen unloading to tissues
High-Altitude Syndromes
o Spectrum of disorders, that have the fundamental etiology of hypoxia and generally occur due to rapid ascent and not enough time of physiological acclimatization
o Principles of management
Do not ascend any higher if patient develops symptoms
If safe, descend if initial treatment fails to improve symptoms
If safe, descend immediately if HACE or HAPE occur
o Acute Mountain Sickness
Incidence varies according to
Rate of ascent, sleeping altitude, genetics
Clinical features
Typically after ascent to altitude >2000m
Occurs rather quickly, usually first 1-6 hours
Headache, nausea, vomiting, weakness, sleep disturbances
Treatment
No further ascent if mild symptoms or descent if moderate/severe symptoms
Oxygen administration (0.5-1 L/m of nocturnal O2 is most helpful)
Acetazolamide
125-250 mg PO BID
Blocks carbonic anhydrase to reduce kidney bicarbonate reabsorption
Helps lower pH to allow respiratory system to further increase RR
Dexamethasone
4 mg PO/IM/IV q6h
Reserved for severe symptoms
Symptom control
Acetaminophen/Ibuprofen PRN
Zofran PRN
Prevention
Graded ascent (avoid abrupt ascent >3000m
Prophylactic acetazolamide (started 24h prior to ascent and continued for first two days)
o High-Altitude Cerebral Edema (HACE)
Pathophysiology involves vasogenic edema in the CNS
Involves increase CBF and a leaky blood-brain barrier
Due to loss of auto-regulation and increased permeability due to inflammatory mediators
Expect T2 signaling on MR imaging
Clinical features
Progressive neurological decline
AMS, ataxia, stupor
Focal neurological signs (usually CN3 or CN6 palsies)
Occasionally seizures and coma
Treatment
If safe, descent is highest priority
If unable, can simulate descent with a hyperbaric bag (i.e. Gamow bag)
Supplemental oxygen
Dexamethasone
8mg IV initially, then 4 mg PO/IM/IV q6h
No evidence for hypertonic saline or mannitol
o High-Altitude Pulmonary Edema (HAPE)
Risk factors
Rapid ascent and associated heavy exertion
Cold environment
Underlying pulmonary hypertension
Pathophysiology involves non-cardiogenic pulmonary edema
Due to increased pulmonary vascular resistance in response to global hypoxemia
Clinical features
Progression of dyspnea is hallmark of HAPE
Early in disease process
Dry cough, dyspnea on exertion, poor exercise tolerance, localized rales, reduced SpO2 readings
Later in disease process
Wet cough, dyspnea at rest, generalized rales, tachypnea, tachycardia
Treatment
If safe, descent is highest priority
If unable, can simulate descent with a hyperbaric bag (Gamow bag)
Supplemental oxygen
Nifedipine
20-30mg extended release PO q12h
Reduces pulmonary artery pressure
Tadalafil
10mg PO q24h typically started for prevention of HAPE 24h prior to ascent
Generates nitric oxide to blunt pulmonary hypoxic vasoconstriction