Grand Rounds Recap 6.8.22
/Pneumothoraces with Dr. Harward - snake bites with dr. otten - junctional and ventricular escape rhythms with dr. Jackson - qips: building a culture of safety with dr. thompson - wellness: nutrition in residency with dr. roblee - metabolic/endocrine disorders of the neonatal period with dr. ketabchi
Spontaneous and traumatic pneumothoraces WITH Dr. harward
Pneumothorax: gas within the pleural space
Pressure due to accumulating gas causes compression of lung parenchyma
Large volume pneumothorax will compress and displace mediastinal structures
Tension pneumothorax
Mediastinal shift places superior and inferior vena cavae under tension
Intrathoracic pressure and tension on cavae decreases venous return
→ decreases preload
→ decreases cardiac output
→ obstructive shock
Primary spontaneous pneumothorax: absence of underlying pulmonary pathology
Subclinical structural and functional abnormalities
3-6x more common in males
Young, thin males
Secondary spontaneous pneumothorax: presence of underlying pulmonary pathology
80% due to COPD
Tumor necrosis, ablation
Necrotizing infection
Traumatic Pneumothorax
Blunt or penetrating
Iatrogenic
Barotrauma
Small PTX
<3cm from apex to thoracic cupola
<2cm between visceral and parietal pleura at level of hilum
Variation depending on which guidelines you follow
PTX findings on AP CXR
Deep sulcus sign
Floating cardiac fat pad sign
Double diaphragm sign
Crisp cardiac silhouette
Other imaging modalities
Ultrasound:
Absence of lung sliding
Other causes of absence of lung sliding: apnea, fibrosis
M-mode: barcode sign suggestive of PTX
CT scan: most accurate but not always clinically feasible depending on stability of patient, external factors in the emergency department
Secondary spontaneous PTX
Stability if:
RR <24
HR > 60 and <120 beats per minute
Normotensive
SpO2 >90% on room air
Able to speak in full sentences
Secondary spontaneous PTX patients are inherently more likely to be clinically unstable
Very likely to require admission
Supplemental O2 reduces failure 50%
Always treat the underlying lung disease
Tension PTX- clinical diagnosis
Diminished breath sounds
Hypotension
Jugular venous distention
Summary:
Defined by gas within the pleural space
May occur spontaneously, secondary to pulmonary pathology, or as a consequence of trauma
If large enough, will create tension on venae cavae and result in obstructive shock
CXR and US may be used in rapid diagnosis. CT is most accurate
Management depends on size and clinical stability of the patient
Snake bites WITH Dr. Otten
~6000 reported snake bites by indigenous venomous snakes (2016) in the US
~3-5 deaths in US per year
~2.5 million venomous snakes worldwide
~100,000 deaths worldwide
Venomous snakes of North America
Medically important New World venomous snakes fall into 2 major families:
Crotalidae (crotalines/pit vipers)
Elapidae (coral snakes)
Pit Vipers
All 48 contiguous states except Maine have at least one pit viper species (Alaska and Hawaii do not have native venomous snakes)
Rattlesnakes (Crotalus)
Pygmy rattlesnakes (Sistrurus)
Copperheads, water moccasin (Agkistrodon)
Anatomy
Paired thermoreceptor organs (infrared detectors)
Extremely sensitive to temp delta (<0.1C)
Locating prey, aiming strikes, adjusting venom dose
Elliptical pupil
Triangular head
Large, anterior, mobile fangs
Single row of subcaudal scales
Elapidae
Outside the Western Hemisphere
Cobras, mambas, kraits, many snakes of Australia
North America
Coral snakes
Phospholipases A2
Neurotoxin that can increase the lethality of venom 10 to 100 fold
Noncompetitively binds to presynaptic calcium channels, inhibiting acetylcholine release
Blocks neurotransmission at the NMJ
Damages muscle cell membranes
Can lead to myonecrosis and rhabdomyolysis
Metalloproteinases
Locally destructive effects
Activate tumor necrosis factor alpha
Hemorrhagins
Leakage of RBC out of vasculature
Pit Viper Venom
Thrombin-like enzymes: coagulopathy
Disintegrins: prevent clot formation
Bradykinins: hypotension, vomiting, pain
Hyaluronidase: allow venom to spread
Lysolecithin: histamine release
Pit Viper: clinical presentation
Depends on species and size of snake, health of snake, age/health of patient, amount of venom injected, number of bites and anatomic location
Many bites occur during intentional handling (illegitimate bites)
25-35% of bites are “dry” (little or no venom is injected)
Epidemiology of snake bites
Males 17-27
April-December
Alcohol intoxication
Southern U.S.
Extremities
Deliberate exposure (legitimate vs illegitimate bite)
Local signs/symptoms
Severe burning pain
Progressive soft tissue edema
Ecchymosis
Hemorrhagic/serous vesicles
Bullae
Systemic effects
Nausea
Muscle fasciculations
Rhabdomyolysis
Systemic hemorrhage
Metallic/rubbery/minty taste
Pulmonary edema
Myocardial depression
Hypotension
Prehospital Care
Factors that reduce morbidity/mortality
Rapid transport
Intensive care
Antivenin
Prehospital care
Airway support
Cardiac monitoring
IV fluids
Removal of jewelry/tight clothing
Mark area of edema
What NOT to do
Incision
Suction
Tourniquets
Electric shock
Ice
Alcohol
Folk therapies
Hospital care
Airway management
Bites to face/neck
Fluid resuscitation
Analgesia
Wound care
Tetanus prophylaxis
Antivenin
Definitive therapy for snake envenomation
Imparting passive immunity to victim against circulating snake venom antigen
Irreversible binding
Should be given as soon as possible, though may be useful in treatment of coagulopathy days after the bite
CroFab
Available for commercial use in 2000
Derived from sheep serum
C. adamanteus, C. atrox, C. scutulatus, Agkistrodon piscivorus
Papain digestion of IgG to yield Fab fragments
Ovine IgG not glycosylated
Less immunogenic
Fab fragments incapable of cross-linking immune complexes
Small molecular size
More rapidly cleared by renal system
Current date: 14% acute reaction, 3% serum sickness
Antivipmyn- Polyvalent equine anti-viper serum
F(ab’)2 antibodies
Horse derived
From Bothrops, Crotalus, Sistrurus, Agkistrodon species
May replace CroFab for some bites
Crofab vs Anavip
Anavip FDA approved 2015
Fab2 decreased allergic reactions
Equine derived
Stays in system longer
Prevents coagulopathy
Less expensive
Antivenin administration
Supplied in lyophilized form- requires reconstitution
Slow rate for 1st 10-15 minutes
Initial control
Reversal/attenuation of local effects
Stable/improving coagulation studies
No worsening systemic effects
Recurrence phenomenon
Pharmacokinetic mismatch between venom and antivenom
Separation of circulating venom/antivenom complex after initial effective binding
Late onset venom components different from those initially active
Development of host anti-antivenom immune response
Surgery?
Incision- No
Excision- only 3-4 days later of necrotic tissue
Fasciotomy- toxic effects mimic compartment syndrome, give more antivenin
junctional and ventricular escape rhythms WITH Dr. Jackson
Heart conduction basics
SA node
RCA 55% people
Lcx 45% people
AV node
RCA 90% people
LCx 10% people
Bundle of His
Right and Left Bundle Branch
Definition of escape
Junctional (AV junctional)
Narrow QRS
Rate 40-60
Regular
Good reliability- ability to perfuse
Patient usually stable
Ventricular
Wide distorted QRS
Rate 20-40
Regular
Poor reliability
Patient symptomatic and unstable
Causes
Increasing age
MI
CT surgery history and scarring
Aortic stenosis
Hypothyroidism
Chagas disease
Viral
BB, CCB, digoxin
Electrolyte disturbances, hyperkalemia
Amyloidosis
Bradycardia in acute MI
Risk with inferior MI due to ischemia affecting AV node or SA node
Junctional or ventricular escape rhythm possible
Typically reversible with perfusion
Complete Heart Block
Old age most important risk factor
If block is at the AV node or above bundle of His
Junctional escape
Increased stability
Unstable with ventricular escape rhythm will require pacemaker
Lyme Carditis
Incidence of 0.3-4%
1-2 months after infection
Does not require permanent pacemaker
Treatment with ceftriaxone
Summary
Escape rhythms are a safety net for the heart when conduction abnormalities occur
Type of escape rhythm is dependent on where the conduction abnormality occurs
There are several etiologies that lead to escape rhythms
In most cases, treatment of underlying cause will result in resolution of the dysrhythmia
QIPS: building a culture of safety WITH Dr. thompson
Medical errors in medicine are unfortunately not uncommon
“Approaches that focus on punishing individuals instead of changing systems provide strong incentives for people to report only those errors they cannot hide. Thus, a punitive approach shuts off the information that is needed to identify faulty systems and create safer ones. In a punitive system, no one learns from their mistakes'' - Dr. Lucian Leape
The Just Culture Doctrine
Honest mistakes should not be penalized unless there is malicious intent, substance use, impairment, or ongoing threat
Penalizing mistakes discourages speaking up about safety threats and instead encourages concealment
“Just Culture” asks what, not who, is responsible
Human imperfection is expected
Embraces those caught in faulty systems
Individual failure is managed fairly
Seeks to balance safety and accountability
A Just Culture Tool is available
Adverse outcome causative factors- multifactorial
Patient’s age and health
MD and RN staffing
Hospital capabilities
Medication choice
Sleep
Time of day
On call specialist
Reliable history
Timely results
Prompt presentation
Psychological safety
An environment where speaking up is encouraged with any question, idea, concern, or mistake
Second Victim Syndrome
The second victim syndrome (SVS) is defined as the healthcare providers who commit an error and are traumatized by the event manifesting psychological (shame, guilt, anxiety, grief, and depression), cognitive (compassion dissatisfaction, burnout, secondary traumatic stress), and/or physical reactions that have a personal negative impact.
Action: What can you do?
Frame the work you’re doing as a learning opportunity with inherent uncertainty
Model curiosity. Ask questions. Embrace messengers.
Acknowledge your own fallibility and imperfections (with your team)
Be the change you want to see
wellness: nutrition in residency with dr. roblee
Eating healthy is hard
Grueling hours
Difficulty eating during working hours
Stressful work environment
Circadian rhythm disruption
Poor dietary habits lead to…
Metabolic disease
Irritability
Fatigue
Cognitive effects
Meal prep
Use your day off
Plan ahead
Go shopping with a list
Make your food for the week
Portion out snacks
Eating schedule tips
In a 24 hour period plan for 3 meals and 2-3 snacks
Eat every 3-5 hours
Eat your biggest meal right before you go to work
Don’t eat too much before you go to bed
Don’t go to bed hungry
Macros- carbohydrates
Avoid simple carbs and refined sugars
Look for complex carbs
Foods high in fiber (4g or more) will keep you fill
Examples: brown rice, lentils, ezekiel bread, quinoa, beans, chickpeas, barley, buckwheat, oats, whole grain pasta, peas, sweet potato
Macros- Fats
Omega-3 and omega-6 are both essential fatty acids
Omega-6 fatty acids are ubiquitous in Western diets
Prioritize omega-3 fatty acids (anti-inflammatory properties, promote cardiovascular health)
Omega-3: salmon, mackerel, flaxseed, chia seeds, walnuts, olive oil, avocado
Omega-6: sunflower oil, corn oil, soybean oil, sunflower seeds, pumpkin seeds, meat, dairy
Macros-protein
Keeps you full and energized
Protein needs vary depending on activity level
Generally, daily protein requirement is 1gm per kg of body weight
Examples: dairy, nuts, beans, tofu, fish, lean meats, eggs
Hydration
Body weight (kg) x 30 = daily fluid requirement (mL)
Avoid drinks with added sugar or sodium
Ex: Bubly, LaCroix, water
Meal Replacement Drinks
Can be a good option if you need something quick
Liquids will not keep you full for long- pair with snack
Check nutrition label- many are low in fiber or too high in protein
metabolic/endocrine disorders of the neonatal period WITH dr. ketabchi
DDx of the ill-appearing neonate
Sepsis
Congenital heart disease
Congenital adrenal hyperplasia (CAH)
Inborn errors of metabolism (IEM)
Mitochondrial disorders
Presenting symptoms
Vomiting
Poor feeding
Lethargy
When to suspect CAH
Hypoglycemia
Hyponatremia
Hyperkalemia
Initial Management of CAH
Treat hypoglycemia
2ml/kg of D25 or 5ml/kg of D10
Stress dose hydrocortisone bolus: 100mg/m2
25mg IV if <3 yo
50mg IV if 3-12 yo
100mg IV if >12 yo
Maintenance dose: same dose as above divided QID
Treat hyperkalemia
Treat shock with NS bolus(es)
When to suspect mitochondrial disorder
H&P: FTT, lethargy, hypotonia, seizures
Variable age of presentation, not necessarily neonate
Labs:
Lactic acidosis (upregulated glycolysis)
AA may be normal or elevated
Initial management of mitochondrial disorders
Treat hypoglycemia
Prevent catabolism with dextrose-containing IVF
Even if hypoglycemia not present
Stroke-like episodes
Treat with IV arginine HCl
AVOID lactated ringer’s solution
If possible, avoid
Over-bolusing
Anesthesia/paralytics
Valproic acid
Statins
Metformin
Macrolides
Tetracyclines
Inborn Errors of Metabolism
H&P: poor feeding, vomiting, lethargy, coma
Labs: (any of the following)
Metabolic acidosis or respiratory alkalosis
Elevated ammonia
Hypoglycemia
Ketones may or may not be present
Initial management of IEM
Fluid resuscitation with normal saline
Avoid LR, may be a lactate metabolism defect
Treat hypoglycemia
Initial bolus: 5ml/kg D10 or 2ml/kg D25
Maintenance: D10 + electrolyte at 1.0-1.5 x mIVF
AVOID enteral nutrition until Dx
Protein could trigger crises
Bicarbonate administration- unlikely to help if organic acidemia
In hyperammonemia, may cause cerebral edema and decrease ammonia excretion
Hypoglycemia (or Maintenance)
Doesn’t matter → give dextrose
Disorder of carb metabolism
Fatty acid oxidation disorder
Amino acidemia
Organic acidemia
Mitochondrial
Timing of presentations
Utilization disorders: within first few weeks
After fasting
Ex. carb metabolism, FOAD
Toxic metabolites: within first few weeks
After protein feeding
Ex. acidemias
Storage disorders: variable, often later
Can have phenotype features
Mitochondrial disorders: variable, often later
Neonatal Seizure Etiology
CNS infection
When can you call it a febrile seizure? → after 6 months old. If younger, consider CNS infection or disorder
Metabolic disturbance, hypoglycemia
Cofactor deficiency
Stroke
Structural
Neonatal Seizure Treatment
General
Phenobarbital 20-30mg/kg initial
10-20mg/kg additional
Max 50mg/kg in 24 hours
Electrolyte disturbances
Treat accordingly
Cofactor deficiency
Pyridoxine (B6) deficiency: 100mg IV q5-15min
Folic Acid deficiency: 2.5 mg IV leucovorin
Other thoughts
Ask if family has care plan
Know how to obtain newborn screen results
Know how to contact nearest specialist
There is an exception to every rule
Summary
Dextrose is your friend
Initial bolus: 5ml/kg D10 or 2ml/kg D25
Maintenance: D10 + electrolyte at 1.0-1.5 x mIVF
Avoid enteral nutrition if unclear Dx
Stress dose hydrocortisone
25mg IV if <3yo
50mg IV if 3-12 yo
100mg IV if >12 yo
Maintenance: same dose as above, divided QID
Consider B6 (100mg) then Folinic Acid (2.5mg) for refractory seizures