Trauma Informed Care (Lund, 3/26/2025)

  A recording of this presentation is available HERE. 

Thanks so much to Dr. Erin Lund for a very impactful presentation this week on Trauma Informed Care. I have to confess that I have seen this presentation (or a previous version) before, but I DO need to hear and rehear and rehear this topic. 

If you remember nothing else, take pearl in: In our daily work should use "universal trauma principles" with ALL patients and then add "extra carefuly trauma informed care" with those whom we KNOW have had extra trauma. 

This includes things like asking for consent, empowering patients over their own bodies and histories, and resisting retraumatization.

I love/hate this image she shared, reminding us of the context of trauma that extends far beyond a person's individual experience. The medical trauma many of our patients have experienced primes them to respond in particular ways to our care provision, and we need to be prepared, but the collective and structural trauma is also ever present.

© Lewis-O’Connor, A. 2015 © Rittenberg, E 2015 © Grossman, S. 2015 UPDATED, April 2020, Feb 2022

Trauma abounds. 

Many of us are well-versed in the original Adverse Childhood Events (ACES) study, which found that 61.7% of CA adults had experienced at least one ACE, and 1 in 6 (16%) had experienced 4+ ACES. You can see the most common ACEs in the image below.

But trauma doesn't end in childhood. Adult traumatic experiences are also common; these include: intimate partner violence, gun violence, sexual assault, incarceration, birth trauma, accidents, racism, sudden loss of a loved one, and more. 

The actual "traumatic experience or incident" matters much less than how we respond to the trauma. What are our resources? Do we have resilience? What are our protective patterns? Do we have time to recover?

The image below is a schematic of a stress trigger, the natural response, and then what follows. Note the time of calming down, depletion and recentering. If we have the tools to pass through these stages, we can recover from the trigger. If not, we may not be able to. Traumatic experiences can lead to developing toxic stress physiology. And repeated stress can impact our neurodevelopment, interfering with executive function

www.dovetaillearning.org

Toxic Stress and Caring Adults - KABOOM!

 
A local non-profit does trainings/workshops to promote resilience. In their workshops, they teach us that our protective patterns, which we develop over time, can be helpful and keep us safe. But when overused or used in incorrect situations, they can be harmful, self-destructive, and inhibit connection with others. Those patterns are seen in the slide below:

SAMSHA (2021) says that to be trauma-informed we must 1) Realize the widespread impact of trauma and understand potential for recovery 2) Recognize the signs/symptoms of trauma 3) Respond by integrating this knowledge about trauma into policies and procedures and practices and 4) Seek to active Resist retraumatization. 

We can create a safe context, restore power, value individuals. We can use universal trauma precautions and stay patient-centered. Being trauma-informed in the medical setting involves empowering patients, giving choice when we can, collaborating, offering safety and trustworthiness. In addition, get curious, learn the back story, listen to patients' fears. Ask yourself and the patient, "How can we help you get through this?"

Resilience is protective. I very much recommend you listen to Dr. Lund's presentation, where she goes on to really talk about heartfelt listening, growing empathy to connect, not defining people by their trauma, and making a real difference through trauma-informed care. 

She ended her presentation with a seminal paper on Trauma informed care in the ED from Ashworth et al (2023). A link to that paper and very helpful tables is available HERE. 

Pediatric Ophthalmology (Qureshi, 3/19/25)

 A recording of this presentation is available HERE. 

My notes:

In pediatric patients, any condition that affects the amount of light passing through the eye will negatively affect the brain's ability to learn and see and result in permanent vision loss. 

Therefore, it is essential to treat pediatric eye disorders as quickly as possible!!

Common causes of childhood blindness, worldwide

• corneal scarring
• vitamin A deficiency
• measles
• opthalmia neonatorum
• harmful eye practices
• infective corneal ulcers
• congenital cataracts
• uncorrected refractive errors
• retinopathy of prematurity
• congenital glaucoma

WHO estimates 19 million visually impaired children worldwide, 1.4 million preventable blindness

Common pediatric eye disorders

• Amblyopia: a decrease in visual development that occurs when the brain doesn't get visual stimulation from the eyes (one or both eye send distorted image to brain, even when glasses are use). Only children get amblyopia, can result in permanent vision loss if not treated in child. Most common cause of vision loss in adults 20-70 is untreated amblyopia
• refractive amblyopia is treatable with glasses/patching
• patch the good eye, let the bad eye function, it works! but does not fix strabismus
• alternatively, drop of atropine in the good eye, to allow bad eye to see better (limits vision in good eye to a certain amount)
• deprivation amblyopia: if you have cataract or congenital ptosis blocking the pupil, very bad for visual development (poor prognosis within even 6 weeks, e.g. cataract, corneal ulcer, congenital ptosis)
• the primary care physician detects amblyopia (e.g. red light reflex), ophthalmology treats it
• asymmetric red light reflex>> urgent eval < 6 weeks of age
• Strabismus: ocular misalignment, "to squint or look obliquely", affects 4% of children <6 years, 30-50% results in reversible amblyopia (vision loss)
• strabismus testing: light reflex is the key (see image below)
• pseudostrabismus: looks like esotropia but light reflex is centered on the pupils (common in kids of Asian descent)
• surgical repair

• Congenital Cataracts: 1/3 hereditary, 1/3 associated with other disorder, 1/3 idiopathic
• must remove within 3 months to prevent irreversible vision loss
• Congenital Ptosis: must be able to see pupil, if kid is using a chin up position, vision is not a threat (ptosis is there, but vision is safe) 
  
  
  
• Horner Syndrome: when you see ptosis, check the pupils. The ptotic eye (SNS innervates the eyelid mm but also the iris dilator), if pupil assymetry with ptosis, patient needs brain/neck/upper chest imaging to follow nerve plexus to make sure there is no problem along the plexus causing the ptosis (e.g. tumor)
• Nevus of Ota: low percentage develop glaucoma (see R eye below, grey in sclera and skin)
• 
• Congenital Glaucoma: enlarged cornea, tearing eyes, spasmodic to light, can develop serious vison loss, need urgent treatment. Very different than an adult. In a kid you should be able to see swollen cornea,  almost like a corneal ulcer or maybe like one eye is bigger than the other. Should be referred urgently

• Retinoblastoma of childhood 
• most common ocular tumor or childhood
• usual onset < 4 years
• 25% present with strabismus
• treatment: radiation, chemo, possibly enucleation
• require systemic work up, including r/o pineal gland and bone tumors
• 
  
  
  
• Red eyes
• Nasolacrimal duct obstruction is very common, usually presents as tearing, common, 5% of newborns, 
• no rush to refer >>90% regress by 12 months (95% by 18 months)
• surgical treatment occurs 18-24 months w/nasolacrimal probe
• Dacryocystocoele (image below): within first few weeks of life, infection and bump w/preseptal cellulitis due to imperforate valve. Have to treat preseptal cellulitis with IV abx and then sedate and probe. It looks better after abx butu if you don't create the passage, it will recur.
  
  
  
• Blepharitis: Very common, redness in conjunctiva and redness in eyelids>> treat the eyelids (warm compresses, abx drops despite no infection> glands work and eyes work better). Can also have stye. Erythromycin ointment doesn't work, but Maxitrol drops do work.

• Neonatal conjunctivitis: neonatal gonorrhea (very violent, first day of life), chlamydia, chemical, HSV (4-5 weeks of life).
• need systemic treatment AND ointment
• Allergic conjunctivitis: itchy red eyes, papillae, zaditor drops OR systemic allergy treatment, temporary steroids okay w/taper if really bad
• vernal conjunctivitis is severe form of allergic, can lead to shield ulcers, giant papillae, often in young men
• Styes: obstruction of meibomian glands, very common 
• hordoleum is a blocked gland
• chalazion is the more chronic granulomatous form
• warm compresses, maxitrol (neomycin/polymyxin/dexamethasone) ointment, only if superinfection can consider antibiotic
• 

Pediatric Vision Screening

Direct visual acuity screening is gold standard

• Start screening age 3/4 w/HOTV or heart/house/square tools for refractive problems

(Tumbling E hard to do with young kids)

• Age 4-5, use HOTV card but can use "match card", looking for 20/40 vision (doesn't have to be better), one eye should NOT be way better than the other> this should trigger referral
• Age 5+, looking for 20/30 or better, move to Sloan Letters and repeat  q1-2 years

Phenobarbital for Severe Alcohol Withdrawal Syndrome (Aguilar & Bowen 3/12/2025)

 A recording of this presentation is available HERE. 

My notes:

• 10.9% of US adults have alcohol use disorder (AUD) at some point in their lifetime (!!)
• AUD costs the US $249 billion/year
• 178,000 excess deaths due to AUD in the US 2021
• Compared to opioids, higher rates of alcohol use, misuse, ED visits, and deaths see below)

Alcohol Withdrawal Syndrome (AWS)

• 500,000/year episodes of AWS requiring pharmacological treatment
• 5-20% of people admitted to the hospital have AWS
• highest risk of seizures in first 1-2 days of AWS, DTs 4-6 days with looooooooong tail
• Reminder of difference between hallucinosis vs. DTs (autonomic instability)

Neuropharmacology of Alcohol

Dopamine>> reward>> addiction

GABA agonism during intoxication>> sedation

Chronic use>> GABA downregulation, Glutamate upregulation

Lots of other neurotransmitters involved: opiate R, serotonin R, cannabinoid R, etc

When we take away alcohol (after chronic use), our GABA system is completely depleted, and our glutamate is "going wild"

Phenobarbital is a barbiturate

• GABA agonism, suppresses glutamate
• PO>> onset 60 minutes, IV>> onset 5 minutes
• metabolized in the liver, excreted renally
• 1/2 life ~79 hours (range 53-118 hours)
• this prolonged half life allows for a built in taper
• has a predictable pharmacokinetics at 10mg/kg (deal body weight), though no RCTs that study "ideal drug level" for AWS
• no documented barbiturate resistant alcohol withdrawal

Traditional treatment of AWS is with benzodiazepines. We know benzos can cause paradoxical agitation and delirium. In addition, a lack of endogenous GABA in chronic alcohol use can make benzos less useful.

What does the current  literature say about Phenobarbital vs benzos?

• Retrospective cohort study, 42-bed ICU, 120 participants (2018, Am J of Critical Care)
•  shorter ICU stays (2.4 vs 4.4), shorter hospital stays (4.3 vs 6.9).  lower rate of mechanical ventilation (2% vs 23%), fewer adjunctives including precedex (7% vs 28%)
• RCT with ED pts requiring admission – single dose phenobarb vs symptom-based BZD, 102 participants (2013 Journal of Emergency Medicine)
• decreased ICU admission rates (8% vs 25%), decreased BZD use
• Retrospective cohort over 2 years, 606 participants (2021, Cureus)
• shorter hospital stay (2.8 vs 3.6), lower all-cause 30-day readmission (11%  vs 19%), fewer 30-day ED visits
• 2 different Metanalyses (2021) findings: may shorten hospital LOS, unclear if shortens ICU LOS but does decrease ICU admission, benzo sparing, may result in less intubation

Some suggestion that we should move away from CIWA for scoring AWS. One proposed alternative is RASS scoring, which should be familiar to people who work in ICUs

Proposed Phenobarbital Protocol DRAFT

Notes:

• For HIGH risk patients (CIWA>20 OR CIWA>16 with Risk factors)
• 10-12 mg/kg (IDEAL body weight) loading dose
• Use ideal body weight calculator (MD Calc)
• should happen in monitored setting (ED vs. ICU) only
• For patients who may be at lower risk for AWS, consider lower dose than the loading dose (e.g. 130mg, 260mg IV/IM) q30 minutes-1 hour
• Patients who have already been treated with benzos CAN receive phenobarbital but should be lower dose (due to risks of sedation)

References:

1. SAMHSA Center for Behavioral Health Statistics and Quality. (2022). National Survey on Drug Use and Health (Table 5.9A—Alcohol use disorder in past year: among people aged 12 or older; by age group and demographic characteristics, numbers in thousands, 2021 and 2022, Issue. https://www.samhsa.gov/data/sites/ default/files/ reports/ rpt42728/NSDUHDetailedTabs2022/NSDUHDetailedTabs2022/NSDUHDetTabsSect5pe2022.htm#tab5.9a  

2. Centers for Disease Control and Prevention. (February 29, 2024). Excessive Alcohol Deaths. Retrieved April 1 from https://www.cdc.gov/alcohol/features/excessive-alcohol-deaths.html#:~:text=About%20178%2C000%20people%20die%20from,or%20488%20deaths%20per%20day

3. Fixed-Dose Phenobarbital Versus As-Needed Benzodiazepines for the Management of Alcohol Withdrawal in Acute Care General Internal Medicine https://pubmed.ncbi.nlm.nih.gov/38151248/#:~:text=There%20was%20no%20difference%20in,%25%2C%20P%20%3D%200.03).

4. National Institute on Alcohol Abuse and Alcoholism. (2024). Alcohol-related emergencies and deaths in the United States. Retrieved April 1 from https://www.niaaa.nih.gov/alcohols-effects-health/alcohol-topics/alcohol-facts-and-statistics/alcohol-related-emergencies-and-deaths-united-states

5. Maldonado, J. R. (2017). Novel Algorithms for the Prophylaxis and Management of Alcohol Withdrawal Syndromes-Beyond Benzodiazepines. Crit Care Clin, 33(3), 559-599. 

6. Tidwell, W. P., Thomas, T. L., Pouliot, J. D., Canonico, A. E., & Webber, A. J. (2018). Treatment of Alcohol Withdrawal Syndrome: Phenobarbital vs CIWA-Ar Protocol. Am J Crit Care, 27(6), 454-460. 

7. Rosenson, J., Clements, C., Simon, B., Vieaux, J., Graffman, S., Vahidnia, F., . . . Alter, H. (2013). Phenobarbital for Acute Alcohol Withdrawal: A Prospective Randomized Double-blind Placebo-controlled Study. The Journal of Emergency Medicine, 44(3), 592-598.e592. 

8. Hawa, F., Gilbert, L., Gilbert, B., Hereford, V., Hawa, A., Al Hillan, A., . . . Al-Sous, O. (2021). Phenobarbital Versus Lorazepam for Management of Alcohol Withdrawal Syndrome: A Retrospective Cohort Study. Cureus, 13(2), e13282. 

9. Murphy, J. A., Curran, B. M., Gibbons, W. A., & Harnica, H. M. (2021). Adjunctive Phenobarbital for Alcohol Withdrawal Syndrome: A Focused Literature Review. Annals of Pharmacotherapy, 55(12), 1515-1524. 

10. Hammond, D. A., Rowe, J. M., Wong, A., Wiley, T. L., Lee, K. C., & Kane-Gill, S. L. (2017). Patient Outcomes Associated With Phenobarbital Use With or Without Benzodiazepines for Alcohol Withdrawal Syndrome: A Systematic Review. Hospital Pharmacy, 52(9), 607-616.

Chagas Disease: Why a Neglected Tropical Disease Matters for US Clinicians (Heindel, 3/5/25)

 A recording of this presentation is available HERE. 

Dr. Leah Heindel gave a wonderful Grand Rounds presentation this week on Chagas Disease. Perhaps the most important moment of the presentation was this slide:

"Look," Dr. Heindel, urged, "look at how this little "kissing bug" (aka triatomine) creates a cascade that has impact on immigrant health justice, reproductive health, whole-family care, global health, and how we think of screening and prevention in the US in 2025. This is family medicine."

Family medicine, indeed, is all of these.

Epidemiology and Disease Burden

Chagas Disease, which infects 7-8 million people worldwide, mostly in Latin America, presents a health burden seven times higher than malaria in the Western Hemisphere. There are an estimated 300,000 people living in the US with Chagas disease, many of whom are immigrants from Mexico, El Salvador, Guatemala, and Honduras. Unfortunately, only about 1% of those have been identified. Both vector and vertical transmission occurs in the US (22-100 cases congenital chagas in the annually).

Chagas disease has both an acute and indolent phase. The overwhelming majority of people infected with Chagas disease (90%) will be asymptomatic in the acute phase, but chronic impacts (especially GI, cardiac) typically appear 20-30 years after initial infection. 

Seroprevalence in immigrants from endemic countries is believed to be about 1% in the general population, though it varies widely depending on how these estimates are made. For example, you can see in the table below from the IDSA that there is a MUCH higher seroprevalence in immigrant patients from endemic areas with otherwise unexplained non-ischemic cardiomyopathy (13-19%). 

Vertical transmission occurs in 2-13% of cases, most congenital infection is asymptomatic, but Chagas has been associated with preterm delivery, low birthweight and low APGAR scores. 

Clinical manifestations

Chagas disease is generally spread via the bite of the "kissing bug", usually on the neck and face at night while people are sleeping; the same bug defecates close to that area, then the disease is transferred to the bloodstream via scratching at the site and introduction of bug feces to the broken skin. The acute phase of Chagas (only in about 10% of people infected) presents as a non-specific viral syndrome, including fever malaise, and anorexia. One pathognomonic sign of acute Chagas is Romaña's sign, pronounced swelling of the eyelid (as seen in image below). Domesticated and farm animals serve as reservoirs of the disease, and thatched roofs are a known risk factor in endemic areas.

After decades long latency, most common manifestations include cardiac (sudden cardiac death as #1 cause of death from Chagas, 55-60% of people, also HFrEF (25-30%) and embolic disease (10-15%). It seems that the parasite has a particular predilection for the electrical and conducting system. 

GI effects are also well-documented and occur in 10-21% of people with chronic Chagas, including both esophageal and colonic manifestations. In the esophagus, dysphagia and regurgitation are common; in the colon sigmoid rectal dilatation and progressive constipation. 

Neurologic effects including peripheral neuropathy and even dementia have been suggested. In addition there is a reactivation syndrome that can affect people with transplant or other immunosuppression.

Screening and Diagnosis 

The earlier Chagas is detected, the better the outcomes. Once someone has chronic cardiac or GI effects, treatment has shown to be unhelpful.

Diagnosis is done via is a serum IgG test with reflex to confirmation (goes to CDC), which is available through most laboratories. 

Both the CDC and IDSA recommend targeting screening based on risk factors, in particular being born in or lived in endemic areas, having a family member with Chagas Disease. 

Screening during pregnancy has been shown to be cost effective and may be something we should be integrating locally in our at-risk population-- more on this to come. Options for pregnancy-screening include pre-pregnancy screening (this MOST preferred because cannot treat during pregnancy) vs. routine OB screening vs. L&D serum IgG vs. newborn cord blood or PCR and even the possibility of universal newborn screening.

Diagnostic testing is warranted in patients who come from endemic areas AND present with electrocardiogram abnormalities (wide range, including 1st degree AV block, afib, PVCs, RBB, low voltage), thromboembolic phenomenon, HFrEF otherwise unexplained, and megacolon or megaesophagus.

Treatment

There are two approved treatments for Chagas Disease, both for extended duration (see image below for dosing)

1) Benznidazole x 60 days

2) Nifurtimox 90 days

Both treatments have high side effect profiles (GI, CNS, marrow suppression). They are contraindicated in pregnancy, though safe in lactation, and contraindicated in severe hepatic and renal dysfunction. These medications also may be hard to come by locally.

The IDSA offers guidelines for who should and should NOT be treated. On the list for who should be treated includes: anyone with acute Chagas, all children with acute/chronic infection, reproductive age women, and people with impending immunosuppression. On the list of people NOT to treat, includes adults with advance cardiac and/or GI manifestations (treatment doesn't reverse these), unless people have impending immunosuppression. Also, not during pregnancy and not in severe hepatic or renal dysfunction. 

Finally, Dr. Heindel recommends this book, The Kissing Bug, written by a first generation immigrant journalist and author, whose family was directly impacted by this disease and who follows the socio and geopolitical forces that influence the management of Chagas in the US immigrant population today.