A recording of this presentation is available HERE.
Check back for a written summary!
Anticoagulation (Nguyen, 12/10/2025)
A recording of this presentation is available HERE.
***
Thanks to Dr. Bao Chau Nguyen for a great review of Anticoagulation this week, with a quick review of warfarin, heparin/LMWH, and a particular focus on the Direct Oral Anticoagulants (DOACs), which have become the mainstay of anticoagulation.
Dr. Nguyen reminded us of the current 2025 indications for Vitamin K antagonist (warfarin), which have dwindled to three at this point
- mechanical heart valves
- atrial fibrillation with mod/severe mitral stenosis (esp rheumatic disease)
- antiphospholipid syndrome (APLS)
She also reminded us of the many challenges with Vit K antagonists, which include frequent monitoring, drug-food interactions, and drug-drug interactions.
Current indications for DOACs as first line:
- non-valvular Afib
- treatment of VTE (DVT/PE)
- prevention of VTE (extended)
- select stable PAD/CAD
Summary of indication and dosing of available DOACs:
Dabigatran
- AF: 150 mg BID, reduce to 110 mg BID (age >80, high bleed risk, interacting drugs), Avoid if CrCl <30 (varies by region)
- VTE: 5 days parenteral therapy, then 150 mg BID, 110 mg BID if elderly or high bleeding risk
Apixaban
- AF (stroke prevention): 5 mg BID, Reduce to 2.5 mg BID if ≥2 of the following: Age ≥ 80, Weight ≤ 60 kg, Creatinine ≥ 1.5 mg/dL (or CrCl <30–50 depending on guideline nuance)
- VTE: 10 mg BID x7 days, then 5 mg BID
- Extended therapy (>6-12 months): 2.5 mg BID
- AF: 20 mg once daily with food, reduce to 15 mg daily if CrCl 15–49 ml/min
- VTE: 15 mg BID x21 days, then 20 mg daily with food
- AF: 60 mg daily, reduce to 30 mg daily if CrCl 15–50, Weight ≤ 60 kg, certain P-gp inhibitors
- VTE: 5 days of initial parenteral anticoagulation, then 60 mg daily (or 30 mg if meeting criteria above)
Reversal agents for DOACs:
Factor Xa inhibitors (Apixaban, Rivaroxaban, Edoxaban): Andexanet alfa (preferred when available), 4-factor PCC 50 units/kg if andexanet unavailable
Dabigatran: Idarucizumab 5 g IVAdjuncts: tranexamic acid, local control, supportive care.
There are now practice guidelines for pausing and restarting DOAC in setting of non-urgent surgery
Finally, Dr. Nguyen presented three important 2025 updates on DOACs:
1) DOAC vs. warfarin in CKD patients (SCr<25), a metanalysis of >71K patients with Atrial fibrillation and CKD, which found that standard dose of DOAC compared to warfarin showed decrease risk of CVA, systemic embolism and ICH, with similar risk of bleeding. HOWEVER, inappropriate dose reduction of DOAC resulted in increased risk of CVA and death. Take home: DOACs are safe and effective in patients with AFib and decreased GFR but should be regular/full dose.
https://www.jabfm.org/content/early/2025/01/16/jabfm.2024.240155R0?utm_source=chatgpt.com
2) DOAC for patients with BMI >50: retrospective cohort study of 754 patients that compared DOAC to warfarin and found a non-statistically significant trend toward favoring DOAC (outcomes CVA, all cause mortality, major bleeding). Take home: DOACs are probably better than warfarin for morbidly obese patients with BMI>50.
https://www.sciencedirect.com/science/article/pii/S240584402417627X?utm_source=chatgpt.com
3) Reduced dosage of DOAC in extended treatment of VTE: systematic review and metanalysis of 5 RCTs looking at recurrent VTE, major bleeding. Found no significant increase in recurrent VTE between reduced vs. full dose, significantly lower bleeding risk in reduced dose group. Take home: It appears safe and effective to reduce DOAC to half dose after treating for acute VTE (usually 6 months).
Family Communication in Palliative Care (Wagner, 12/3/2025)
A recording of this presentation is available HERE.
***
Thanks to Dr. Andrew Wagner, who gave a really thoughtful and important Grand Rounds this week entitled, Palliative Care Pearls. He spent the bulk of the time showering us with pearls about how to connect and communicate with patients, particularly at the end of life. He touched on spirituality in medicine and lifted up the notion that good communication is good medicine. The sound quality on the recording isn't excellent, but still is worth watching so that you can experience directly his wisdom and experience.
I highlighted the key pearly questions in bold below.
He highlighted listening and relationship, generous listening, and presence/compassion/empathy. He talked about how death is a part of the life cycle (not a failure) and that healing is coming to peace with mind, body, and soul relationships with spirits on a higher power. If we reframe death as a life cycle event, we can help patients find peace.
One question: "What needs to happen so you can lay your head on your pillow, and say 'I am good'?"
Dr. Wagner talked extensively about centering the patient's identity, values and meaning, which lends itself toward shared decision making: align decisions with values and what matters most, explore "what are you hoping for and what are you most worried about"?, present options in terms of burdens and benefits, and ensure patient and family understand prognosis realistically.
We have the opportunity to offer "a sense of calm", which can be achieved by making eye contact, touch (if/when appropriate), reading the room, modulating voice, sitting down (and ensuring everyone has a chair), arranging the room.
Another possible question: "How are you doing? How is this going for you?"
Imagine if we regarded death as a final stage of growth. Could we then turn toward death as a master teacher and ask "How then shall I live?"
A third question: "What do you know about what the doctors have been telling you?"
Normalize things for patients, "most people in your situations are anxious/fearful-- how are you doing?", OR "Many people are afraid of dying, is that you?"
Palliative care is understanding people's values and goals and creating care plans that are consistent with those values and goals. Everyone gets tired and frustrated with serious illness, but if someone is feeling that way consistently, "it's important for you to tell us that because there are care plans for people who are tired of doing those things".
When dealing with surrogate decision makers, it is extremely important to help the surrogate bring the patient into the room: Tell us about [Joe]. Who was he? What did he love? What made him happy? What was important to him?
A fourth question: "Imagine [Joe] had a crystal ball and could hear all the things we have been talking about; what would [Joe] say?". And then a follow-up once you have elicited Joe's ideals, "I recommend, given what we know about what [Joe] cares about, I recommend . . ." (is this consistent/not consistent with Joe's values.
Dr. Wagner reminded us that physicians can and should be more directive when it comes to Code/CPR decisions.
And when it comes to families that do not want information disclosed to patients, try this fifth question: "I understand you don't want me to tell grandma, but is it okay if I ask grandma if she wants to know more about what is going on?"
Lean into the mystery. Nobody knows.
He also reminded us about self care-- I am enough (see below) and I am not alone (we have teammates, colleagues, chaplains, pastoral consultation), and we should be sharing stories as a means of self-healing.
For those of you interested in the resources he references, here are some:
- Rachel Naomi Remen, MD (Kitchen Table Wisdom and My Grandfather's Blessings) "Healing and the Inner Life: The role of clinician is witnessing>> connection>>healing
- "I am enough" (this he lifted up as important to physicians to remember and recite before stepping into challenging situations. We meet patients AS THEY ARE; our presence is enough"
- "All healing is mutual" (physicians are also healed by the encounter)
- Generous listening-- listening to understanding, NOT fixing, the quality of listening
- Blessing each other-- seeing wholeness beneath illness
- Ira Byock, MD "The Four Things:
- Please forgive me
- I forgive you
- Thank you
- I love you
- Balfour Mount, MD "Human Question": What would you want me to know that will allow me to give you excellent care?
- Harvey Chochinov, MD, "Dignity Therapy"
- continuity of self: "What do you most want remembered about you?"
- role preservation
- generativity
- hopefulness
Finally, some clinician take-aways: 1) holding safe space 2) healing at the end of life 3) honoring intuation and wisdom ("trust your gut, your intuition, your wisdom"). A final useful statement: "We are helping [Joe] to die".
Tumor Lysis Syndrome (Truong, 11/19/2025)
Thanks so much to our Pharmacy Resident, Lam Truong, who gave an excellent Grand Rounds this week on Tumor Lysis Syndrome.
Recording will be posted HERE when available.
In the meantime, enjoy the cliff notes (thanks Cherie Green!)
Tumor Lysis Syndrome
- Oncological emergency from rapid breakdown of malignant cells leading to massive release of intracellular contents into bloodstream
- Overall in hospital mortality is 21%
- Most common in NHL(30%) > solid tumors (20%) > AML (19%)> ALL (13%)
- TLS can either present at initial dx with very aggressive tumors (usually lymphomas/leukemias but occasional very aggressive solid tumors), OR onset can be 3-7 days after chemotherapy - so patients with upcoming chemotherapy get labs 3 days prior to chemotherapy both to make sure they are not already in TLS and to compare post-chemo labs
Diagnosis: Prompt recognition and tx are essential….
4 Lab abnormalities for dx:
Hyperkalemia (tumor cell lysis), Hyperphosphatemia (cell lysis), Hyperuricemia (from breakdown of DNA/RNA-crystal nephropathy), and Hypocalcemia (binds the excess phosphate)
Result:AKI (uric acid crystals, direct cytotoxicity), cardiac arrhythmias (hyperK), and seizures (metabolic disturbances), neuromuscular dysfunction (rigidity)
Symptoms: n/v/d, weakness, muscle cramps, paresthesias, seizures, arrhythmia, hypotension, HF, syncope, oliguria, hematuria, edema, joint pain - so keep your differential broad if patients present with these sxs!
Causes: chemo causing cytotoxic effects, molecular targeted therapies and immunotherapies, can occur spontaneously in setting of large tumor burden even in absence of treatment initiation
Monitor Uric acid, K Phos, Ca, Cr, LDH (high LDH represents rapid cell turnover)
Prevention of Tumor Lysis Syndrome:
Hydration protocol, closely monitor UO, dc nephrotoxins, stop all K agents
Hypouricemic Agents for prevention and tx
Allopurinol xanthine oxidase inhibitor used in intermediate risk patients, prophylaxis in TLS but has slower onset than…
Rasburicase recombinant urate oxidase inhibitor for high risk patients and tx of active hyperuricemia works rapidly (risks: hemolytic anemia in G6PD deficiency). Loading dose 3 mg IV x 1
Management: Use Tumor Lysis Order Set
- Look at criteria and lab monitoring - some need additional doses of rasburicase and q6 hr labs
- HyperK: use protocol
- Hyperphos: treat first with binders and concurrently treat hypocalcemia
- HypoCa: look on the line above, don't treat first. Treat Phos first!
- HD for usual indications (refractory hyperK, fluid overload, etc)
Acute Liver Injury (Deis, 10/29/25)
A recording of this presentation is available HERE.
Many thanks to Dr. Faith Deis for an awesome presentation this week on Acute Liver Injury (ALI). For those impatient folks out there, the most important take home points are:
1) While the combination of alcohol and acetaminophen can actually be hepato-protective, a pattern of heavy ETOH use + fasting followed by moderate to high dose of APAP can be particularly hepatotoxic and make vulnerable patients more susceptible to ALI.
2) N-Acetylcysteine (NAC) replenishes glutathione with is hepatoprotective and shows benefit for ALI of multiple etiologies (not just APAP intoxication); when in doubt and/or when in the midst of a work-up, give NAC empirically for any undifferentiated ALI, even if APAP level is normal.
A few more pearls from Dr. Deis's talk follow. . .
Acute Liver Failure= Acute liver injury (as indicated by elevation in AST/ALT) + Coagulopathy (INR>1.5) + Hepatic Encephalopathy
Much like many of us use LactMed for breastfeeding safety, there is an excellent NIH source, LiverTox, which compiles all the evidence we have on liver toxicity of medications. Just last night while precepting, a resident and I used this resource to understand whether GLP-1 medications may be implicated in rising transaminases in a patient with poorly controlled DM2. This is a great resource!
Dr. Deis introduced us to the idea of using the "R factor" to help distinguish between intrahepatic and cholestatic patterns of liver injury.
From the 2021 ACG Guidelines. You can see how both the LiverTox and the R factor are involved in your clinical decision about 1st line testing for abnormal liver enzymes:
A little physiology and pathophysiology of APAP Toxicity, which you will note involves the CYP-2E1 pathway (5-9% of hepatic metabolism of APAP) and NAPQI, which leads to hepatocyte necrosis. In APAP overdose, more of the pathway is pushed to the NAPQI pathway! This is important in consideration the mechanism of action of NAC, which actually helps to replenish glutathione, and therefore shift the ASAP metabolism pathway away from the toxic one and back to the healthy one.
Dr. Deis also shared an interesting set of studies on the interaction between APAP and Alcohol on liver metabolism. This is super interesting! It turns out that if APAP and alcohol are ingested simultaneously, alcohol's metabolism actually has a protective effect on the liver's metabolism of APAP, keeping it in the non-toxic pathway. BUT if alcohol is ingested prior to APAP administration (and particularly in the setting of prolonged fasting, which is not uncommon during an alcohol binge), then the use of APAP is pushed toward the NAPQI pathway and is more likely to be hepatotoxic. Practically speaking, then, if a patient has an alcohol binge, and then consumes even moderate doses of APAP at the tail end/after the binge, those moderate doses may lead to a disproportionately toxic impact on the liver. This means, then, that you can have acute liver injury (and even failure) from a therapeutic dose of APAP.
What about NAC?
Turns out that NAC's protective effect on the liver extends beyond APAP ingestion. In a 2021 Metanalysis , authors found a small but stastitically significant mortality benefit in patients with non-APAP induced liver injury and improved mortality (see table below). There are actually few downsides to NAC (the only absolute contraindication is allergy to NAC itself, care with volume needed to infuse for patients for whom volume could be problematic). In sum, American College of Gastroenterology 2024 Guidelines actually recommend NAC be administered to all patients with ALI while work-up is in progress.
A bit on Alcoholic Hepatitis (which may be on your ddx in someone with binge drinking behaviors)
-Remember the Alcoholic hepatitis rarely has AST/ALT elevated above 400-500 and the AST/ALT ratio should be somewhere around 1.5 and the Total Bilirubin is almost always >3.
The 2024 ACG guidelines on alcohol associated liver disease have a really nice set of flowsheets (for those of you who love flowsheets) that nicely outline the evaluation of Alcoholic hepatitis and the subsequent decision tree around using (or not using) steroids, remembering that steroids have downsides (infection, GI bleed, hyperglycemia, AKI, psych) and should only be used in appropriate candidates.
On a final note, we must be careful with patients with ALI who also undergo alcohol withdrawal. Phenobarbital, which has become widely used in our institution in the last year, is relatively contraindicated, as are sedating medications (e.g. benzos). That being said, alcohol withdrawal is a dangerous condition that could result in ICU transfer and/or even death, so we need to be treating them. A reminder that librium/chlordiazepoxide, which has widely fallen out of favor, may be the best option in these patients.
So much good learning!
Thanks for making it to the end.
Dr. Deis' references:
Ghosh, A., Berger, I., & Remien, C. H. (2020). The role of alcohol consumption on acetaminophen-induced liver injury: Implications from a mathematical model. Journal of Theoretical Biology, 510, 110559. https://doi.org/10.1016/j.jtbi.2020.110559 ouci.dntb.gov.ua+1
Forget, P., Wittebole, X., & Laterre, P.-F. (2009). Therapeutic dose of acetaminophen may induce fulminant hepatitis in the presence of risk factors: A report of two cases. British Journal of Anaesthesia, 103(6), 899-900. https://doi.org/10.1093/bja/aep322 OUP Academic
Ghosh, A., Berger, I., Remien, C. H., & Mubayi, A. (2020). The role of alcohol consumption on acetaminophen-induced liver injury: Implications from a mathematical model. Journal of Theoretical Biology, 510, 110559. https://doi.org/10.1016/j.jtbi.2020.110559. (Note: duplicate to #1 – keep one)
Lee, W. M., Kaplowitz, N., et al. (2020). Acute liver injury with therapeutic doses of acetaminophen (≤ 6 g/day): A prospective study. Hepatology, (in press). https://pubmed.ncbi.nlm.nih.gov/33306215/ PubMed+1
Whitcomb, D. C., & Block, G. D. (1994). Association of acetaminophen hepatotoxicity with fasting and ethanol use. JAMA, 272(23), 1845-1850. https://doi.org/10.1001/jama.272.23.1845 (from PubMed 7990219)Alzheimer's Disease 2025 (Mendius 10/15/2025)
A recording of this presentation is available HERE.
***
Thanks to Dr. Mendius, SMGR Neurologist, for a practice-changing Grand Rounds presentation on Alzheimer's Disease (AD) in 2025. Dr. Mendius shared that he had updated this presentation from 2022, and whereas in 2022, he was filled cynicism and despair regarding the diagnosis and treatment of AD, just three years later, he is filled (and filled us) with tremendous hope.
Gosh, don't we all need a little more hope these days?! Well. . .here it is, in the form of GR notes on AD!
Two important primary care practice changers right up front:
- Primary care providers should be ordering a serum blood test for diagnostics-- Lumipulse G pTau217/ß-Amyloid 1-42 Plasma Ratio -- for patients with cognitive impairment and in whom you suspect Alzheimer's Disease
- Primary care providers should refer ALL patients with cognitive impairment/concern for dementia to neurology for assessment for new anti-amyloid treatments if they meet indications
Major neurocognitive disorder criteria
- Acquired
- disabling decline from prior level of function (be aware that if you are declining from a relatively high level of function, you may still have a significant dementia)
- single cognitive area sufficient
Cognitive domains
- learning and memory (ability to acquire, store, recall info)
- language (comprehend, repeat, produce in reading/writing/speaking)
- executive function (plan for something, e.g. get to store and back with all the things)
- complex attention (sustained focus/attention on something, divided attention)
- perceptual motor (take a visual, auditory or tactile stimulus and make a complex response)
- social cognition (can you process social cues, appropriateness of their and your own behavior, theory of mind-- understand their processes)
Ddx of Dementia
- Alzheimer 60-80% (most common by far)
- Vascular 15-20%
- Lewy Body 10%
- Frontotemporal 2-10%
- Parkinson's Dementia 2%
- Mixed 10%
- Other: Huntington, CJD, CTE
Life Expectancy: at age of 70, 3-10 years at time of diagnosis. Average is 7 in AD, but 6-20 years is what Dr. Mendius quotes to patients.
"Reversible" Dementias: Alcohol, Depression, Metabolic (Thyroid, Parathyroid, B12/folate), Infectious (HIV, syphilis, long COVID), Structural (NPH, subdural hematoma, tumor)
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| Top Score=30, 26 is lower limit of normal |
Dr. Mendius prefers the MOCA due to combination of executive function, language function, visuospatial function and memory. Formal neuropsych testing costs thousands of dollars and 2 days of work. Comprehensive Dementia Review (CDR) is used a lot in research studies but not used much in clinic.
A few pearls on Parkinsonism and Dementia
- Parkinson's Disease (PD) has significant dementia component, 40-60% of PD patients "dement" during the course of their disease
- There is an important difference between Lewy Body Dementia and PD Dementia>>stiffness/tremor/slowness/postural instability presents WITH the dementia at time of onset. Also presents with REM sleep, visual hallucinations, vivid dreams.
- In PD, dementia presents late, 5-8 years after the onset of tremor/movement disorder
Mild Cognitive Impairment: 20% of population >70 has MCI. Most will remain stable, about 25-40% progress to dementia (10-15% per year). People with MCI presenting with primarily short term memory group is most likely to progress to AD
RF: age, smoking, obesity, lack of exercise
Alzheimer's Disease
Genetic Autosomal Dominant occurs in <1% of AD, mutation amyloid precursor
Only 7.5% of AD presentation presents <65 years (some genetics, some non-genetics)
Cardinal features of AD:
- Memory impairment-- generally begins with declarative episodic memory (time/place) BEFORE semantic and procedural memories. Anterograde long term episodic amnesia. Trouble laying down new memories. In MOCA task, give 5 words to remember>> if unable to recall words with hints indicate more significant Alzheimer pathology
- Executive functioning-- anosognosia "I don't know I have a problem" (If someone comes in worried about their memory, they usually don't have dementia, if their spouse is worried>> more likely to be a problem)
- Visuospatial impairment: ability to draw cube, numbers on clock
- Language difficulties: "like pruning a tree", language becomes very simple, words to describe things begin to disappear, circumlocution (talk all around a word to describe something)
- Behavioral Symptoms: apathy and social disengagement, irritability/wandering/aggression tend to be late. Capgras phenomenon: "this is not my wife"
- Apraxia: motor tasks, e.g. show me how you brush your teeth, use a razor to shave
- Olfactory dysfunction is typically late
- Sleep disturbance: frequent arousal
- Seizures 10-20% of patients with AD have seizures
- Motor: myoclonus, frontal release signs late in the course
Neuroimaging reveals specific atrophy patterns:
Alzheimer Molecular Biomarkers
- Currently studying and targeting amyloid and tau, microglia
- NEW this year!!!! Lumipulse G pTau217/ß-Amyloid 1-42 Plasma Ratio (17970) is a serum test that is sufficiently diagnostic for AD, some pretty good numbers: 91% positive predictive value and 95% negative predictive value (Palmquist 2025). You can reduce the "indeterminate population" down to about 10%. Seems to be covered by insurance!
- Can be used in the amnestic/MCI population
- This test should not be done on a "normal" (i.e. not cognitively impaired) patient
- Lumipulse is necessary to get into trials for antibody infusions
Amyloid is in the brain for a reason>> part of the innate immune system, involved in synaptic formation and repair, organizing long term memory and synaptic organization, also involved in moving things from cell bodies into dendrite and axons
There are TWO Current anti amyloid antibodies that are available:
1) Lecanemab: against protofibrils, used in MCI and mild AD dementia, 10mg/kg every other week. Infusion reactions are common 26% (need to watch 4 hours after first three infusions). need frequently MRI scans to look for flare/T2 for edema, hemorrhage and hemosiderin (12-17% of patients, most asymptomatic, but 9/900 had significant hemorrhage)
-Efficacy demonstrated in study of 1800 patients, 18 months, outcome: CDR, 30% slowing of decline, marked reduction of amyloid in the brain, improvement best if amyloid reduced to 15-20% of what you expect in AD population. Efficacy is maintained to a couple of years for those who respond. NEW Subq injection (weekly) just approved.
2) Donanemab: goes against deposited plaques, this is a monthly injection, need frequent MRIs
-Efficacy : similar to Lecanemab -- 30% slowing in decline, side effects: 24% edema, hemorrhage/hemosiderin in 30% (vs. 13% in placebo arm)
FUTURE????
Tau seems like major target we will be treating in the future>> tau stabilizes microtubule bundles (internal cytoskeleton of the neuron). Also involved in transport functions. Functional tau has a specific distribution, pathologic tau clumps and destabilizes the microtubule>> neurofibrillary tangle. Stages of AD seem related to Tau.
Microglia also seems like future possibility>> microglia is brain's immune system (lymphocyte infiltrated into the tissue)
170 drugs in various stages of development!
Lifetime interventions for dementia prevention: see the Lancet image below: ~30-40% of dementia is preventable over a lifetime.
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| 2024 Lancet standing commission |
Methamphetamine Associated Heart Failure (Gordon, 10/8/25)
A recording of this presentation is available HERE.
***
Thanks so much to Dr. Lily Gordon for a really impactful presentation on Methamphetamine Associate Heart Failure. We see SO much of this condition in the hospital, and at times it can literally feel like the Wild West. Having a structured presentation helped me to understand where to focus my medical an advocacy efforts, as well as contextualizing the problem within our current times.
Epidemiology and Trends
For example, it was helpful for me to hear that methamphetamine use rates have increased significantly in the last decade (see graph below), that the entire west coast is experiencing an disproportionate burden of meth-induced heart disease (see map below), and that patients with meth-induced heart failures have a documented longer length of stay and higher cost and disease burden.
My lived experience as a hospital-based family doctor was confirmed that patients with this disease carry a high burden of social determinants of health, including housing instability and low SES, as well as disease occurring at a younger age and male-gender predominant.
I was fascinated to revisit the physiology and pathophysiology of meth-induced heart failure to be able to understand that there are two dominant pathways through which methamphetamine impacts cardiac output, leading to heart failure: 1) direct myocyte toxicity as well as 2) sympathetic activation.
Interestingly, for patients who use methamphetamine, binge pattern of use (leading to higher rates of inflammation), co-use with alcohol (even in low and moderate range), and an as-of-yet undiagnosed genetic predisposition are associated with meth-induced HF, whereas route of use (IV vs. smoke vs. snort) and duration. This has also been my experience-- that some patients can use for decades and not develop cardiomyopathy, whereas others can use in binge-like fashion for a relatively short period of time (less than a year) and develop heart failure.
Diagnosis and Treatment
A reminder from Dr. Gordon that Meth-associated Heart Failure is a diagnosis of exclusion. There are no consensus guidelines on diagnostic criteria. In point of advocacy, patients with a new diagnosis of heart failure AND concomitant meth use tend to have a longer delay in getting an ischemic evaluation, as shown in the data from this 2024 paper from Kersey, et al (see below). A reminder that most patients with a new HF diagnosis should get an ischemic evaluation as part of their diagnosis.
1) Is the damage from methamphetamine permanent?
answer: limited data from Germany (Schurer, 2017) found that the ejection fraction in patients with hear failure OFTEN improves significantly with meth cessation (as compared with continued use). This, in my opinion, may offer our patients some true HOPE.
2) Are there treatment options to help me stop meth?
answer: there is good data that CONTINGENCY management (i.e. payment/gift cards and/or rewards) is the most effective intervention to decrease methamphetamine use and get to sustained cessation.
Non-FDA approved (but evidence based) interventions that can be effective in helping with meth cessation include naltrexone+ bupropion (contraindicated with concomitant opioid use), mirtazapine (ideal for co-treating depression), and psychostimulants (in case of underlying ADHD).
3) What if I cannot stop?
answer: GDMT is still indicated and can improve outcomes. Patients with ongoing methamphetamine use should still be offered full GDMT. We could do better! Active meth use is not reason to withhold lifesaving treatment. The chart below shows evidence that we can be more diligent about providing full GDMT for these patients.
answer: GDMT is still indicated and can improve outcomes. Patients with ongoing methamphetamine use should still be offered full GDMT. We could do better! Active meth use is not reason to withhold lifesaving treatment. The chart below shows evidence that we can be more diligent about providing full GDMT for these patients.
Empric Antibiotics and the Antibiogram (Patel, 9/24/25)
A recording of this presentation is available HERE.
Thanks to Omi Patel, PharmD for an excellent presentation on Empiric Antibiotics, Antibiotic Stewardship and Diagnostic Stewardship in the Hospital. We are so lucky to have a close working relationship with our pharmacists who offer interdisciplinary team care.
I don't know about you, but I LOVE antiobiograms! I love local data. I love the compilation of local data into a useful tool and I love evidence-based medicine.
See a piece of current local SSRRH Antibiogram below. Note Omi's reminder that organisms with <30 isolates should be interpreted with caution. As a small hospital, some of our bugs are reported out with under this number. This means the sensitivities should be assumed with more caution.
Unsurprisingly, the overwhelming majority of our Gram negative bacteria are E Coli, and it is important to note that E Coli's sensitivity to various antibiotics has changed over time. See the graph below to see how our local E Coli's resistance to Ceftriaxone has increased (also note how poor our sensitivity to Cipro is!)
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Anal Cancer Detection (Mejia Powell, 9/17/25)
A recording of this presentation is available HERE.
Dr. Rob Mejia Powell gave a really awesome talk this week about Anal Cancer Screening. He reminded us that, while anal squamous cell carcinoma-- almost entirely HPV-related -- is rare in the overall population (1-2 cases/100K person years). While most people are not high risk and should NOT be screened, there are higher risk populations who should definitely be screened with anal pap smears and referred to high resolution anoscopy (HRA), which is available through SRCH for internal and external referrals. Take a look at his presentation for some really great info. If you just want the brief notes, you'll miss out on the butt jokes.
Here's a reminder of what patients with anal cancer "look like", survivors of anal cancer: https://youtu.be/QYR3GWWAmjE?si=kolJuD1TrdgWXMBU
"Say the word 'anal anal anal' a million times until your friends get used to it."
Take a look at this table to see the relative incidence in certain risk categories:
Known risk factors include age, HPV infection (especially vulvar neoplasia in women), receptive anal intercourse, and immunosuppression (e.g. HIV, chronic steroid/immunosuppressants). Also note that the highest growing group in women.
Pathogenesis of anal cancer is similar to cervical cancer: Exposure to HPV > persistent infection > precancerous high-grade squamous intraepithelial lesions (HSIL, anal intraepithelial neoplasia (AIN grades 2 or 3)) > invasion to ASCC
Who should be screened?
- People with HIV
- MSM (especially with HIV)
- Women with history of cervical/vulvar/vaginal neoplasia
- Transgender women
- Solid organ transplant recipients, IBD (esp perianal Crohn's) and those on chronic immunosuppressants
Does screening work?
The ANCHOR Trial, published in NEJM 2022 was a multi-site RCT that showed that, YES, screening at risk populations does work to prevent anal cancer. Primary outcome: anal cancer. Test subjects: Men with HIV age >35. Study found 9 anal cancers in the treatment group (those screened>> HRA>> treatment) vs. 21 cancers in the observation group. This equates to a 60% decrease in anal cancer.
How to approach the topic of anal cancer screening with patients:
1) Explain what an anal pap smear is: what are we looking for? what are we trying to prevent?
2) Get an HPI: anal itching? bleeding? pain? difficulty stooling? presence of anal lesions?
3) Anal Pap: get cytology and HPV prior to digital exam>> use Dacron swab (wet with water, place 2-3 inches across anal verge, aggressive angling)
4) Digital anal rectal exam (DARE)
5) Refer abnormal anal paps to high res anoscopy (HRA) (see chart)
Summary chart:
Ehlers-Danlos Syndrome, Dysautonomia, and MCAS: Diagnosis and Management in Primary Care (Ohringer, 9/3/25)
A recording of this presentation is available HERE.
This week's Grand Rounds, by Dr. Alison Ohringer, was so phenomenal that I have literally been thinking about it nonstop since she finished. The topic-- Ehlers-Danlos Syndrome, Dysautonomia, and MCAS-- doesn't exactly sound titillating, but after years in primary care taking care of patients with chronic symptoms that I don't always know what to do with -- I had a serious physician "AHA moment".
Dr. Ohringer started with a silly meme that has now become an earworm for me: "If you cannot connect the issues, think connective tissues."
I have long thought of rheumatology and/or autoimmunity as a linking factor for non-specific symptoms in patients, particularly in women with fatigue, dizziness, and other systemic malfunctions. I also have long dreamed of studying how our enteric nervous system interacts with the central nervous system (leading to diarrhea, constipation, and anxiety), but I cannot say I had specifically tied in connective tissues to the issues-- until yesterday.
If you are a primary care provider, I definitely recommend watching this one! If you just want my notes, here goes. . .
Hypermobility= the ability of a joint to move beyond the normal range (can be isolated and/or benign (e.g. gymnasts) or generalized and/or symptomatic, impacting multiple joints and leading to pain, fatigue and can be associated with other symptoms)
Spectrum of severity of hypermobility:
Ehlers-Danlos Syndrome (EDS): a group of conditions characterized by one or more of several common features: skin hyperextensibility, joint hypermobility, and tissue fragility, with subtypes distinguished by family history, clinical criteria, and oftentimes genetic testing.
Hypermobile Ehlers-Danlos Syndrome (hEDS), previously referred to as EDS type III, the most common subtype, is diagnosed by hx and clinical criteria. There is no genetic test. Many experience symptoms of Mast Cell Activation Syndrome (MCAS), Postural Orthostatic Tachycardia Syndrome (POTS) and related dysautonomia, small fiber neuropathy, and migraine
Hypermobility Spectrum Disorder (HSD) is diagnosed by history and clinical criteria, on a spectrum ranging from asymptomatic to chronic pain. Some may have some of the hEDS comorbidities, though they may be less severe
Prevalence:
- EDS 1/20-40,000 (vascular EDS 1/100K)
- hEDS 1/3000-5000
- HSD: ~1/500
This schematic below depicts Dr. Ohringer's explanation for the relationships between the issues. Note that MCAD=Mast cell activation disorders.
Symptoms of mast cell activation include a variety of organ systems, including not only allergy, but also cardiologic (hypotension, tachycardia), GI (diarrhea, cramping), and constitutional (fatigue and even memory/concentration problems).
MCAS (mast cell activation syndrome) = MCAD + abnormal labs
Dysautonomia and POTS:
Dysautonomia: all disorders of the autonomic nervous system resulting from imbalanced sympathetic/parasympathetic activation - can be a clinical diagnosis, can be diagnosed with certain tests
POTS: a form of dysautonomia meeting 2 specific diagnostic criteria: - History of orthostatic intolerance with or without systemic symptoms - Correlation of symptoms with a sustained increase in upright HR by at least 30 bpm (40 bpm if pt <20yo) within 10 minutes of standing or head-up tilt, without orthostatic hypotension
Common symptoms in patients with MCAD and POTS/dysautonomia
General: fatigue, night sweats, anaphylaxis, weight changes
HEENT: itchy/watery eyes, nasal congestion, itchy throat
Cardiac: light headedness, pre-syncope, palpitations, tachycardia, labile BP
Pulm: shortness of breath, wheeze, cough
GI: refractory acid reflux, intermittent abdominal pain, nausea, vomiting, diarrhea
GU: bladder irritability and frequent voiding, uterine cramps, heavy menstrual bleeding
Derm: hives, itch, flushing, rash MSK: long bone pain
Neuro: LH/dizziness, brain fog, neuropathy
Diagnosis and Evaluation:
- Assess for hypermobility using the Beighton Score (score results dependent on puberty and age)
- Assess for EDS "red flags" (screening for vascular EDS and risk for ruptures, see image below)
- Eval for hEDS then possibly for HSD once the red flags for the high-risk, genetic EDS subtypes have been ruled out
- Eval for comorbid dysautonomia and/or MCAD
- Rule out mimics (e.g. iron-deficiency, vit D deficiency, allergy, GERD, etc)
Management
This was my favorite part of the presentation-- for a cohort of patients that almost feel untreatable, Dr. Ohlinger gave us SO many ways to consider treating these patients. The general idea is outlined again on her schematic in green (details below). Trigger avoidance, mast cell stabilizers, Autonomic Nervous System regulation, and H1/H2 blockers.
Trigger Avoidance:
Low-Histamine Diet
AVOID • Aged cheeses/Cured meats
• Fermented foods (sauerkraut, kimchi, yogurt)
• Alcohol (especially red wine)
• Vinegar-containing foods (pickles, soy sauce)
• Certain fish (tuna, mackerel, sardines)
• Leftover meats and fish
• High histamine fruits: strawberries, citrus fruits,
bananas, pineapples, papayas, plums, etc.
• High histamine vegetables: spinach, eggplant,
avocado, tomatoes, pumpkin, etc.
INCLUDE: Foods that are generally safe include:
• Fresh meat and freshly caught fish
• Fresh fruits (excluding those listed above)
• Fresh vegetables (excluding those listed above)
• Dairy substitutes (rice milk, coconut milk)
GOOD Eating Habits
• Eat fresh, home-cooked meals.
• Freeze leftovers immediately to prevent
histamine formation.
• Limit processed and packaged foods
Mast Cell Stabilizers:
Autonomic Nervous System Regulation
- Systemic symptoms: Glycemic control [1st line], Duloxetine or venlafaxine [1st line]
- Compression: Compression socks (ideally to thigh) [1st line] Abdominal binder IF no pelvic floor dysfunction [2nd line]
- Electrolyte repletion: Daily oral rehydration solution [1st line] • Normalyte powder, or LMNT powder, or DIY with ¾ tsp table salt, 2 tsp powdered sugar, ¼ tsp cream of tartar, squeeze of lemon for taste, all in 750 mL water 1-2x/day
- Autonomic nervous system retraining: Vagal tone exercises [1st line] see image below
- Symptomatic orthostatic tachycardia from POTS: Cardio-selective beta blocker (or propranolol if no asthma/resp sx) [1st line] Ivabradine (Corlanor) 5mg bid [2nd line] Fludrocortisone [3rd line] Midodrine [4th line]
H1/H2 Blockade
H1: allegra, loratadine, etc
H2: high dose famotidine
Pro Tips:
1) IF you cannot get a patient in with a genetic counselor, primary care CAN order an Invitae Genetic Panel
• Iron repletion for goal ferritin >50 (or >100 if baseline inflammation)
2) Low hanging fruit for everyone:
• Ferrous sulfate or iron bisglycinate M/W/F (Pure Encapsulations OptiFerin-C) if GI sx from other iron
• Vitamin D repletion for goal vitamin D >30
• Magnesium glycinate before bed is good for everyone who doesn't have diarrhea
I particularly appreciated how Dr. Ohlinger finished off her talk: with primary care strategies for managing what is a patient population that has often been dismissed, stigmatized, mislabeled, and struggled with a undeniably fragmented system. . .
Validate lived experiences: “Your symptoms are real and recognized.”
- Lean in to the "I don't know" with a commitment to find solutions together.
- Use structured frameworks (Beighton, consensus criteria) when possible to guide workup.
- Document functional impact clearly to support referrals and accommodations
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