Spine Surgery for the PCP (Athanassious, 7/15/26)

A recording of this presentation is available HERE.

Many thanks to Dr. Christian Athanassious, orthopedic spine surgeon, who gave a really great Grand Rounds Treatment of the Spine for the PCP. The recording is worth watching! For those who prefer the written word. . .

Key learning points:

-The cervical and lumbar spine contains mobile segments>> most likely to develop problems (in contrast to thoracic spine)

-Cervical DJD can often radiate to the scapula

-Be sure to give high enough doses of gabapentin (e.g. 300mg QHS) for acute back pain, helping pts sleep improves pain

-Myelopathy with acute change in function (e.g. ability to hold a cup, balance) needs urgent eval

-If patient has >6 months pain with stenosis on MRI, they are unlikely to get better and should be referred to spine surgeon

-Spinal precautions: no twisting, bending or lifting > 10 pounds (fusion x  6 weeks, then can increase weight to 25 pounds x 3 months, laminectomy x 6 weeks)

Neck Pain

-Radiculopathy: compression of cervical nerve roots: deep aching, electrical feeling, stabbing, numbness/tingling (must be differentiated from carpal tunnel syndrome)

-DJD means "less hydration in the disk level" (doesn't mean there is compression nerve or pain generator)-- most adults will have 1-2 levels of DJD on imaging, must always correlate with history and physical exam findings

-Most common cervical problem is C5/C6:  neuroforaminal narrowing will affect the C6 nerve root (weak biceps, wrist extension, deltoid weak)

-Second most common: C6/C7: numbness and tingling over forearm, 2nd and 3rd digit (radial), wrist flexion weakness, triceps weakness

-if a cervical problem > 6 months, should refer to spine surgery

-Myelopathy: can present as a step-like decline (from one day to next), more urgent than radiculopathy. Pain doesn't follow dermatomal distribution because whole spinal cord is being compressed

-while nerve roots can recover (even after 1-2 years of injury), spinal cord injury does not recover as well

-surgical emergency if acute change in function

-"I was walking with a cane independently, and now I feel like I am drunk, I cannot control my feet, I do not know where my arms/legs are in space">> needs cervical and thoracic MRI and spine surgery consultation, may need ED visit

-sudden change in handwriting, in ability to hold a cup

-bowel and bladder dysfunction are rare (need major compression)

Lumbar Pain

Less urgent low back pain: sciatica/back pain

More urgent: cauda equina

L1-L5/Sacrum (6 vertebrae)

Discs: annulus fibrosis (outer fibrous layer), nucleus pulposus (gelatinous)>> pain from annulus being torn, another part is nerve roots being compressed or the pulp putting pressure on the nerves  caustic to nerve root, can cause pain). Acute annular tear, release of NT and tear can cause acute pain>> PT, back precautions, NSAIDSs vs. oral steroids

Non-operative management of acute lumbar disc herniation

-NSAID
-Physical therapy

-gabapentin/lyrica: make sure to dose gabapentin high enough

-oral steroid

-referral to pain mgt for epidural steroid injection

-brace (for fracture, first line for fracture tx unless severe compression of nerve root, patient with a body habitus that doesn't allow, or emphysema dx cannot tolerate) >>vertebroplasty/kyphoplasty: spine surgeon, IR, pain mgt surgeon (okay to call spine surgery if we have questions about what to do)

Ddx lumbar Pain: arthritis, stenosis, DJD (if bad enough), facet disease

Back symptoms:

-axial back pain: doesn't radiate (stenosis, arthritis in facet, severe DJD leading to bone on bone)

-radicular: irritates the nerve root, radiates down legs or out to arms, or to scapula (if thoracic, can radiate mid back toward ribs)

-loss of balance (spinal cord compression)

-loss of dexterity (spinal cord compression)

-weakness (can happen with nerve root or spinal cord compression)

***

Neck surgery:

-Most common: Anterior cervical discectomy and fusion (ACDF), less common disc arthroplasty (if disease limited to 1-2 levels)

-Disc removed, spinal cord and facet decompressed>> spacer placed. If fusion, plate placed over the top (if just arthroplasty, no plate placed)

-Disc arthroplasty: not indicated for >2 disc levels, facet disease often a problem. Usually indicated only in young patient with little facet disease, short hx of axial neck pain, acute issue 2/2 fall or accident (disc replacement). Many will eventually need a fusion

Normal ACDF recovery: 

    -some degree of difficulty swallowing (no need for swallow study), have to chew longer, cut smaller. Pay attention when swallowing. Can last weeks to 1-2 months, almost always resolves

    -pain in front of neck

    -mild swelling in front of neck>> make sure breathing okay, can speak, eat and drink. Can consider TXA post-op to prevent seeping

    -mid-scapula pain: spacers cause stretch on facets and capsule and can cause posterior neck that radiates to scapula

    -strength doesn't come back right away, can continue to see recovery up too 2 years post-op

    -neck braces after fusion (1 level 4 weeks, 2 levels 8 weeks, 3 level 12 weeks in brace)

Abnormal ACDF recovery:

    -C5 radiculopathy (difficulty lifting shoulder) common after severe spinal stenosis due to posterior drift, not permanent, give brace so arm not hanging, will resolve over time

    -redness/infection of surgical site (if no fever, can rx cephalexin; if fever, may need admission for IV abx, MRI to ensure infection is superficial)

    -any NEW dense weakness>> get MRI

    -Horner syndrome: symptomatic treatment, lubricating drops for eyes

surgical decompression (microdiscectomy)

Low Back Surgery

    -microdiscectomy most common

    -laminectomy (full removal) vs. laminotomy

    -#1 indication for spinal fusion is mobile spondylolisthesis (pt flexes and extends and has >3mm motion between flexion/extension). If spinal stenosis and symptoms correlate, not improving 3-6 months, intolerable of pain

    -Why fuse?

        -DJD with stenosis

    -Adjacent level disease

        -degenerative scoliosis

Access lumbar spine from the 1) front (anterior retroperitoneal approach): incision in midline of stomach, go around peritoneum, fuse in retroperitoneal. 2) lateral anterior retroperitoneal approach, 3)  posterior fusion

ALIF: anterior lumbar interbody fusion. Very stable, access via vascular surgery (higher risk of bleeding), powerful way to treat patients IF treating L5/S1 (cannot be accessed frmo the side). Downsides: post-op bleeding, post-op infection (superficial vs. deep (abnormal labs, fever/vital sign instability), DVT/PE (increased due to vessel manipulation), sympathetic chain compromise 

PLIF: posterior lumbar interbody fusion. Less effective, more problematic. Have to take down a lot of paraspinal musculature, removal of bone and ligament from posterior canal. Cannot correct deformity as well as ALIF. 

EXLIF: minimally invasive procedure, eXtreme lateral interbody fusion. Much smaller incision (compared to PLIF). Can use large cage. large graft to increase stability. L5-S1 cannot be accessed due to the anatomy (pelvis in the way). Can get anterior thigh numbness/hip flexion weakness (psoas mm)

What requires urgent spine surgery attention?

-Myelopathy: quick change in function, send to ED, call spine surgeon

-Severe radiculopathy with weakness

-If symptoms > 6 months, doesn't need ED eval but should refer to spine surgery (especially if MRI finds stenosis)

-Cauda equina: severe excruciating back pain, weakness on exam, numbness ins addle, bowel/bladder incontinence. Usually caused by acute event (should be treated within 48 hours, bowel and bladder function may not return)

From Reactive to Proactive: Building Systems to Prevent Patient Harm and Improve Quality of Care (Krishan, 5/27/26)

A recording of this presentation is available HERE.

Human Papilloma Virus: what's new in 2026? (Jordan, 5/20/26)

A recording of this presentation is available HERE.

Cardio-Obstetrics (Soneji, 5/13/26)

A recording of this presentation is available HERE.

Thanks so much to Dr. Nisha Soneji, a new local expert in Cardio-Obstetrics! She joined SMGR in the fall and gave us a great presentation this week that was very family medicine friendly-- on the overlap of cardiovascular disease (hypertension, pre-E, valvular disease) and the peripartum time. It's a great presentation, and she is going to be an awesome resource to have here in our community.

"Pregnancy itself is a major stress test-- you are basically on a treadmill all the time".

US has a shocking rate of maternal mortality-- the highest among developed countries, 49.5/100K live births (highest for black women in the US) and CVD is the major contributor to maternal mortality. Significant racial and ethnic disparities are seen: black women 2.6x risk of death compared to white women. Advancing maternal age increases risk of maternal mortality (87.1 death/100K births)



CVD accounts for 33% of all maternal deaths. Whereas infectious risk of maternal mortality have decreased over the last decade, CVD related deaths are increasing, 2/3rds are considered preventable.

Most common cause of CVD death:

• congenital heart disease
• ischemic heart disease
• valvular heart disease (esp stenotic disease: aortic stenosis, mitral stenosis)
• hypertensive heart disease
• congestive heart failure (peripartum cardiomyopathy, esp post partum)Contributing factors; delayed response to warnings (pregnancy symptoms mimic CVD), ineffective care, misdiagnosis, lack of continuity post partum (risk continues up to 6 months after delivery)

2/3 of maternal deaths occur during post partum period, when women tend to make less time to be seen (caring for newborn, going through hormonal changes, PP depression, etc)

CV changes during pregnancy: "Pregnancy itself is a major stress test-- you are basically on a treadmill all the time". If you are at risk for CVD, in can present in pregnancy or post partum.

See image below:
Normal findings in pregnancy: systolic murmur, elevated JVP, displaced apex, edema, increase in chambers on TTE, small pericardial effusion
NOT normal in pregnancy: S4, diastolic murmur, fixed splitting second heart sound, moderate to large pericardial effusionNOTABLY Unchanged in pregnancy: LVEF, REF, PASP


American College Cardiology


Who should be referred to Cardio-OB?
change in functional status
asthma not responsive to therapy
palpitations
chest pain/tightness that doesn't improve
syncope
SBP not controlled on med
oxygen saturation <90%
hx chemo can lead to HF in pregnant women (10% risk)
existing cardiac conditions: valvular disease, CHF


Risk Assessment:

Modified WHO 2.0 risk calculator


CARPREG

Who doesn't need referral: isolated sinus tachycardia, benign ectopy, mild hypertension managed on meds, normal BNP or TTE. If in doubt, refer!

Preconception counseling: high risk patients should get preconception counseling when risk of death is so high that they really should NOT get pregnant.
Assess risk
medication review (cannot use ACE/ARB)
genetic consultation (if CHD, increased risk of fetal CHD)Testing:
TTE: echo is first line monitoring tool
Troponin, BNP not routinely monitor, but good idea to check baseline if risk factors and/or symptoms. Can then compare post partum to antepartum BNP. Troponin can be ordered routine at the lab.BNP>200 can be normal in pregnancy
BNP >300 VERY suggestive of heart failure
CXR for shortness of breath
Treadmill stress tests in pregnancy can be done safely
Zio/holter
CT chest with angiogram can be considered if benefit>> risk
Hypertension in pregnancy
Chronic hypertension (<20 weeks), gestational hypertension (>20 weeks), preE (+organ dysfunction, Pre-Eclampsia with severe features, Eclampsia (with seizures)
BP Goal <140/90
Daily low dose ASA during pregnancy for preE/eclampsia prevention >12 weeks EGA in moderate to high risk patients
Benefit>>Risk
Pre E: 71% increased risk CVD, 2.5 risk CAD, 4x risk HF

Meds for BP: labetolol (shouldn't be used in asthma, decompensated cardiac function), can use nifedipine

Arrythmias
pregnancy increases aryrthmias due to increased blood flow and hormonal changes. Most common CV complication. Increases with age >41 years.
Preventable
SVT: vagal maneuvers, beta blockers, calcium channel blockers, digoxin (can be added if BB don't work) flecainide
Defer ablation to post partum (due to risk)
Afib: BB, digoxin, 2nd line calcium channel blockers, can be safely cardioverted
Can get implanted devices if need pacemaker

Heart Failure should be treated during pregnancy, cannot be deferred to post partum
-bad outcomes for moms and babies


Peripartum Cardiomyopathy
diagnosis of exclusion
new EF <45% without reversible cause
RF: maternal age, htn, preE, prior cardiomyopathy
present in 3rd trimester to 1 month (up to 6 months PP)
20% recurrence rate, contraception is important
risk of death 5-10% at 1 year
most people with recover EF, but future pregnancy brings higher risk
Meds: loop diuretic, hydralazine, isosorbide dinitrite, digoxin, beta blocker, ((IV dobutamine can be used), AVOID: ACE/ARB/ARNI, SGLT2
Vaginal delivery is recommended unless cardiogenic shock (safer than LTCS)

Valvular Disease
preconception counseling important, especially with L side valve disease (even if asymptomatic)
send to cardiology, need to get stress test pre-conception
TTE q trimester for mild-mod valve disease
R sided valvular disease (e.g. TR), need fetal echo, rarely need intervention>> vaginal delivery preferred
L sided valvular disease: regurgitation well-tolerated, stenotic disease NOT well tolerated in pregnancy (e.g. AS or MS, even if mild). At high risk for atrial arrhthmias

CAD in pregnancy
1/10K hospitalizations after pregnancy
Risk increases 3x
RF: age, black race, eclampsia/preE, known CAD, traditional risk factors (e.g. DM)
Spontaneous dissection (SCAD) most common cause of pregnancy-related MI (conservative tx recommended)

Gout: An Update (Maniscalco, 5/6/26)

A recording of this presentation is available HERE.

Thanks to Dr. David Maniscalco, SMGR Endocrinologist, for an update on Management of Gout. 

1st MTP

Common signs/symptoms

• 80% of gout is monoarticular process (single ankle, knee, 1st MTP, wrist, olecranon bursa)

• significant pain ("cannot even let a bedsheet touch it")

• red/hot/swollen

• flares commonly overnight and early morning (pts may describe this)

polyarticular gout (<20%) becomes an issue in pts with longstanding gout that hasn't been treated, can be seen in hospitalized patients, can be associated with fever, can mimic sepsis
tophaceous gout: pts who haven't received care as outpatient, develop significant tophi, pain can hit critical point with severe pain

Diagnosis

• ideal: presence of uric acid crystals on synovial fluid analysis (crystal-proven gout)

• less ideal: often diagnosed on typical clinical presentation + hyperuricemia

NOTE: serum uric acid level can be erroneously low when a patient is in the midst of a gout flare, so don't be fooled (should recheck uric acid after flare resolves)

Management
Based on 2020 American College of Rheumatology Guidelines for Management of Gout
Indications for urate lowering therapy:

• 2 or more gout flares within a year

• no need to start after first attack>> monitor and see if repeated attacks

• tophaceous gout (rheum should manage)

• radiographic damage attributable to gout (erosions on x-ray)

• hx multiple flares over time (even if <2/year)

• first gout flare with CKD >3

• uric acid >9 (significantly high) or hx nephrolithiasis

no need to start with incidental elevation of uric acid in the absence of gout symptoms
Urate lowering therapy:

• Allopurinol is PREFERRED first-line agent

• recommended including for pts with CKD>3 (safe)

• allopurinol does not cause kidney injury (safe in AKI as well)>> decreased GFR can increase risk of side effects, e.g. severe cutaneous reactions (Stevens Johnson, DRESS), which are rare but do happen>> lower dose if rash develops

• in pts of southeast Asian descent (Han Chinese, Korean, Thai) and African American>> check for alelle HLA B5801 before starting allopurinol

• Feboxostat is used as an alternative to allopurinol

• previously concerned recommended for patients with CKD>> now no longer an indication

• used rarely

• per current guidelines, contraindicated in pts with hx CVD (increases risk of CV death, mixed data)

start lowest dose and titrate up monthly, need serial uric acid measurements to titrate
Goal uric acid <6mg/dl (for non-tophaceous) <5mg/dl (for tophaceous, managed by rheum)

• starting dose: allopurinol 100mg daily (lowest dose), feboxostat 40mg daily (lowest dose)

• decreases risk of hypersensitivity reactions, decreased risk of flares with initiation

• there is no inherent danger in increasing allopurinol>> max dose 800mg

• max dose of feboxostat is 80mg

• about 1/3 of patients will be at goal with 300mg allopurinol

• for pts with CKD3, start with 50mg allopurinol (titrate up by 50 mg/month until goal uric acid)

• There is NO need to stop allopurinol in AKI in hospitalized patients

• can lead to gout flares and do not worsen AKI

Acute flare management
Colchicine is first line most effective within first 36 hours of flare (doesn't work better if started after): 1.2mg, followed by 0.6 mg 1 hour later, then 0.6mg BID until flare resolves
If not resolving, transition to prednisone
If attack is going >48 hours, choose something other than colchicine (prednisone preferred)
Prednisone: 0.5mg/kg 2-5 days, then taper over 7-10 days
NSAID: naproxen 500mg BID, indomethacin okay (often cannot be used due to comorbidities)
ICE!!!!
Medication Prophylaxis

• Any time you are starting urate lowering therapy, you need prophylaxis at the same time!!

• Colchicine is preferred agent for ppx: 0.6mg daily, okay in CKD (CrCl<30, 0.3mg/daily or 0.6mg qod)

• If cannot do colchicine (diarrhea is common), NSAID, e.g. Naproxen 200 or 250mg BID (limited by CKD)

• Last option is prednisone  for those who cannot tolerate colchicine or NSAID: pred 2.5-7.5mg (usually start with 5mg), if worried about diabetes, try to get away with lower dose (e.g. 2.5mg daily)

• Titrate up q2-4 weeks (with uric acid via lab to direct)

Duration of prophylaxis: continue for 3-6 months AFTER target uric acid (longer for tophaceous gout)
Lots of crystal still in joint, take a long time to dissolve, people tend to have flares until treated for a long time

Medication monitoring
Allopurinol is safe (stop if rash), CBC/CMP after initiation, liver issues are not much of an issue, can monitor periodically q6-12 months (CBC, CMP), more frequently if renal impairment. Similar for colchicine.
Diet: low purine diet, low alcohol, reduce high fructose corn syrup, no concrete evidence on cherry juice, avoid red meats/organ meats/scallops, mussels, meaty fish
HCTZ increases uric acid>> change and may help uric acid improve
Losartan is gout-friendly-- evidence it decreases uric acid

Myth busters:

• No need to stop urate lowering therapy while having a gout flare

• No need to stop urate lowering therapy in AKI (can lead to bad flare)

• Okay to start urate lowering therapy DURING a gout flare (despite what UptoDate says)

• Colchicine is safe and NOT highly toxic and can be safely taken as long as adjusted for renal impairment, drug interactions

Refer to rheum:
polyarticular gout
tophaceous gout
unable to be treated with allopurinol/feboxostat

Defensive Medicine (Bialostozky, 4/29/26)

A recording of this presentation is available HERE.

Hooray for Generalism Finding Meaning and Purpose in a World of Hyper-Specialization (Gerlach, 4/15/26)

A recording of this presentation is available HERE.

Immigration Status and Negative Health Impacts (Yadira Raya-Cervantes, 4/1/2026)

A recording of this presentation is available HERE.

Northern California Center for Well Being: HeartWorks Cardiac Rehabilitation Program (Roosen, 3/25/26)

A recording of this presentation is available HERE.

Thanks so much to Erin Roosen, program manager for our local Center for Well-Being's Cardiac Rehabilitation Program, HeartWorks, located at 500 Doyle Park Drive, Santa Rosa 95405. She gave an inspiring presentation on the value of Cardiac Rehabilitation. She certainly inspired me to give a more robust bedside recommendation for my cardiac patients. 

Cardiac Rehabilitation is an evidence-based intervention that literally saves lives. . .

HeartWorks offers: 

• A 3 month focused exercise program for patients with heart failure, any cardiac procedure (valve replacement or repair, stent, CABG), and recent STEMI/NSTEMI
• Cardiac rehab
• decreases need for hospitalization by 25%
• helps people increase activity level
• improve quality of life (65% improvement on PHQ9)
• improves diet
• decreases mortality (47% decrease in mortality if you complete the program, compared to attending only 1 session)
• Cardiac rehab includes pre and post exercise vitals and 3 lead EKG monitoring
• Phase II is 36 sessions (2-3 days/ per week, depending on availability): goal is to improve aerobic capacity (by increasing the 6 minute walk test and/or improve MET levels). This is generally covered by Medicare insurance
• Phase III is an additional 3 month non-monitored program paid for by participants (24 sessions, 2/week)
• Once participants complete cardiac rehab, they are offered a 3 month voucher for our local YMCA

What was most moving about Erin's presentation was the improvement of patients' quality of life and mental health, as well as a recognition that decreasing loneliness (we are in an epidemic) improves mortality as well. 

We are working with HeartWorks to ensure more of our patients complete cardiac rehab with a special personal focus on our Spanish speaking patients (Erin said they have both a Spanish speaking MA and physiotherapist).

Of note, referrals must be done through a patient's cardiologist!

Update on Hormonal Treatment of Menopause (Mason, 3/18/26)

A recording of this presentation is available HERE.

Many thanks to Dr. Antoinette Mason for an important presentation on Hormonal Treatment of Menopause. Dr. Mason is a graduate of our residency program and is also a graduate of our integrative medicine fellowship.

Her stated goal of the presentation: to empower clinicians to use menopausal hormonal therapy (MHT) 

Before 2002, menopausal patients regularly received MHT. After 2002, when the Women's Health Initiative (WHI) was stopped early due to concerns regarding increased rates of breast cancer, blood clots, dementia, CVD and more. This led to a lot of fear and an abrupt change in practice-- as a result, most clinicians have been trained to avoid hormones in menopause.

Over the past 15 years, there has been lots of re-evaluation of the data. Also formulations of hormones used today are not the same as those used in the WHI. Timing matters, age of start matters. 

We are now reckoning with fear, beliefs, lack of evidence, training. . .many of our leading organizations (Menopause Society, ACOG, Endocrine Society) have guidelines that confirm that MHT is safe and appropriate for many populations. 

bio-identical means "same compounds made by the ovaries" (estradiol  (E2) + micronized progesterone), but there are LOT of different formulations of these as well.

Risks of MHT:

• blood clots: associated with oral estrogen (including OCPs, conjugated equine estrogen, oral estradiol). Oral estradiol safer than OCPs, 3-4x risk OCP vs. oral estradiol. But transdermal (patches, gels, cream) do NOT increase risk of blood clots. 
• gallbladder disease: cholelithiasis, cholecystitis, low but increased
• endometrial hyperplasia/cancer: unopposed estrogen therapy (need to give estrogen therapy)
• breast cancer: WHI showed small increase in rate of breast cancer, but estrogen alone actually reduced breast cancer. Risk for breast cancer seems driven by progestin >5 years (when use mircorinized progesterone NO increased risk of breast cancer but no good RCTs). Safest approach: use MHT<5 years. We may never have RCT with clear data. 

Hormonal Cheat Sheet:

FDA approved indications for MHT:

• vasomotor symptoms: hot flashes, night sweats
• genitourinary syndrome of menopause: urinary/vaginal symptoms, dyspareunia
• prevention of osteoporosis in people who are high risk (e.g. family hx, comorbidities), do NOT treat osteoporosis but does prevent fractures
• treatment of early ovarian failure or surgical menopause

Additional benefits (not FDA approved)

• musculoskeletal syndrome of menopause: changes in joints, connective tissues, muscles (pain, stiffness, new joint pain that is NOT arthritis)
• mood/cognitive changes/sleep
• quality of life
• miscellaneous short and long impacts: fractures, colon cancer, breast cancer (estrogen alone), diabetes, improvement in insulin resistance, better blood glucose control for people with DM, LDL reduction (transdermal estradiol), reduced CVD, dementia (mixed studies, ?vascular)

Timing hypothesis: earlier is better (age <60 years of age or <10 years since menopause onset)

How to rx MHT:

• use bio-identical hormones
• use transdermal estrogen whenever possible
• start early, use lowest effective dose (titrate to symptom control)

Absolute contraindications: current breast cancer or hx of breast/endometrial cancer, current or hx VTE, severe liver disease, pregnancy, uncontrolled severe hypertension (get BP under control first)

Assess risk: If high risk for VTE, do NOT use oral estrogen. If high risk CVD, look at lipids, A1c, recommend yearly mammogram, osteoporosis risk

1. Do they need birth control or do they not want to ovulate? (if yes, consider IUD/OCPs)
2. Do they have a uterus? (if yes, they need some progesterone)
3. Are they having regular cycles? (if yes, luteal dosing of progesterone, if no, can use continuous progesterone)

Progesterone decline

For most people in menopause, progesterone starts to decline and estrogen gets chaotic. Eventually post-menopause, both get low but in the transition it's very unpredictable. A lot of people have symptoms associated with low progesterone state initially. Most common: anxiety, insomnia, shortening cycles, headaches. Can just use micronized progesterone alone in early menopause symptoms: e.g. start with 100mg orally or vaginally (same capsule) just 2 weeks after ovulation (in luteal phase).  . .Can later increase dose or add estradiol. If cycles are irregular and unpredictable, can use continuous progesterone at night. Vaginal progesterone can be less sedating.

LOOP events

LOOP events (luteal out of phase event): ovulatory event, and then in the luteal phase (week or two after ovulation, you get another ovulation>> can cause anemia, other issues for people).

OCP can work, but for those who don't' want OCPs, can use progesterone to stabilize the endometrium and try to reduce bleeding. Start 100mg QHS (lowest dose), can increase to 200-300mg to stabilize bleeding. Adding estradiol can help (oral helps more than transdermal but have to balance safety and benefit). Don't forget birth control!

Common Progesterone side effects: constipation (fiber/magnesium/water), morning grogginess (can try earlier in the evening, switch to vaginal formulation)

Estrogen Decline

estrogen decline symptoms: vaginal symptoms, hot flashes, irregular period

Can start estradiol (start with lowest patch>> twice weekly better than once weekly, smaller, adhesive less sticky). Currently supply chain issue, harder to get right now

Follow up 4-8 weeks because hot flashes should respond quickly>> if they don't get better, need more estrogen

Vaginal Estrogen 

Vaginal estrogen should be used liberally for genito-urinary symptoms of menopause. Vaginal estrogen can be used SAFELY for almost everyone, including post partum. Can decrease UTIs in elders. Cheap, easy, effective tool. Note there are TWO vaginal rings (one rx'd for local therapy, one for systemic therapy. Make sure you know which you are rx'ing)

Testosterone: Low dose topical testosterone VERY low dose for sexual dysfunction of menopause (1/10th male dose). Always optimize estrogen and progesterone first to see if symptoms improve. Do not put testosterone gel on clitoris.

OB and GYN update: highlights and practice changing articles from 2025 (Lund & Bacon, 3/11/2026)

A recording of this presentation is available HERE.

(late entry)

Many thanks to Drs. Allison Bacon and Erin Lund for an excellent review of important practice-changing literature from the fields of OB and Gyn in 2025. It's obviously important for us to keep track of practice-changing advances, but the task can be overwhelming and burdensome, particularly if it's an area you are not using on a daily basis. 

Dr. Bacon started us off with 3 practice-changing OB papers:

1) Quality-Improvement (QI) Strategies for the Safe Prevention of Preterm Birth, ACOG Committee Statement 17, May 2025

Key take homes:

• current US NTSVD (normal term spontaneous vaginal delivery) rate is 25.6% but ranges 18.5-84.6%, and the WHO goal is 23.6%>> the variability represents opportunity for improvement through local QI projects
• in fact the CMQCC initiative in California reduced rates from 26% to 22.8% (from 2014 to 2019)
• suggested strategies to improve vaginal delivery:
• local policies and procedures to support vaginal birth
• labor support huddles
• team trainings for interpretation of fetal heart rate monitoring
• unit based policies for oxytocin and management of labor dystocia

2) FIGO good practice recommendations on preconception care: A strategy to prevent preterm birth, Int'l Journal of Gynecology/Obs 2025

• preterm delivery is responsible for most neonatal and infant deaths
• many risk factors for preterm birth can be targeted outside of pregnancy
• baby-centered assessment as a part of preconception care
• examples risk factors and interventions
• teen pregnancies>> preconception counseling 
• optimize screening/treatment of chronic conditions (e.g. hypertension, DM, thyroid)
• mental health>> screen for mental health and eating disorders
• infectious disease>> HPV vaccination, screen for STIs, preserve oral health
• nurtitional status>> discuss BMI, dx/tx iron-deficiency

 

3) Air Pollution Linked to Risk of Spontaneous Preterm Birth, Celeste Krewson, 2025, Contemporary Ob/gyn

• talk to patients about PM2.5 as mechanism for for social drivers of health, use of air filters?
• solutions driven by housing, community, city planning

Dr. Lund presented the second half on the important gyn literature:

1) ACOG Clinical Consensus #9: Pain Management for in-Office uterine and cervical procedures

• healthcare professionals tend to underestimate the pain people with uterus may feel during a procedure, providers may deem pain management not needed and therefore not offer to patients
• despite discrepancy between level of pain between patients and providers, patients still do report high degree of satisfaction with in-office gyn procedures
• higher pre-procedural anxiety and anticipated pain are 
• associated with higher pain scores
• THEREFORE options for pain management should be offered to all patients for in-office procedures
• IUD: topical anesthetic is more effective over placebo or misoprostol
• lidocaine spray>> lidocaine injection (?2017 RCT)
• no evidence to support pre-procedure NSAID, though may help for post-procedure pain
• use of ultrasound has been shown to decrease pain of IUD insertion

• EMB: 10% lidocaine spray (3 puffs before), naproxen 30 minutes prior reduced pain in one study, performing EMB with full bladder may reduce pain
• Uterine aspiration: paracervical block, NSAIDs pre-procedure (for post-procedure pain), oral benzos do not reduce pain but do reduce anxiety
• Colpo: topical/intracervical lidocaine recommended for biopsies and LEEP

• Trauma-informed care: universal trauma precautions, given patients control over procedure, ask permission to begin/continue procedure, careful with words used (e.g. not bed, table)

2) Management of Recurrent Bacterial Vaginosis, ACOG Clinical Practice Guideline Update 12/2025

• Recurrence is common! 66% of patients experience recurrence of BV within 12 months of initial diagnosis
• Recent RCT comparing partner therapy for recurrent BV (treating partner with oral and topical) showed marked decrease in recurrence (35% vs. 65% at 12 weeks), absolute risk was BIG -2.6 recurrences per person per year
• Increasing evidence that BV should be considered an STI: predominantly occurring in sexually active populations, associated with new/multiple sexual partners, there is microbiological evidence that sexual partners exchange bacteria
• Ideal people to partner treat: monogamous male/female partners (shared decision making for other scenarios)
• Coverage may vary-- CA extended partner therapy applies to STIs (GC/CT), MAY be applied to BV (pharmacy dependent)
• Note clindamycin gel can weaken latex condoms
• Also note, recent evidence based guidelines say it's okay to drink alcohol and take metronidazole!! 

Slow Medicine: finding the balance between knowledge, care and humanity (Paul Nguyen, 3/4/26)

A recording of this presentation is available HERE.

Many thanks to Dr. Paul Nguyen, who gave a moving and important Grand Rounds this week, which he entitled "Slow Medicine: Reflections from a 3rd year resident". What was so compelling about his presentation was how he brought us back to the basics of why most of us came to family medicine in the first place and wove in his reflections on where the rub occurs, and how we might approach it to make it better for patients and for us.

I particularly appreciated his inclusion of two Vietnamese proverbs, which I will leave here for your consideration:

Translation: You only know you're hungry after eating.

Meaning: You may only understand the importance of something once you have experienced it yourself.

Translation: Keep grinding the metal, one day it will turn into a needle.

Meaning: If you keep putting in the hard work, you may wind up with something beautiful and useful

In between these two beautiful proverbs, Dr. Nguyen introduced us to Victoria Sweet's book, Slow Medicine (if you haven't read it, both he and I highly recommend it!) and highlighted some of the core tenets she promotes in her book:

1) Gevuld (Dutch for "stuffed"), in the contest of medicine the idea that wounds can literally fill themselves in, that the body knows how to repair itself, that illness is not always an enemy to defeat. In this model, physicians are stewards of processes, not commanders of outcomes. 

2) Slow ≠ passive: medicine doesn't always require an intervention, time itself may heal. Sometimes the best intervention isn't doing more-- it's doing less. Not ignoring or neglecting but allowing the body's processes to work. 

3) Observation: observation is itself an active clinical skill, paying attention matters, and watching the body heal itself may be our only duty. Tolerating uncertainty is another part of our job. 

I particularly appreciated this slide from Dr. Nguyen, summarizing Sweet's argument and contrasting "fast medicine" (how we do things) to slow medicine (how he wants us to consider doing them):

In this section, he talked about the contrast of metrics vs. meaning, of productivity vs. presence and shared some of the data regarding burnout in the primary care workforce as well as patient perceptions of being held/cared for based on time spent with them. 

And for those of us who have been through residency and/or are witness to our residents going through residents in this era, we can related to these tensions, the feeling of not having enough time to sit with patients BUT wanting nothing more than to have the time to do so. The feeling of data overwhelm without a true understanding of the patient's lived experience.

Dr. Nguyen shared with us two meaningful patient experiences he has had during his residency training-- one that ended with a peaceful death, the other that left a patient without a diagnosis but getting better (who knows why? perhaps it was the time he spent with her?).

And, finally, some wisdom for his juniors and colleagues:

Metabolic Dysfunction Associated Steatohepatitis (MASLD) (Holt, 2/25/2026)

A recording of this presentation is available HERE.

Deep gratitude to Dr. Will Holt, CPMC Hepatologist, who drove to SSRRH from Piedmont at the literal crack of dawn to teach us about Metabolic Dysfunction Associated Steatohepatitis (MASLD) and Alcohol-Associated Liver Disease (AASLD) and then changed hats to spend the morning with our residency leadership as a faculty leader for graduate medical education within Sutter. 

His talk was fantastic! I recommend you watch it.

For those of you who prefer to read, the highlights:

First, MASLD

• We all known that the prevalence of obesity and diabetes have both skyrocketed over the last several decades-- nearing 50% in some regions of our country. 
• 
• Along with these metabolic issues, comes MASLD-- world prevalence is estimated to be 29.8% lowest rates for those of African descent (thought to be both genetic and food access/lifestyle related)
• Risk factors for MASLD include age >50, high BMI and DM2
  
• MASLD is a risk factor for death
• Assume that people are high risk (>50, high elevated BMI, DM2) have MASLD>> screen them for MASH with via fibroscan
• For everyone else with any component of metabolic syndrome (e.g. overweight, a1c>6%, hypertension, HDL<40 (F) and <50 (M), triglycerides>150)>> use FIB-4 to screen first
• if the FIB4>1.3>> Fibroscan,
• unless they are >65yo, then use FIB-4>2.0
• Fibroscan uses a weighted hammer/pulse to measure liver stiffness-- this is available through Sutter Airway)

• Fibroscan <8 is normal (=reassuring, low risk), >14 demonstrates cirrhosis
• for those with a normal fibroscan, focus on lifestyle modification for metabolic disorders
• for those with an abnormal fibroscan, refer to hepatology
• Fibrosis predicts liver-related mortality (see graph below from J. Hepatology 2017)
• stage 0/1 fibrosis: no increased mortality
• stages 2, 3, 4>> increased liver mortality 
• 

As per the 2024 AASLD Guidelines for clinical suspicion of steatotic liver disease

What are the treatment options for MASLD and MASH?

• Pharmacologic:
• Vitamin E: 96 week RCT: reduced fibrosis 41% vs. 31% (placebo)
• Pioglitazone: meta-analysis, reduced fibrosis vs. placebo OR 1.77
  
• There are two FDA approved medications:
• Resmetirom (2024): TRH-beta agonist, 52 week RCT vs. placebo, reduced fibrosis 24% vs. 14%
• Semaglutide (2025): GLP1 agonist, 72 week RCT vs. placebo, reduced fibrosis 37% vs. 22% 
• Non-Pharmacologic: diet/exercise/weight loss
• weight loss improves liver histology! Even 5%!!!
• 
  

Now, a little bit on ALD

• Defining Alcohol use disorder (AUD)
• 
• Biomarkers for ETOH
• Urine tests (EtG, EtS) have a very short detection window (<48 hours)
• PEth is current "truth serum", gives us information about the last 30 days, though there are some false positives in the lower ranges (20-40). Very high results (>400-1000 are very reliable)
• Diagnosing Alcoholic Hepatitis can be tricky!
• elevated MCV (100), elevated WBC, jaundice

• Treatment of alcohol-associated hepatitis with prednisolone (rather than prednisone due to first pass metabolism, when not available, prednisone is acceptable) FOR: 
• Patients WITH Maddrey Discriminant Function >32>> 
• AND WITHOUT
• evidence of biliary obstruction on ultrasound
• uncontrolled infection (especially bacteremia)
• AKI with SCr>2.5
• UGI bleeding
• Severe shock/hemodynamically unstable
• Expect 3 month recovery (bili will remain high)
• You can wait a couple of days before starting prednisolone (e.g. if any of the above active), pts can still benefit with delayed start
• Use the Lille score to predict (7 days) who will respond

• N-Acetylcysteine= mixed bag, there does appear to be a mortality benefit at 30 days but not at 3 months/6 months (NEJM 2011, see image)
• 
  
  
  
• What about liver transplant (LT) in ALD?
• 2011 RCT from France (NEJM 2011) was practice changing, randomized patients with AH without sobriety and first decompensating event  to LT vs. no LT (only <10% deemed candidates)>> found that 1 and 3 year survival was the same for patients with ALD as any other liver disease
• This led to a change in practice in which transplant can/may be considered for alcoholic hepatitis in select patients, not specified as a specific duration of sobriety>> at CPMC, this is called the "limited sobriety pathway to LT"
• Careful patient selection for LT (with ALD) is key. 
• Family support
• Absence of untreated psychiatric disorder
• Agreement by patient with support to LIFELONG abstinence (this can be harder to get to that you might imagine)
• This assessment is done by LT SW at CPMC (often via video visit prior to Transfer)
• We know that patients with AUD will relapse

Ethical Deviations and Inequities in the Delivery of Health Care (Matthews, 2/11/26)

A recording of this presentation is available HERE.

***

Special thanks to Dr. Adora Matthews, Sutter's CME of Inclusion and Belonging. She gave an important presentation on Inequity in the Delivery of Health Care-- as a celebration/reminder of Black History Month and a reminder of our commitment to delivering equitable and excellent care to every patient we serve. 

Dr. Matthews reminded us of four important historical occurrences that still contribute to fractured trust in the medical system for black Americans:

1) Dr J. Marion Sims, often referred to as "the father of modern gynecology", a white man, who operated on black slaves without anesthesia, perfected his hysterectomies and vesico-vaginal fistula repair on black slaves without consent, and contributed to a long-held notion in medicine that "black people don't feel pain the same as white people". After  all surgical assistants resigned due to discomfort with his work, he ultimately forced three black slave women (named Anarcha, Betsy, and Lucy) to assist him in these experimental surgeries.

A statue to honor these three women, the "Mothers of Gynecology" stands today in Montgomery, Alabama. 

2) The Tuskegee Syphilis experiment, which took place from 1932-1972, in which 400 black male sharecroppers were knowingly observed to study the natural history of syphilis, even after cure/treatment for syphilis was widely available (in the form of penicillin!). Spouses were infected, babies were born with congenital syphilis, extreme pathology was documented. This is widely considered the greatest failure of medical ethics in our country. This experiment didn't end until it was leaked to the press in 1972. A formal apology rendered by President Bill Clinton in 1997, calling the experiment "shameful and racist". 

3) Henrietta Lacks was a black woman who was treated in 1951 for cervical cancer at John's Hopkins University. After she died that same year, her cell line (HeLa) was used (without consent) for countless projects, including vaccine development, medical research, most recently for the COVID vaccine development. 110,000 publications are attributed to her cell lines, which are still in use today. The Lacks family was unaware of this use of her cells until 1973, when they were approached by a scientist who wanted to study them. 

These historical truths (and many others) contribute now to systemic inequity and mistrust. We must be aware of these histories, warned Dr. Adora Matthews, when we are caring for black American patients. We must be aware of them when we see current inequities. And while being aware isn't enough, it's a start.

Four current inequities for Black patients:

1) Healthcare access: black and brown patients have higher rates of being uninsured, are less likely to have preventive care, and less likely to have a regular PCP.

2) Chronic disease management: black American women have some of the highest rates (40%) of metabolic syndrome, which doubles CV risk, increases all cause mortality, and is associated with DM, CKD and stroke.

3) Maternal and fetal health outcomes: black women have highest rates of maternal mortality and fetal mortality, even when controlling for SES (see graphs below)

4) Pain management: Biased beliefs about black patients and pain tolerance dating back centuries with no evidence-- still exist today. There is literature from emergency rooms, hospitals and clinics that black patients are less likely to receive pain medication for the same painful condition.

Dr. Matthews reminded us that knowing the history (and the current inequities) is where we begin-- from here we begin to look at systems and address systemic racism in the daily work we do. We turn our grief, sadness, anger and despair into hope for our patients. We confront our own biases by attending lectures like these and participating in unconscious/implicit bias assessment ( Harvard's can be found HERE). 

"Hotter than Ever" Menopause and Non-Hormonal Therapies (Kareer, 2/4/2026)

A recording of this presentation is available HERE.

Update on Atrial Fibrillation (Goyal, 1/26/2026)

A recording of this presentation is available HERE.

***
Many thanks to Dr. Rajat Goyal for a fantastic Update on Management of Atrial Fibrillation, which has really changed over the last few years. Many of us trained in a time where we were taught that "rate control is as good as rhythm". We got pretty accustomed to starting a rate med (beta blocker or calcium channel blocker) and a DOAC and leaving it at that. . . that mantra of the 2000s is not quite right anymore. Turns out that rhythm control is the way to go!

Practice changing pearls:

• Afib begets Afib
• Everyone with atrial fibrillation (including paroxysmal) should be referred to EP 
• Ablation shows better outcomes (decreased progression, improved morbidity and mortality) than medication management alone
• The earlier the ablation, the better (i.e. within first year of onset) because AF is a progressive disease
• Patients with heart failure and AF definitely benefit from ablation
• Patients s/p ablation who show no AF at one year can safely discontinue anti-coagulation
• Lifestyle modification is important: weight loss, alcohol/tobacco use, hypertension and DM management, OSA, and stress

Rhythm vs Rate Control: 

Older studies showed no difference in M&M, BUT subsequent analysis found that patients in sinus rhythm and on anticoagulation had lower risk of death (AFFIRM trial). 

EAST-AFNET trial showed that early rhythm control associated with lower M&M (death, stroke, HF admits, coronary events). Of note, many were treated with anti-arrhythmic, not all were converted via ablation

Once in persistent AF, rhythm control efforts no longer effective. Essentially, AF begets AF due to the structural changes that lead to permanent changes in the conduction system

Ablation:

• Goal is to kill triggers that initiate afib and kill unhealthy tissue. They approach the pulmonary veins and electrically isolate them, but also look at LA, LA appendage, RA, etc.
• Ablation is MORE effective than ablation in controlling AF and maintaining sinus rhythm, and the earlier the better.
• Fewer progress to eventual persistent AF after ablation

What about in setting of HFrEF?

• Yes, they benefit from ablation!
• AF causes decreased CO, RVR, loss of atrial systole and increased MR and TR so in patients with HF, maintaining sinus rhythm is VERY important.
• The CAMERA-MRI study 2017 showed that after ablation the EF improved 18% after ablation compared to 4% with medical rate control.
• A follow up study also showed reduction in mortality, hospitalization after ablation thus became a Class 1 indication (including paroxysmal AF)

 

Ablation Modalities: Pulsed Field Ablation (PFA) created at UCSF in early 80s and alters cell membranes. The mapping is done via catheter which maps the LA and PVs and able to find high areas of voltage to ablate. Pulsed Field ablation a bit more effective than Thermal ablation

Technique isolates PV about 80%.

Complications of ablation: atrial-esophageal fistula. PFA allows more selective injury and less injury to esophagus (so far 0 events). Tamponade < 1%, stroke <.05%, AE fistula <1%, vascular events <3%, coronary spasm 0.14%

Who needs to be on Anticoagulation?

Left Atrial Appendage is where many clots form, so closing that area with Watchman after ablation helps reduce stroke significantly

Ablation + closure vs Ablation + anticoagulation: no difference in strokes long term

See image below:

• for patients with a low CHADS2VASC score (<2 for men and <3 for women), if you can prove no AF at 1 year post ablation, they can safely STOP anticoagulation
• for patients with a higher DHADS2VASC score, most should either be continued on anticoagulation OR be referred for a LAA occlusion.

Smartwatches?

What about everyone with their smart watches? Turns out that smartwatches have terribly sensitivity but pretty good specificity. SO, if a patient has NO AF on their watch, they probably don't have AF. On the other hand, just because the watch shows AF doesn't mean they actually have AF. Intermittently monitor every few months, but consider encouraging your patients to get a smartwatch

Lifestyle modification 

Lifestyle modification is still a mainstay of treatment/prevention of Afib. Patients with AF really need to be counselled on weight reduction, blood pressure management, glycemic control (if DM), alcohol and tobacco use, stress management. They should also be assessed and treated for OSA. Working on these risks is essential for long term maintenance of sinus rhythm