Inflammatory Bowel Disease (Memel, 8/19/26)

A recording of this presentation is available HERE.

Thanks to Dr. Memel for a super packed fact-filled presentation on Inflammatory Bowel Disease (mostly focused this time on ulcerative colitis  with an important preamble on nutrition). Thankfully, she is coming back to do Part 1 in December, because we were all on the edge of seats and we didn't get through the whole slide deck and we want to learn more about Crohn's Disease!

My take homes:

• Ultra-processed foods (containing additives like dyes, emulsifiers, and excess salt) are bad for our gut. In particular, emulsifiers are to be avoided!
• The Mediterranean Diet is the best for patients with IBD and everything else)
• FIBER is actually good for patients IBD (contrary to old thinking), just need to modify the texture as needed for tolerance
• Fecal calprotectin is an excellent screening test for IBD and can be used to trend over time to monitor treatment response
• 5ASA is mainstay of UC treatment (lifelong), budesonide can be added on for flares (less systemic effects than prednisone)

IBD is an idiopathic autoimmune disease with objective inflammatory evidence>> chronic inflammation is key, and it tends to progress in severity

IBD incidence is rapidly increasing worldwide (in both developing and developed countries). Older adults getting more and more IBD>> keep on ddx

Genetic susceptibility (163 genetic loci identified, very genetically inherited) is an important factor. Crohn's has higher genetic risk than UC. Higher risk of passing to first degree relatives.

Environmental triggers causing patients to express the phenotype. Immune system is "over reacting>> changes in gut microbiome>> expression of IBD. Ultra-processed foods, sugar (highest risk factor for developing IBD). Chemicals that allow foods to be shelf stable are the most problematic part of ultra-processed foods. Excess salt causes inflammation in GI tract. Artificial sweeteners disrupt the microbiome. Once bacteria get past the mucosa>> inflammatory cascade!

Emulsifiers (that allow oil and water to mix) are used widely in the food industry (ice cream, peanut butter) are TERRIBLE for the GI tract. Disrupt a mucous layer causing an inflammatory environment. Try to avoid emulsifiers as much as possible, read labels and look to eat things with LESS chemicals in the food label.

What you can do?

• Breastfeeding is protective and beneficial to the  microbiome.
• Pets in the home under 2 benefits children's microbiome (hygiene hypothesis)
• Mediterranean diet (2023 practice update) is the best diet for people with IBD, first degree relatives less likely to develop IBD
• People who eat more fruits/veggies/whole grains have less inflammation in their gut
• Fiber is GOOD for the gut (unless they have a stricture/penetrating disease). All the data suggests them more fiber, less likely they are to flair. Not all fiber is the same. Can cook fruits/veggies and make them softer. Texture can help them be better tolerated (smoothies, cooked veggies)
• Red meat is bad for the colon-- Crohn's and UC, specifically processed red meats (salami, prosciutto)
• Dr. Memel says she always starts with breakfast: oatmeal, fruit smoothies (frozen fruit is cheaper, blended is tolerable), chia seeds can be integrated into everything (and cheap at TJs)

Dieticians for IBD:

Crohn's vs. UC

Labs to evaluate a patient with IBD:

• CRP helpful to track inflammation
• albumin used to assess severity of inflammation in IBD (albumin can inform the dose of infliximab)
• enteric pathogen panel important because infection can provoke IBD flare

Fecal calprotectin: protein released by neutrophils. Most helpful in someone with chronic diarrhea and trying to determine if this is inflammatory or not. If normal fecal calprotectin, much likely NOT IBD. Borderline levels can be tricky, trending in 4-6 weeks can be helpful. Very high needs colonoscopy. Used in IBD to trend over time and track in place of colonoscopy.

Mayo endoscopy score, GI uses as standard objective assessment 

UC Treatment has two parts:

1-induction (put out the fire)

2-maintenance (prevent fire from coming back)

Stride 2 guidelines recommend three goals for treatment of patients with IBD:

1-Clinical remission (living life again)

2-Endoscopic remission (no disease evident on colonoscopy)

3-Complete histologic healing (no inflammation on biopsy)

Treatment protocols are driven by risk to progression to colectomy. Low risk involves mild disease with limited anatomic extent. High risk include younger (<40), extensive colitis, severe disease (Mayo 3), elevated CRP, low albumin (admit to hospital for IV steroids)

IF Mild UC>>5-ASA or budesonide

5ASA formulation and rx depends on where UC is anatomically

3 phenotypes: 

• Proctitis (5ASA suppositories are often good enough), if really struggling can do steroid suppositories as well, can do daily 5 ASA>> taper to qod> taper to q 3 days (for life, otherwise will flare)
• Left sided colitis (5 ASA enemas can reach further): oral + enema at the beginning, if they don't respond, can add budesonide (selective steroid), budesonide foam can be squirted up the rectum (not as far as an enema but easier to use). For maintenance, oral 5 ASA because patients hate doing enemas the rest of their life
• Pancolitis (need oral 5 ASA as well): can do oral budesonide + 5 ASA. Very rare risk of AIN (renal function should be checked once a year)

Budesonide used by GI a lot! Added on as a flare treatment Much LESS side effects than oral prednisone (safer, lower risks of systemic side effects). Not as strong as prednisone

Patients should be on lifelong therapy for UC (to prevent flares!!!)

IF Mod-Severe disease>> Tx is Biologics (see chart below)

There are MANY many biologics. Many more than just infliximab (the original anti-TNF). Patients google biologics and get very scared but the options are many and they are much safer than they used to be. See the triangle of safety down below. Dr Memel tells patients now, "The risk of developing colon cancer from recurrent flares is greater than the risk of being on today's biologics".

Decisions about which agent the gastroenterologist will choose are complex, including insurance/comorbidities/physical needs/travel needs, etc. . .

There is still emerging data on how long patients need to be on biologics. . .Dr. Memel tells people that biologics are "life long therapy" due to the risk of relapse/flare. 

Treatment of acute UC flares

-always order stool cultures, including CDiff (infection is risk for flare)

-always order CRP (GI trends daily)

-trend bowel movements (by nursing)

-DVT ppx is important even if bloody bowel movements due to 3-5x increased risk of VTE (flares are inflammatory)

-40-60mg IV methylprednisone in AM (to reduce insomnia)

-check PPD/quant gold  and Hep B serologies on admission (because they take a long time to come back)

-Try to avoid opioids and NSAIDs due to risk of toxic megacolon

Kratom and 7OH (Dembar & Rubin, 8/12/26)

A recording of this presentation is available HERE.

Thanks so much to our Addiction Medicine Fellows, Drs. Allie Dembar and Rebecca Rubin for a super super important presentation on Kratom and 7OH, two opioid like substances with high dependence risk and rising rates, despite a 2026 California ban on sale of such products.

Please watch their presentation if you don't know what 7OH is and/or if you work in primary care, emergency rooms, with children, etc. . .

Here are my notes:

Kratom is a plant from Southeast Asia, formal name, mitragyna speciosa. The active ingredient, mitragynine, has a mild stimulant effect when the leaves are chewed (think coca leaves from S. America) as well as a mild opioid effect at higher concentrations. 

7OH is a synthetic version of mitragynine, which is much more potent (and only present in <2% of the plant substance). It appeared in the US market ~2024. Some studies suggest higher potency than morphine

Both have been available for sale across the US, mostly in gas stations and smoke shops and until recently were not regulated. In 2026, Governor Newsom announced a ban in California of their sale (though they can still be found in local smoke shops per reliable reports). 

The increase in Kratom/7OH availability has led to an increase in kratom toxicities. By 1200%!

Men>> Women

Age group most affected is 20-39 year olds, followed closely by 40-59 year olds

There have been 233 Kratom-associated deaths between 2015 and 2025, 79% included multiple substances, and opioids are often co-reported

There are advocacy groups pushing for liberation of Kratom/7OH across the country, most of whom are being led by  chronic pain patients who feel abandoned by the medical system and looking for an answer to treatment for their chronic pain (in light of opioid prescription reduction over the last decade+). Kratom and 7OH are largely unregulated. This map below is produced by a pro-Kratom advocacy group. Notice the variance across traditionally aligned red and blue states and even the discrepancy up and down the Pacific coast.

The political landscape is evolving quickly

On July 1, 2026, the DEA "moved temporarily schedule 7OH and related substances to protect public safety". This federal action was aimed at synthetic 7OH (not directly at the plant based Kratom). A Schedule 1 label means that the drug has a high potential for abuse with no accepted medical use. 

Note that 7OH intoxication and withdrawal closely mirror that of opioid intoxication and withdrawal. 7OH is a potent mu opioid receptor full agonist. Small amounts can lead to euphoria>> larger amounts to respiratory depression. 

Withdrawal is functionally similar to opioid withdrawal. Half life is 1-5 hours (patients usually start withdrawing within 2 hours of stopping-- use habits require frequent use during the day, up to 6 times per day). You can increase the half life with chronic use up to abou 24 hours.

Treatment of Kratom withdrawal is buprenorphine, buprenorphine, buprenorophine. . .

Unlike with fentanyl, you will not precipitate withdrawal and you do not need to micro-dose, but can go straight to micro-dose-- 16mg SL plus don't forget your adjunct (ondansetron, loperamide, gabapentinoids, hydroxyzine, and if inpatient, can consider benzos for anxiety/agitation). 

Of note, you can order a sendout lab checking for mitragynine in urine (but this will typically not show up as an opioid in our standard utox).

Functional Disorders, Somatic Symptoms and Chronic Pain (Jones, 8/5/2026)

 A recording of this presentation is available HERE

Thanks to Dr. Kendall Jones for a fantastic opener for R3/Senior Grand Rounds presentation this week. She borrowed from a lecture she attended last spring at the Family Medicine Colloquium by Kaiser Family Medicine teachers. . .but really brought it home to our patient population. 

If you are a primary care clinician caring for patients with functional disorders (think IBS, migraine, fibromyalgia. . .and all those unn-nameable conditions), you should watch this!

Functional Disorders

Medical school trains us well to investigate mechanical/structural abnormalities (e.g. SBO, carotid stenosis, hip fracture), assess for biochemical abnormalities (e.g. low hb, elevated a1c, hyperthyroidism), but does not prepare us for functional disorders-- which, by definition, have no specific tests. Functional disorders are diagnosed with symptom assessments, validated tools, in combination with negativing imaging/labs or other work-up. 

And yet, in primary care, we see a LARGE number of patients with functional disorders. Here are a few:

These patients are challenging. They bring up a lot in clinicians, and they don't always get the care they need. Sometimes they are left to steer their own ship (which doesn't reliably make them better), they get HUGE work ups (all of which turn out negative or equivocal), and they get labels that do not really apply, labels that are hard to remove. 

Dr. Jones reminded us that we use clinical judgement all the time to make diagnoses-- think a viral URI or a migraine. For these patients, we use illness scripts and confidence in our experience. This same notion applies to patients with functional disorders.

Central Sensitization

Central sensitization is a state of persistent CNS hyper excitability in which the brain and spinal cord amplify incoming signals beyond their objective magnitude. The "volume of the nervous system" is literally turned up. This is not psychological. It is driven by neuroinflammation, HPA axis dysregulation, synaptic plasticity in the dorsal horn, reduced descending inhibition, and more. This phenomenon is propagated via ACEs, chronic stress, trauma, perception, expectation, and neuroplasticity. 

I LOVE this fire alarm analogy!

Reminder: our job is NOT to keep searching for a fire.

We need to be able to recognize patterns of central sensitization:

• multi-system symptoms with no unifying biomedical lesion (though don't forget connective tissue and EDS)
• severity out of proportion to objective findings-- the gap is the signal amplification
• symptoms fluctuate with stress, sleep
• prior extensive negative work up but patient remains symptomatic
• presence of ACEs or chronic stress (which patient may not have insight into)
• hypervigilance: symptom tracking, googling, frequent visits, lots of messages
• sensory hypersensitivity: light, sound, temperature, touch, odors (more than just pain)

Language matters

When tests come back negative, avoid "everything is fine", "your tests are normal", "nothing is wrong", "maybe you're stressed". These statements do not explain what IS happening for the patient and leave them searching for another explanation. 

Communication is key!

Remember patients can have central sensitization AND something else!!!

Validated Tools for assessing for Central Sensitization include:

• Somatic Symptom Scale - 8. Gierk B et al. JAMA Intern Med. 2014.

• Eight items rated 0-4 over the past 7 days (GI, back pain, limb/joint pain, HA, CP/SOB, dizziness, fatigue, sleep)

• 8-11 = medium, 12-15 = high, 16-32 = very high.

• Each category increase is associated with 53% more healthcare visits

• CSI: Central Sensitization Inventory. Mayer TG et al. Pain Pract. 2012; Neblett R et al. J Pain. 2013

• Part A: 25 items, scored 0-100 

• Part B: Prior CSS diagnoses (unscored, clinical context)

• Cutoff ≥ 40: 81% sensitivity, 75% specificity for CS syndromes

• <30 = subclinical, 30-39 = mild, 40-49 = moderate, 50-59 = severe

Treatment of Central sensitization:

Education: normalize, reframe: "Your symptoms make sense to me. Let's try to understand what is going on." Discuss the context/ask the question: "What do you think is making your nervous system so sensitive?" Help change their relationship with their symptoms-- to decrease their fear. Remember, having somatic symptoms is part of living inside a body.

Nervous system retraining: mindfulness based pain reduction, breathing exercises, cold exposure (resets the mamalian dive reflex), singing, humming, yoga, meditation, massage (feet and neck)

Central sensitization and Chronic pain

• nociplastic pain happens over months to year; it can be at least partially reversed with desensitization of the oversensitized alarm
• patients have to be patient (months to years) to notice improvement
• patients and physicians benefit from moving away from "symptoms" into acceptance, understanding an rehabilitation>> goal is improving quality of life and increasing function
• movement is key: motion is lotion

Primary care needs united partnership with specialists.

We don't need to get it all done in one visit, even 2 minutes can help shift mindsets

We are not just asking patients to relax, we are helping them re-calibrate their nervous system.

Central sensitization does not invalidate the patient's experience, it only offers an explanation with evidence-based interventions.

Clinicians must NOT miss red flags

References:

Mohabbat AB & Wilkinson J (2023). Central sensitization: when it is not all in your head. Am Fam Physician. 101 (1):92-96

G. Lorimer Moseley & D Butler (2017). Explain pain supercharged: the clinician’s manual. 

tamethebeast.org (refer patients with chronic pain to this website)

Van Oosterwick J et al. (2013). Pain physiology education improves health status in fibromyalgia. Clin J Pain. 29(10):873-82.

Difficult (aka Dysregulated) Patient Encounters (Pimental, 7/29/26)

 A recording of this presentation is available HERE

***

Thanks to Dr. Britni Pimental, who gave us a fantastic presentation on Difficult Patient Encounters. She started by changing our word choice from "difficult" to "dysregulated".  When we label patients as difficult (angry, demanding, emotionally intense), we should be really calling them dysregulated-- shifting this label can help us shift in how we see patients. 

There were SO many pearls in this presentation, I definitely recommend listening to it yourself. But for the notes version:

It's not surprising that patients being seen in the clinic or hospital are dysregulated-- their nervous system is literally being stressed-- they are scared, in pain, feeling a loss of control, triggering old trauma and sensing systemic pressures.

When people get overwhelmed, their executive function goes down. They cannot listen. They cannot process high level medical information.

Clinician response to dysregulation can lead to to an unfortunate feedback loop:

Trigger>>>> Arousal>>>> Behavior>>>>Clinician Response>>>Trigger 

We are not neutral. We are human beings too.

Countertransference is the phenomenon in which our own emotional reaction to the patient is shaped by our own previous experiences. This can lead to helplessness, frustration, avoidance, over compensation, and assertion of control. 

We must strike a balance between empathy and limits/boundaries. Empathy does not require agreement. Most people do better with limits and effective boundary setting helps people who are dysregulated. Rather than being exclusive, empathy and boundaries are complementary.

3 steps to empathic boundary setting:

1. Validate the emotion
2. Set clear limits (without excessive justification-- see above, people's ability to tolerate info is low)
3. Offer alternatives (a small # of choices) to give control back

Restore regulation

Our tone, posture, body language and pacing will impact our patients' behaviors.  Clinician regulation is the most powerful de-escalation tool. Patients are highly attuned to non-verbal cues from clinicians (pacing, tone, body language)

The goal of de-escalation is NOT to win the argument or to convince the patient of a particular viewpoint. The goal is to maintain a functional relationship, create a safe and collaborative environment. 

Self-regulation for clinicians

-lower tone

-slow speech

-adapt a non-threatening posture

-sit down (if safe)

NURSE

Name

Understand

Respect

Support

Explore (options)

Offer choices as much as possible. Patients want to feel they have some say in their care.

Allow for pauses>> to avoid rushed decision-making. People need wiggle room. 

Ask open ended questions

Practice reflective listening

Avoid escalation

-avoid interrupting

-avoid power struggles

-avoid defensive responses

-avoid arguing the facts

A simple self-check re. countertransference:

What am I feeling right now?

What is this patient activating in me?

How is this helping/hurting their car?

Re-engage with your own executive function

-pause

-slow breathing

-relax your shoulders

-consciously slow your speech

-decrease your own physical arousal

RESPOND INTENTIONALLY RATHER THAN REACTIVELY 

The clinician-patient alliance builds trust, creates psychological safety and decreases emotional arousal. Regulation+ relationship + respect= safer encounter

Diagnosis and Management of Osteoporosis (Hamann 7/23/2026)

 A recording of this presentation is available HERE. 

***

Thanks so much to Dr. Kendal Hamann, SMGR Endocrinologist, for an outstanding Grand Rounds presentation on Osteoporosis. Dr. Hamann covered the basics and the nuances of osteoporosis diagnosis, reminded us that the DEXA scan results are only part of the clinical picture, and clarified when bisphosphonates should be first vs. second line.

Please watch the recorded version above if you want all the details.

4 clinical pearls:

• Use the FRAX score (10 year fracture score) to guide who should be treated for osteoporosis
• Even patients whose T score doesn't improve on bisphosphonates, there is a 30-50% decrease in fractures
• Rebound fractures are real. Never start denosumab (Prolia) without a plan for bisphosphonates after completion
• Check DEXA 2-5 years into treatment, at start of drug holiday (which is generally 5 years into bisphosphonates), then 2-5 years later

Osteoporosis= decreased BONE STRENGTH, which is a combination of Bone DENSITY (BMD) + Bone TURNOVER + Bone ARCHITECTURE

Normal BMD T>1.0, osteopenia BMD 1>T>-2.5, osteoporosis T<-2.5

Diagnosis of osteoporosis= 

• Fragility fracture (most commonly, fracture of wrist spine, hip from standing height) 

OR 

• T-score of <-2.5 by DEXA scan. 
• Of note, 50% of people with fragility fractures will NOT meet criteria by DEXA

Normal aging vs. Disease

Bone density peaks around 30 years in women and decreases p after that, with a particular drop after menopause. It is part of the normal aging process BUT also leads to significant morbidity and mortality. 

• Vertebral fractures cause pain, loss of mobility, loss of height, even restrictive lung disease and abdominal issues. Plus, once you have a vertebral fracture, you have 20% risk of a second one in the next year. 
• Hip fractures: 30% 1 year mortality (higher in men), 40% of people never walk independently after hip fx, 25% wind up needing care in long-term care facility

Bone density scan (i.e. DEXA) is a screening tool. But it only captures 60-80% of bone strength. You should be using  the FRAX score (10 year risk of fracture) in addition to the T score to direct treatment

• FRAX: >3% risk of hip fracture, >20% risk of any fracture are indications for treatment
• Usng a T score of <-2.5, about 30% of menopausal women will qualify as having osteoporosis
• 1/2 of women with fragility fracture do not qualify as having osteoporosis on DEXA (i.e. T score will be >-2.5)
• Indications for DEXA:
• women and trans-people >65
• men >70
• any adult over 50 with a fragility fracture
• monitoring treatment
• lots of other people:
• primary hyperparathyroidism
• chronic steroids
• hypogonadism
• premature menopause
• longstanding hyperthyroidism
• celiac disease
• pregnancy w/fragility fracture
• people on GnRH agonists

Risk factors for Osteoporotic Fractures:

Age

History of previous fracture

FALL risk

Family history

Cigarette smoking (1/8 people with hip fx are smokers see below)

ETOH >3 drinks/day

Immobilization

Inadequate Ca and Vitamin D (during childhood, leading to low peak in 30s)

Smoking!!!

Treatment:

Don't forget fall prevention!

Calcium and Vitamin D were given to every patient in every treatment arm of every trial for osteoporosis. They are still the mainstay of osteoporosis treatment and prevention. There is old data demonstrating they definitely decrease risk of fracture. Dosing is all over the place, but Dr. Hamann generally recommends 1000mg of Calcium and 800u of Vitamin D/day. It's fine to get your calcium through dietary means (particularly if you have a history of kidney stones and cannot tolerate supplements), just make sure you're getting 1000mg/day. 

Who should receive treatment?

-anyone with T score <-2.5

-anyone with hx of vertebral/hip fracture from standing

-anyone with 10 year fracture risk (FRAX) > 20%

-anyone with 10 year hip fracture risk (FRAX) >3%

-clinical judgement

Bisphosphonates are the mainstay of osteoporosis treatment. They inhibit osteoclast. Data for fracture risk reduction is robust-- decreased fracture risk 30-50% reduction after about 6 months on bisphosphonates. Cost is low. We have 25+ years of experience now with these meds. 

PO alendronate, ibandronate, risendronate

IV zoledronic acid, ibandronate

Risk of osteonecrosis of the jaw (ONJ) is low but real 1/10,000, risk of atypical femur fracture 1/50,000-1/100,000-- much lower than the number of fractures prevented by the medication.

Side effects: GI 10% (heartburn, upset stomach, nausea), aches (1%), hypocalcemia (check vitamin D and replete  before starting), 1 in 5 people will get a flu-like infusion reaction to zoledronic acid. These should NOT be used in childbearing women. 

Newer agents=Anabolic agents: Romozosumab (sclerostin inhibitor, sq monthly x 1 year, only approved in women), teriparatide & abaloparatide (parathyroid hormone agonists, sq daily x 2 years)

Costly, only approved for 1-2 years

Romozosumab: treat to target T>-2.5, should be used FIRST line for "severe osteoporosis" (T score <-3.0)

Order matters (see image below)-- these anabolic agentsshould be followed by bisphosphonates (not the reverse)

IN particular with denosumab (prolia), fragility fractures of the spine and rebound fractures are real. MUST always be followed by a bisphosphonate. 

order matters!!

Dr. Hamann's General Approach:

Drug holidays and repeat DEXA?

Consider drug holiday after 5 years on bisphosphonate (if not fracturing)

Check DEXA 2-5 years into treatment, at start of drug holiday, then 2-5 years later

When to consult endocrinology?

-intolerance of oral bisphosphonate

-severe osteoporosis (T<-3.0)

-multiple fractures despite treatment

-anyone needing to stop denosumab (prolia)

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.