Understanding Hospice Care (Saeed, 9/30/26)

A recording of this presentation is available HERE.

Penicillin Allergy (Patel, 9/23/26)

A recording of this presentation is available HERE.

Thank you to our Pharmacy Supervisor, Omi Patel, PharmD, for a super interesting presentation this week on Penicillin Allergy. Please do watch the presentation if you have a chance! If not, my notes:

The label penicillin (PCN) allergy is WIDELY used on patient charts. And more often than not, is untrue. Look at the numbers:

And this label, is NOT harmless!

• it can lead to the use of less effective therapies (e.g. cephalosporins are much more effective against MSSA than vancomycin)
• it can lead to more antibiotic resistance and increased risk for c. diff infection
• it can prolong length of stay in the hospital and increase hospital costs (more expensive and less effective abx)
• is can cause paradoxically MORE toxicity (e.g. a septic PCN-allergic patient will get more powerful, less effective, and more problematic drug combinations)

To review, PCN drug reactions fall into four main categories, labeled Type 1( IgE and mast cell mediated), II (cytotoxic and IgG and IgM mediated), III (immune complex, IgG and IgM and complement) and IV (T-cell mediated delayed reactions, which can be benign or severe).

Of note, Type IV (delayed rash) can be everything from totally benign to life threatening (SJS, DRESS). This is important because a patient with Type IVb rash can still be a candidate for re-labeling, whereas a patient with life-thretening Type IVd rash should never receive PCN again!

Immediate/IgE reactions generally occur very quickly, often within the first 1 hour (and almost always within the first 6 hours) of exposure. Also urticaria/hives that lasts longer than a day is generally not life-threatening. An hives reaction that occurs within 1 hour of the 1st dose, lasting less than 1 day (1:1:1 rule) is more likely to be a TRUE IgE allergy.

Patients with a history suggestive of SJS, DRESS, AIN, recent anaphylaxis and/or angioedema should not receive PCN again. Patients with intolerance (n/v/headache) a delayed benign rash (maculopapular, no organ involvement), family history only ("I was told as a child"), or a remote untreated mild reaction (>5-10 years ago) should be considered for a challenge or retesting.

I like these 6 questions for every allergy label:

It's the R chain
Cross-reactivity between PCN allergy AND cephalosporins depend entirely on the R chain (not the shared beta lactam ring). This means that even with a proven PCN allergy, many cephalosporins can be safely used. Omi pointed us to this chart from Northwestern, a link can be found HERE. This can help clinicians and pharmacists safety select a cephalosporin for PCN allergic patients.

PEN-FAST

Omi also introduced us to the PEN-FAST score, which we will be rolling out at SSRRH in the next few months to help de-label patients with PCN allergies. The PEN-FAST score is a way to assess which patients can be safely tested with a direct amoxicillin test (rather than skin testing) as a means to de-label. (of note, regardless of PEN-FAST score, if patients has hx of SJS/TENS/DRESS, they are NEVER eligible for an amoxicillin challenge test). In patients with a PEN-FAST score of 1-2, direct oral challenge (with amoxicillin) is safe and effective.

Patients with a score of 3 need a graded challenge

Patients with a score of 4-5 should NOT be tested with an oral challenge or graded challenge

In a graded challenge, you start with super low dose and see if there is a reaction (if there is, you confirm the label and stop). In a desensitization protocol, patients are treated THROUGH their reaction. 

Of note, in a study done at a Sutter hospital, they found that MOST PCN allergic (37/41) patients are not truly allergic and could tolerated an oral test dose of amoxillin, which then allowed us to de-label them! Some did have mild reactions (e.g. maculopapular rash), but this does not mean they have a true life-threatening PCN allergy. 

PMOS (PCOS): Not Just Irregular Periods (Bongato, 9/16/26)

A recording of this presentation is available HERE.

***

Thanks to Dr. Charlene Bongato for an excellent update on Polyendocrine Metabolic Ovarian Syndrome (PMOS), formerly known as Polycstic Ovarian Syndrome (PCOS). It was recently renamed to capture the reality that the disease, as we now understand it, is not a primary ovarian problem but rather a multifactorial syndrome with environmental influences and characterized by: 

1) hyperandrogenism 

2) ovulatory dysfunction 

3) polycystic ovarian morphologic features

***it is important to note that while insulin resistance is closely associated, it is NOT a defining feature

5-13% of female patients meet criteria for PMOS (by Rotterdam criteria, see below)

it is the most common cause of anovulatory fertility

~70% of patients remain undiagnosed

PMOS is caused by dysregulated ovarian androgen excretion or increased extra ovarian androgen production, characterized by excess LH and decreased FSH.

"Atypical PMOS" is obesity-related

Rotterdam criteria (must meet at least 2/3)

• oligo- or an- ovulation
• clinical or biochemical signs of hyperandrogenism
• polycystic ovaries by ultrasound

Additionally, per ACOG, Anti-Mullerian hormone (AMH) can serve as a diagnostic marker of PMOS when factors such as age, phenotype, BMI, etc are taken into account. 

How to assess for excess androgen?

1) Clinical assessment for hirsutism, using the modified Ferrimen Gallwey Score

additional manifestations of hyperandrogenism include acne (2.8x more prevalent in adolescents with PMOS), androgenic alopecia, seborrhea, hyperhidrosis, hydranitis suppurativa

***note: virilization is abnormal in PMOS and should prompt investigation for other causes of hyperandrogenism

2) Laboratory assessment: total and free testosterone (can consider DHEA, androstenedione if testosterone is normal)

Take care NOT to diagnose PMOS in teens. You need both irregular cycles and hyper-androgenism. Should not assess cycles until at least 2 years of menarched, AND polycystic ovarian morphology (PCOM) should NOT be used within 8 years of menarche. Additionally AMH should not be used.

Typical vs. Atypical

• In functionally typical PMOS, overexpression of DENND1A.V2 leads to hypersecretion of testosterone precursors from the theca cells. Plus 20-30% of the time, there is adrenal contribution with also elevated DHEA.
• In functionally atypical PMOS, obesity mediated insulin resistance and excess leads to stimulation of steroidogenesis and overproduction of androgens within adipocytes

Additional evaluation after diagnosing PMOS should include: 

1. Cardio-metabolic risk assessment: HbA1c, lipids, STOP-BANG (for OSA) 
2. MASLD
3. Depression and anxiety
4. Anovulatory infertility
5. (there is an elevated risk for endometrial cancer but screening is generally NOT recommended)

Management

management of PMOS depends primarily on desire for fertility

goals include: management of hyperandrogenic features, management of underlying metabolic abnormalities, prevention of endometrial hyperplasia and cancer, contraception (for those not desiring pregnancy) and ovulation induction (for those who desire pregnancy)

For those who do NOT want to pursue pregnancy:

Endometrial protection with pills/patch/ring (combined contraceptives) are first line to manage hyperandrogenism, cycle regularity and contraception. Progestin only products are acceptable but do not manage hyperandrogen. Metformin can help with menstrual regularity.

Certain progestins have less androgenic activity (see image)

You can add spironolactone after 6 months for additional anti-androgen effect PRN

For those who DO want to pursue pregnancy:

Ovulation induction is the goal with either letrozole (now first line) or clomiphene

Metformin does not help with ovulation dysfunction except for patients with insulin resistance who have failed lifestyle interventions (diet, weight loss)

Addition of a supplement called inositol has increasing evidence for ovulation induction

Additional dietary supplements to consider: Vitamin D, Omega 3, NAC, berberine

Why Discharge Before Noon. . and other Hospital Metrics (Picetti, 9/9/2026)

A recording of this presentation is available HERE.

Thanks to Dr. Dominic Picetti, hospitalist and physician advisor at SSRRH, who gave an important presentation on Reimagining Care Progression.

He started with this article from the Choosing Wisely Campaign "Things We Do for No Reason", which debunks this oft-used metric as a means to decrease length of stay (LOS) and create more open beds for patients waiting in the ED.



While Dr. Picetti acknowledged that using this metric in isolation does not accomplish the goals stated above, he reminded us that prolonged ER boarding DEFINITELY leads to worse outcome (increased mortality, increased CAUTI, increased CLABSI, increased falls, increased delirium and a poor experience of the hospital).


However, arbitrary clock time metrics fail to solve hospital overcrowding because they target an order entry deadline rather than underlying operational throughput barriers.


How can we improve this quality? We can do so by implementing a multi-disciplinary care progression model, which considers "steps to home" from the beginning-- what is the estimated/target discharge date? what are barriers to this patient going home? There is evidence to support these models (see image below)





AHRQ states that daily multi-disciplinary rounds are the single most effective lever to decrease hospital days in complex patients.


We must consider the concept of throughput:
From ER (where we establish early trust or mistrust)--> Inpatient/on wards, where clarity vs. lack of clarity defines the patient experience (there are plenty of opportunities here for mistrust). One of the goals of multidisciplinary rounds is to establish the anticipated date of discharge and share that with the patient. It is okay if we are wrong, but better to give the information to the patient.


In other words, "discharge should start on day #1".


Dr. Picetti also lifted up the statement Why not home? Why not today? as a conversation to be had with and about each patient each day. Our goal should be for patients to spend LESS time in the hospital (because generally being at home is better for everyone) and ultimate disposition location should be home.


One of our jobs is to inform people when they are medically ready to leave the hospital.


***


Quality Metrics are measure of the quality of care we provider patients.


When patients spend extra days in an acute hospital bed (beyond medical readiness), patients are at increased risk of lots of things: CAUTI, CLABSI, pressure injuries, falls, delirium. All of these contribute to increased readmission AND increased morbidity and mortality.


The Sutter Playbook is a framework for understanding Inpatient progression. It includes:
1) Case management does an assessment <24 hours from admission. Goals are to identify post-acute placement needs, prior living arrangements, PCP, DME, social barriers
2) Daily MDRs why not home? why not today?
3) Real time delay tracking (case management does this in the "avoidable delay" tab on Epic)
4) Touch points (2pm meeting with leaders AND complex care rounds weekly, where all patients > 7 days and other challenging cases are discussed)

Caring for the Post C-section Patient (Morrison, 9/2/2026)

A recording of this presentation is available HERE.

Thanks to Dr. Lily Morrison, R3 for a really thoughtful and important presentation on Caring for the Post-C-section Patient. Dr. Morrison shared her own learning after herself experiencing an emergency c-section last year. She did a wonderful job of marrying the evidence (qualitative and quantitative) and the patient experience (her own and that which is captured online and in the qualitative evidence) in her presentation. I highly recommend you watch it! If you just want the Cliff's notes, here they are:

>1,000,000 c-sections occur annually (about 1/3 of all US births)

C-section is the most common major surgery performed in this country

When Dr. Morrison had her c-section, she admits, she didn't really know what to expect, and as she dove into the literature, she was not alone:

Hospital discharge instructions given to Dr. Morrison did not answer her most basic questions-- e.g. when can I pick up my toddler and when is it safe to drive and return to other typical activity?

Dr. Morrison divided her presentation into first hours>> first days>> first 6 weeks>> first 3 months>> chronic as a way to think about post-op C-section care

The most updated evidence-based immediate C-section Guidelines come from Enhanced Recovery After C-section (ERAC) 2025 Update from the Society of Obstetric Anesthesia and Perinatology. This really outlines important actions while in the hospital after a c-section.

First 48 hours

Pain is obviously an important outcome after c-section and patient experience is highly variable

EARLY pain control is known to have positive impact long after the immediate post-op period

Standard care involves:

1) Neuraxial opioids in the first 12 hours after surgery (spinal/epidural during c-section by anesthesia)

2) For patients who have had a crash c-section under general anesthesia, consider ways to augment pain control including a transversus abdominus plane (TAP) block, which can be done by anesthesia

3) There is good evidence for 1gm of APAP pre-op

4) Scheduled ibuprofen/APAP after surgery (for weeks for some patients)

5) Opiates as a rescue (we generally use oxy in our hospital, oral is preferred to IV and try to limit to <30mg/first 24 hours)

6) Abdominal binders has mixed recommendations but does have evidence for improved early pain 

Early function (i.e. encourage patient to walk) also has evidence. Walking ASAP after surgery leads to fewer complications (9716 steps during hospitalization showed significantly less complications), early showering (after 12 hours is fine, no need to wait 48 hours), early eating and drinking, early foley removal

Psychological healing: normalize the experience, help limit the guilt/shame of not having had a vaginal delivery, recognize for some women they have experienced a trauma, acknowledge their disappointment and grief. Some women really benefit from debriefing early (others needs/want it later)

Infant bonding: also important, pain control and encourage breastfeeding, skin to skin

First 6 weeks

Pain 

median time to opioid cessation is 8 days

median time to analgesic cession 17 days

median time to pain resolution 21 days

There appears to be an inflection point for patients in pain at the 3 week mark-- 22 days +/- 9 (this is GOOD to share with patients). This means that pain is normal to still be experiencing  at the 2 week visit, it is okay to continue APAP/Ibuprofen, keep using the binder

Function

There are really NO evidence based guidelines, really pain should be the guiding factor for everything from lifting to driving to having sex

Psychological healing

there are increased rates of post partum depression and anxiety after LTCS, 20-40% of women with PPD in c-section patients, 4-20% with PTSD

Screen! 

Treat with SSRI (sertraline has the best evidence), CBT

Address PPD and PTSD as a care team: stigma, disappointment, a sense of failure, poor communication, a lack of trust, loss of control, fear of the OR can all be normal>> consider addressing some of these expectations prenatally (since 1/3 pregnancies in the US will end in LTCS)

Post C-section debrief>> some patients do not want to revisit the event, but some DO!

Goal is rebuilding TRUST

Next 3 months

Pain

After 3 months, if patients still have pain, this should be considered "chronic"

~1/4 of patients after LTCS report chronic pain, likely 2/2 nerve entrapment, intrabdominal adhesions

Risk factor for chronic pain include: severe early post-op pain (this is why we want to treat pain EARLY), stress, smoking, pre-op depression or anxiety, and longer/more complex surgery

Treatment for chronic post-c-section pain:

1- rule out something medical (surgical referral for lysis of adhesions)

2-offer meds (SNRI, gabapentin)

3-physical therapy (scare and soft tissue mobilization)

4-topical medications (e.g. capsaicin, lidocaine)

5-acupuncture (there is an evidence based modality called "scar deactivation", protocolized)

6-lidocaine infiltration can be done 30-66 of 0.5% lidocaine significantly can improved pain (has been effective in early post-partum period as well)

Return to Exercise

Day 1: gentle walking pelvic flood exercises

2-6 weeks gentle abdominal engagement, increased walking, aim for 30 minutes 5x/week

6-8 weeks the abdominal fascia has 51-59% of its tensile strength

8-12 weeks high intensity, low impact 

>12 weeks running/circuit training/full exercise

Reasons to slow down: severe pain, increased vaginal bleeding, excessive fatigue

Long term impact of birth method:

~5% of c-section patients still experience pain >1 year after surgery

Life long increased risk of miscarriage, previa, stillbirth and abruption

Of note, c-section patients have lower rates of urinary incontinence and prolapse

Acute Kidney Injury (Kavalam, 8/26/26)

A recording of this presentation is available HERE. 

Thanks to Dr. George Kavalam for an important presentation on AKI. 

Here are my take homes: 

• Baseline creatinine (SCr) is the lowest value in the last 3 months
• KIDOGO criteria defines AKI as a rise in SCr of 0.3 (in 48 hours) or oliguria (urine output <30cc/hour)
• SCr can be falsely low in muscle wasting, liver disease, and volume overload>> use cystatin C in these circumstances to more accurately detect GFR
• SCr and GFR have an inverse non linear relationship, so a rise from 1-2 is MUCH more concerning than a rise from 3-4

Urinalysis with micro is  a "poor man's biopsy"

Urine specific grafity 1.002 is VERY dilue. . . . 1.030 is highly concentrated

Protein: only looks at albumin (cannot assess other proteins, e.g. Benz Jones)

Blood: +blood on dipstick with 0 RBC is rhabdo until proven otherwise

WBC: elevated in infection AND acute interstitial nephritis (AIN)

Ketones: do not detect beta hydroxybutarate

Glucose: a blood glucose >180 will spill into the urine

Urine sediment: 

RBC cast>> glomerulonephritis

WBC cast>> AIN, pyelo (inflammatory process)

muddy brown cast>> ATN

hyaline cast>> dehydration

waxy and broad casts>> CKD

FeNa is historically taught as a means to determine if AKI is pre-renal (<1%) vs. intra-renal (>2%). Really you should think about it as a way to support the clinical picture, not to make the diagnosis itself. 

• FeNa answers the question: "What are the tubules trying to do with the sodium"
• only helpful if pt is oliguric
• use FeUrea if patient on diuretics

Urine sodium (Na) is NOT helpful in AKI (only in hyponatremia)

Urine Osms can range normally between 50-1200, trust that the kidneys know what they are doing

+Proteinuria

-nephrotic syndrome (>3.5g)

-overflow>> multiple myelolma

-tubointerstitial>> ATN, AIN, Fanconi's

-transient/isolated>> dx of exclusion (e.g. post exercise)

And an important footnote from Dr. Kavalam: Note, due to historic and systemic racism in medicine, race was used to calculate GFR in black patients for decades. In 2023, race was finally dropped from MDRD, restoring 457 days for African American patients on kidney transplant lists

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.