A link to a recording of this presentation can be found HERE.
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A summary will follow.
An Integrative Approach to Substance Use Disorder (Adachi Serrano, 12/13/2023)
A recording of this presentation is available HERE.
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Many many thanks to Dr. Katya Adachi Serrano, SRFMR Alumna class of 2014 and Integrative Medicine Fellow (2015) on An Integrative Approach to Substance Use Disorders. Dr. Adachi Serrano blends her family medicine background with training in herbal and integrative medicine, plus a board certification in addiction medicine. In so doing, she spoke thoughtfully on topics from buprenorphine induction to herbal supplements for SUD to spiritual support. This is definitely a presentation worth watching! The link is above.
For those of you who prefer the written word, my notes below:
Dr. Adachi Serrano took us through the case of a young man suffering from alcohol use disorder (AUD) and repeated episodes of alcohol withdrawal syndrome (AWS). She started by grounding us in the concept of the tribal MAT Echo Clinic Wellness Wheel (see below): consideration of the mind, body, spirit, and community, as a means to think about the care of patients with SUD.
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| Tribal MAT Echo Clinic "Wellness Wheel" |
The Body
Medication assisted treatment -- or medication for addiction treatment (MAT)-- is the gold standard for treatment of patients with many SUD. SUD is just like any other chronic disease, Dr. Adachi Serrano argues: SUD has a gradual onset, affects all races/ethnicities/SES, it relapses and remits, is partially relieved by lifestyle changes. And so, we should approach SUD like any other chronic disease.
AWS; Typical treatment for acute alcohol withdrawal involve either long-acting benzodiazepines (chlordiazepoxide or diazepam), or gaba-ergic meds (e.g. gabapentin) tapered by either dosing interval or amount daily. See these patients daily, says Dr. Adachi Serrano.
AUD: The best medication option we have for chronic management of AUD is naltrexone, which decreases cravings and suppresses the pleasure people get from drinking ETOH. This can be dosed 25-50mg qhs, Precaution with: acute hepatitis, liver enzymes 3-5x normal, decompensated cirrhosis, active opioid use. Common adverse events include headache, nausea, drowsiness. Some people also experience anhedonia.
Another option is long-acting naltrexone (aka vivitrol), which is an IM injection 380mg given q4 weeks (after a 4 day PO trial of naltrexone oral). An alternative maintenance medication is acamprosate, which is dosed 666mg TID (2 tabs of 333 TID). Side effects include diarrhea and adherence. A third option is Gabapentin 100-300mg daily to TID.
OUD: Standard treatment or opiate withdrawal syndrome (OWS) is supportive measures (e.g. clonidine, hydroxyzine, trazodone, ondansetron). Maintenance for OUD is either suboxone or methadone, usually dosed 2-4mg q2-4 hours, max 8mg on D#1. Sublocade, a long-acting injectable buprenorphine, may be available to better-insured patients, dosed at 300mg SQ x 1-2 doses, then 100mg q28 days. Finally, naltrexone is a third maintenance option, but you must be opioid free for minimum of 5 days (ideally 7-10 days). This is idea for patients who do not use opioids. Clonidine is often used as an adjunct during the withdrawal phase 0.1-0.3mg q1 hour.
Dr. Adachi went on to talk about the value of herbal supplements for SUD, as an adjunct to the standard allopathic medications. Three main categories of herbs: adaptogens, nervine, and nutritive.
1) Adaptogens help the body to adapt to stress, "normalizing influence on physiology". They tend to be derived from the roots of plants that grow in hardy environments and rugged terrain, and their effect is thought to be due to the hormones the plants themselves have generated in these rugged environments.
- Ashwagandha, dosed 400-500mg BID helps to normalize GABA activity in the body. This can be helpful in all forms of SUD. Precautions: nightshade allergy, hyperthyroid
- Rhodiola, derived from arctic regions, is very stimulating. Dosed 100-200mg. Caution: can sometimes be too stimulating, especially in stimulant use, w/d and recovery. Thought to "get the fire burning again"
- Eleutero aka Siberian Ginseng, increased dopamine, thereby increasing energy levels
- Licorice also can be helpful, sweet and easy to take
2) Nervines: have a direct effect on the nervous system. The following nervines are considered "calming nervines" which can be helpful in recovery:
- Skull cap, a GABA agonist, 850-1200mg daily in tincture (very concentrated)
- Valerian, another GABA agonist
- Lavender, 1-2 tsp in 8 oz of water
3) The last category are the Nutritives, which are nutrient rich and thought to support the body. One of Dr. Adachi's favorite is milky oats extract, which is nourishing to the nervous system and also increases dopamine.
The Mind
Mental health treatment should be considered an essential part of MAT. All patients with SUD should be screened for underlying mood disorders (including anxiety, complex PTSD), learning disabilities, and ADHD. These underlying disorders should be treated with both medications and therapy.
Trauma: 90% of patients with OUD report a history of trauma, 80% have child sexual abuse, emotional abuse, or violent trauma. We should see SUD as a marker of trauma and work to normalize in a therapeutic way. Here Dr. Adachi Serrano used the image of a record playing in our ear-- "our early experiences teach us messages, like a record playing in our mind" that we may not even know is playing.
This is where mindfulness practice comes in, also CBT. Introduce the concept of brief CBT for a non-therapist (for those of working in primary care practices where mental health services can be hard to come by). Dr. Adachi Serrano took us through brief CBT (see image) and reminded us that the goal is to rewrite the core message, overwrite the music playing in our head: "I am valuable. I am loved. I matter. I am safe"
She encouraged us to teach residents to cultivate their own dopamine -- "give yourself a high five and do a little dance". But in order to prevent burnout in primary care, really important to use motivational interviewing techniques and meet patients where they are at-- know the stages of change and tailor your intervention to the patient's stage, not your desired outcome.
The Spirit
This leads us to spiritual and somatic treatments. Often in patients with SUD there is a temporal disconnect between what the body is experiencing and the present, i.e. the spirit is not living within themselves. This is categorized in different cultures with different words, including susto, soul wound, etc.
EMDR and somatic experiencing may be helpful treatment modalities.
In addition, there are many other spiritual treatments: sweat lodges, talking circles, spiritual counseling, limpiezas.
Meaning is important, and looking for ways to experience normal emotions -- a safe space to feel both sadness and JOY. To look for one's core values, to recognize safety.
The Community
Healing community is necessary to support recovery. Patients need to ask if their community is supportive to recovery? Is their current community a barrier to recovery? Dr. Adachi Serrano described a person in recovery as being in a "bubble". When you are early in recovery, you are cleaning up your space, trying to keep your bubble strong. If your bubble doesn't have a thick shell, you don't want to be in an environment that is going to stress or test that bubble. You also need the community to provide support around that bubble, to protect the individual while they are vulnerable. This involves tending to the community, offering community -- in whatever healthy forms are available.
Group settings for SUD include: NA, AA, SMART Recovery groups, Talking circles, spiritual communities, etc. Creating connection to community, culture, family. Find space for new identity to grow. We may need to help patients guide them through a change of identity, friends/support circles to see the opportunities that are there.
Multidisciplinary Pain Management (Revelis 12/6/2023)
A recording of this presentation is available HERE.
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Thank you to Dr. Yulia Revelis, SMGR Pain Management physician, for an excellent Grand Rounds presentation this week on Multidisciplinary Pain Management. Dr. Revelis, who is fellowship trained in pain management, is a relatively new addition to SMGR. Dr. Revelis took us systematically through how she assesses and treats pain complaints in her clinic. I was most impressed with her pragmatic approach to pain and her simple advice to believe patients when they complain of pain.
Here are the rest of my notes:
- Acute pain: days to weeks (after acute injury, surgery, etc.)
- Subacute pain: <3 months
- Chronic pain: >3 months
Most common pain, no surprise, is low back pain, followed by neck pain, joint pain (knee, shoulder, hip), and TBD or "total body dolor", which is all-body pain.
Dr. Revelis encouraged us to always go back to the history and physical when assessing pain. Also consider imaging, medications/interventions/treatments, social components, and psychiatric components ("depression and anxiety go hand in hand with chronic pain, and it is a vicious cycle")
She covered a few key tools to help in your assessment of pain. These include the following (links are live when possible)
- Oswestry Low Back Pain Disability Questionnaire
- SF-36
- McGill Pain Assessment
- Fibromyalgia Questionnaire
- Pain in Advanced Dementia (PAINAD)
These are all tools to quantify pain, its impact on activities of daily living and quality of life, and can often be used to track benefit of interventions offered.
To evaluate pain, Dr. Revelis encouraged us to go back to the history: get detailed description of the pain, its location, associated factors, chronicity, family history and social history. Then do a focused exam including inspection, palpation and any indicated special testing. "You don't always have to get imaging," she cautioned, "only when it is clinically appropriate to do so."
Pain management is multifactorial
- Physical therapy
- Medications
- Interventional options
- Counseling/CBT
Physical therapy offers long-term solutions gives people autonomy and self-determination with regards to their pain. She is a big big fan.
Medication options are many:
- topical meds (including lidocaine patches, Voltaren gel, and compounded creams including ones that have TCA or topical gabapentin)
- NSAID (care with elders, contraindications)
- Acetaminophen is an excellent pain med and is often under-dosed!
- Anti-spasmodic (including cyclobenzaprine, baclofen, tizanidine) her first line is cyclobenzaprine (Flexeril) 5mg at bedtime x 2 weeks max, "start low, go slow". Only rx'd as needed and should almost always be rx'd in conjunction with PT
- Gabapentinoids (gabapentin and pregabalin), particularly for neuropathic or radicular pain
- TCA/SSRI/SNRI: duloxetine particularly helpful in fibromyalgia
- Opioids should be A LAST RESORT, really only indicated for cancer-pain and acute pain, not adequately treated with all of the above
Dr. Revelis is able to over her patients injections, when appropriate, using either ultrasound or x-ray guidance. These include injections of neck, epidural injections, knees, hips, etc.
It is important to screen for addiction/addictive behaviors in patients with chronic pain and remember that chronic pain specialists are not the same as addiction specialists. Pts with chronic pain exhibiting addictive behaviors should be evaluated by addiction specialists.
When to refer to pain specialist?
- chronic non-cancer pain
- cancer pain
- acute on chronic pain
- most importantly, patients who WANT to be helped
Care of Acute HIV in the Hospital (Fenning, 11/29/2023)
A recording of this presentation is available HERE.
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Many thanks to Dr. Reece Fenning for an excellent presentation this week on Acute HIV in the Hospital. A recording of his presentation is available above.
My notes:
- 75% of the HIV+ population in Sonoma County is >40 years old
- HIV disproportionately affect African American and Latinx people, who make up 65% of the new diagnoses each year
- Whereas in California 73% of people living with HIV are engaged in care and 64% are virally suppressed, in Sonoma County, 86% are engaged in care, and 82% are virally suppressed
- Patients with HIV have 1.5x the hospitalization rate as their HIV- counterparts
The CDC recommends that ALL US adults receive a one time HIV screening. People who should be tested more frequently (annually) include: 1) people with partners who are known HIV+ or have a known exposure, 2) pregnant patients, 3) patients who use IV drugs, and 4) people who exchange money (or other goods) for sex.
Luckily, our HIV testing sensitivity has improved in the last decade, and the so-called "window period" is now much shorter than the past -- it is only around 10 days (but up to 3 weeks) between viral acquisition and possibility of a false negative test.
When seeing patients with HIV in the hospital and/or outpatient, you should check their CD4 count AND their viral load. Also, screen for common co-morbid infections: TB (the most common worldwide), acute viral hepatitis (A, B, C), and other STI testing (RPR, GC/CT), and lipids.
HIV is staged based on CD4 count and/or CD4 percentage:
- Stage 1: CD4 count >500
- Stage 2: CD4 count 200-500
- Stage 3: CD4 count <200 and/or CD4 percent <14%
Newly diagnosed HIV should be treated immediately (rapid tx induction), except in rare cases of specific comorbidities. These exceptions include Cryptococcus meningitis and active TB. Both require initiation of treatment of these conditions prior to treating the HIV disease. (see chart below):
- Biktarvy (bictegravir/emtricitabine/TAF) is a single pill containing all three meds
- Alternate options includes a couple of different dolutegavir-containing regimens
- Trivicay + Descovy (2 pills)
- Trovicay + Truvada (2 pills)
- Triumeq (only one pill, but requires HLA testing, so not great for rapid treatment)
What about empiric prophylaxis Opportunistic Infections (OIs)?
You should be worried about OIs if CD4<200 and/or CD4 percentage<14%. The most common OIs for which to consider ppx are PCP pnuemonia (aka PJP) if CD4<200-- ppx is TMP-SMX daily, and MAC (if CD4<50) -- ppx is azithromycin once weekly.
How should we think about OIs in the acute setting? There are a couple of different ways to think about OIs:
Time with HIV
- newly acquired (<6 months)
- previously on treatment but now stopped
- on treatment, but its not working
Presenting symptoms:
- AMS --> think CNS infection (Crypto
- respiratory symptoms --> think PCP, MAC
- dermatologic symptoms --> think HSV, VZV, MRSA, KS
Random acute HIV symptoms and pearls:
- Acute HIV: The large majority of patients will have viral/flu-like symptoms with acute HIV that will self-resolve. Most are not sick enough to present to the ER during this acute illness.
- Immune reconstitution inflammatory syndrome (IRIS) usually appears 2-4 weeks after starting tx, it is a diagnosis of exclusion. Greatest risk with high viral load and very low CD4 (<50). Treatment is NSAID (outpatient) or steroids (inpatient)
- HIV wasting syndrome: acute weight loss (>10% of body weight), often with acute diarrhea. Looks like cancer. May need an EGD and/or colonoscopy for biopsy to diagnose. See testing algorithm below.
- Odynophagia: pain with eating may be a sign of oral thrush and/or esophageal candidiasis
- Dermatologic infections in HIV are very confusing and also often require a biopsy (see images)
(L>R clockwise: Kaposi's Sarcoma, HSV, MRSA Shingles) - Respiratory illness in HIV disease should be evaluated like non-HIV with CXR, blood work, but also add beta-D-glucan (for fungal infections). You likely will need tissue (bronchoscopy or induced sputum) to get a diagnosis.
- Neurologic symptoms in someone with HIV require a head CT, followed by CSF studies. Also don't forget a fundoscopic exam (CMV retinitis)
Additional resources:
ERASE: Interrupting Racism in Medical Training (Stecker)
Recording and Summary will be here once available and completed.
Primary Care for Patients with Alcohol Use Disorder (Lund, 11/15/2023)
A recording of this presentation is available HERE.
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Deep gratitude to our Assistant Program Director and local expert, Dr. Erin Lund, for an excellent presentation on Primary Care Management of Alcohol Use Disorder (AUD). Living in the wine country, this is a medical problem that sometimes hides in the shadows of social acceptability and cultural norms.
Dr. Lund covered a broad range of topics related to AUD, including healthy drinking, screening for risky drinking, assessing severity of the use disorder and treatment (both acute withdrawal and chronic management). Alcohol, consumed around the world, is one of the oldest-used psychoactive substances, 2/2 only to caffeine. There is documentation of humans indulging in alcohol dating back 9,000+ years.
(Note: much of the ETOH literature includes gender-based nomenclature. In an effort to be gender inclusive, I will use the following terms in this blogpost: AMAB: assigned male at birth, AFAB: assigned female at birth)
Healthy drinking
Standard drinks vary based on alcohol content and volume: 12 oz beer, 8-9 oz malt liquor, 5 oz wine, 1.5oz distilled spirits (see image below). Healthy drinking guidelines are based on age and gender assigned at birth: for adults under age 65, no more than 4 drinks for AMAB or 3 drinks for AFAB on any one day AND no more than 14 drinks/week for AMAB and 7 drinks/week for AFAB.
Risky Drinking
Rates of risky drinking and AUD are shockingly high in the US: 12-month prevalence of 13.9% of AUD (7% mild, 3% moderate and 3% severe) and a lifetime overall prevalence of 29%. Typically people AMAB have higher rates than people AFAB, but this is changing, as alcohol becomes more socially acceptable for AFAB patients. People ages 18-35 have the highest prevalence.
A binge episode is defined as:
- >4 drinks for AFAB >5 drinks for AMAB,
- at least one day in the last 30 days
>5 days of binge drinking=HEAVY USE
Heavy use is NOT the same as AUD, but intervention should be considered, as heavy use is associated with increased all-cause mortality, earlier death, increased automobile accidents, increased accidental and intentional injuries, and social and legal problems.
Alcohol Use Disorder
DSMV outlines AUD* as "a maladaptive pattern of alcohol use" within the past 12 months, as defined by at least two of the following criteria:
- Drinking larger amounts/longer periods than intended
- Efforts/desire to cut down
- Great deal of time spent obtaining, using, recovering
- Craving
- Recurrent failure to fulfill role
- Continued use despite social/interpersonal problems related to drinking
- Activities given up (social, occupational, recreational)
- Recurrent physically hazardous behavior
- Continued use despite physical or psychological problems
- Tolerance
- Withdrawal
*Mild AUD: 2-3 criteria, moderate 4-5, severe ≥ 6
Screening for AUD
USPSTF gives a grade B recommendation to screen ALL adults for unhealthy alcohol use. Here's the good news: when we screen, it makes a difference! Patients actually cut back and change their use habits. People live longer.
There are a variety of standardized screening tools; these include:
- 1Q screen: How many times in the past year have you had more than 4 drinks/day (AFAB) or 5 drinks/day (AMAB). Positive with answer of >1
- AUDIT-C (which is what is used at SRCH, see image below)
A nice thing about using the AUDIT-C is that the results can be used to guide treatment. An AUDIT-C score of 0-3 indicates low risk drinking (no intervention needed), a score 4-5 is moderate risk (brief intervention indicated). A score 6-7 merits a brief intervention + psychotherapy and consideration of pharmacotherapy. A score of 8-9 is an indication for pharmaceutical intervention + psychosocial intervention+/-specialty care management. A score of 10+ merits urgent specialty referral.
Treatment of AUD
Treatment of AUD includes both psychosocial and pharmacological treatments. It also involves both an acute stage (active use, withdrawal) and a chronic stage (maintenance, harm reduction, reduction).
Psychosocial support involves both formal treatment programs (inpatient and outpatient programs), many of which are based in Peer Support. These include but are not limited to AA, smart recovery, etc.
Pharmacological management involves, at the minimum, 1 of 3 FDA-approved medications. These meds can be started in the inpatient or outpatient setting. We have great room to improve in this area. A study in 2012 found that only 8% of US patients with AUD were being treated with medications.
Considerations in starting meds for patients should include goals (e.g. abstinence vs. reduced use), relevant health factors (e.g. comorbidities like chronic pain, cirrhosis, etc.), and external barriers.
Alcohol Withdrawal Syndrome (AWS)
The slide pasted below demonstrates the timeline for Alcohol withdrawal and some recommendations in terms of who can withdraw in an outpatient setting vs. those who need inpatient support.
Providers should use standardized scores to keep an objective assessment of a patient's alcohol withdrawal. There are several, including the CIWA (10q, objective + subjective report), the SAWS (10q, patient-completed), and the SEWS (7q, clinical assessment)
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| CIWA: <10: very mild AWS, 10-15 mild AWS, 16-20 modest AWS, >20 severe (DTs) |
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| SAWS: patient scores their own symptoms in past 24 hours, <12 is mild AWS, >12 is moderate to severe AWS |
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| SEWS |
The severity of AWS dictates the level of care the patient needs. Patients with mild-moderate withdrawal can be managed in the outpatient setting, assuming they can also 1) have consistent follow-up 2) take PO meds 3) have friend/relative/support person 4) have no prior hx of DTs 5) have no high risk comorbidities (physical or psychiatric) that would make home withdrawal unsafe (e.g. extreme anemia, decompensate cirrhosis) 6) do NOT have polysubstance use.
All other patients should be managed in an inpatient setting.
Pharmacotherapy for AWS
Goal of treatment of AWS is to help patients withdraw safely (prevent DTs, seizures, death) and reduce likelihood of relapse. This can be accomplished using either benzodiazepines (e.g. chlordiazepoxide or lorazepam), which was the previous gold standard, and/or with benzo-sparing protocols, most of which use anticonvulsants and anti-adrenergic medications.
Anticonvulsants: phenobarbital, gabapentin, valproic acid, carbamazepine
Anti-adrenergic: clonidine, propranolol, guanfacine, precedex
Everyone with AWS should get folic acid (1gm/day) and vitamin B1 (thiamine, 100mg/day)
The idea behind the benzo-sparing protocols is that these medications are AS effective in safe withdrawal with less abuse potential than benzos. There are still evolving studies in this area, and some agents have more evidence than others. These protocols vary based on location and experience.
See below the draft algorithm (not yet live) at SRCH, which screens for patients who may safely withdraw outpatient and uses fixed dose gabapentin (300mg TID vs. 600mg TID).
Older algorithms use fixed vs. on demand dosing of lorazepam and/or chlordiazepoxide. You can find a link to those older guidelines HERE.
Chronic Management of AUD
Okay, finally, moving onto medications that prevent relapse and/or help people cut back and/or help people remain abstinent. Most studies look at a period of time of 12-16 weeks of reduced use and/or abstinence, but in clinical practice a minimum of a year of maintenance therapy is recommended, particularly if there is a high risk of relapse.
FDA approved: naltrexone, Acamprosate, disulfiram
- Naltrexone: 50mg PO daily OR 380mg IM monthly, reduces risk to any drinking (NNT 10) and heavy drinking (NNT 12), injectable has evidence for reducing number of heavy drinking days. Reduces craving and pleasurable effect of drinking. Contraindicated in liver failure, concomitant opiate use (within 7 days). Pregnancy is relative contraindication.
- Acamprosate 333mg, 2 tabs TID daily. Reduces return to any drinking (NNT 12), reduces withdrawal associated dysphoria. Has mixed evidence on efficacy compared to placebo. Contraindicated in renal failure (GFR<30) and pregnancy.
- Disulfiram: oldest med on the market for AUD (1949), anticipation of feeling sick discourages use. Blinded studies don't show great effect, but open label studies do show reasonable effect.
Non-FDA approved but have some evidence: topiramate, baclofen, gabapentin, ondansetron, sertraline, semaglutide
- Topiramate: non-FDA approved, may reduce cravings, impulsivity and post-withdrawal dysphoria, 100-300mg/day (titrated up over 6 weeks from 25mg day starting dose, increase by 50 mg per week), BID dosing recommended. Contraindicated in pregnancy and renal failure.
- Gabapentin: non-FDA approved, may be continued after using for treatment of AWS, 300mg-600mg TID for maintenance dosing to reduce cravings and return to drinking
Endometrial Cancer (Delic 11/8/2023)
A link to a recording of this presentation is available HERE.
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Many, many thanks to our speaker this week, Dr. Lejla Delic, a local gynecologist-oncologist, who works with our local oncologists and gynecologists to care for patients in our community with gyn cancers. Her presentation was excellent -- so good, in fact, that we we want her back for a Part 2, on ovarian cancer. Stay tuned. We will get her scheduled in the winter/spring.
In the meantime, my notes:
Gynecological cancers occur in the uterus (most common, aka endometrial cancer), cervix, fallopian tubes, ovaries, peritoneal cavity, vulva and vagina.
In the US, there are ~65,000 new cases of uterine cancer per year --> 12,000 deaths
In the US, there are ~19,000 new cases of ovarian cancer per year--> 12,000 deaths
Unfortunately, mortality from uterine/endometrial cancer is on the rise
Endometrial cancer, the most common type of gyn cancers, has a lifetime prevalence of 3%. Women are average age 60 years old at the time of diagnosis and, because endometrial cancer typically presents with post-menopausal bleeding, 75% are diagnosed in the early stage (stage I and II). When it does metastasize, endometrial cancer typically spreads via local lymphatics to the pelvic nodes and then to the aortic lymph nodes.
Unfortunately, black women in this country are dying at disproportionate rates of endometrial cancer and are diagnosed with more aggressive cancers, younger than white women.
Risk factors for endometrial cancer:
- Obesity (endogenous unopposed estrogen). In fact, every 5 points of BMI increases your risk of being diagnosed with endometrial cancer by 50%.
- Chronic anovulation (obesity, PCOS)
- Nulliparity, infertility, early menarche, late menopause
- Exogenous unopposed estrogen (e.g. HRT without progesterone)
- Tamoxifen (2x risk of uterine cancer)
- Hereditary: these present earlier than sporadic cancers, more typically in non-obese younger women (<50 years old), including genetic syndromes like Lynch Syndrome and MLH1, 2, 6, etc.
Risk reduction for endometrial cancer:
- OCPs (combined)
- Weight loss
- Hysterectomy (offered to women with Lynch syndrome after age 45 or when fertility is accomplished)
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| NEJM: Association with race and BMI and endometrial cancer |
Historically, endometrial cancers have been divided in two groups: Type 1-- or non-aggressive, more excess estrogen type-- and Type 2, more aggressive, poorly differentiated, frequently metastasize (40% of women with Type 2 have +LN at time of diagnosis. Increasingly, however, new molecular characterization studies are changing the way we think about and treat endometrial cancer and are being integrated into the categorization. This is because prognosis is variable depending on these molecular characteristics.
90% of women with endometrial cancer present with post-menopausal (PMP) uterine bleeding. All cases of PMP bleeding should be investigated but it is important to note that only 9-14% of women with PMP bleeding have cancer. Abnormal uterine bleeding (AUB) in premenopausal women may present more like "intermenstrual" bleeding.
Evaluation of AUB:
1) Pelvic ultrasound: in PMP women, >4mm endometrial stripe necessitates and EMB. Of note, endometrial stripe thickness in premenopausal women is totally useless. Also, in someone with repeated bleeds, even a thin stripe should not prevent you from getting an EMB.
2) Endometrial biopsy (EMB)
Of note, Type 2 Endometrial cancers, an EMB has a 25% false negative rate.
If the patient has recurrent bleeding, even if they have a normal EMB, refer for hysteroscopy and D&C
Treatment of endometrial cancer:
1) Surgery
All gyn cancers (except for cervical, trophoblastic and vaginal) need surgery to be staged.
Surgery includes hysterectomy, bilateral salpingectomy, and lymph node assessment (sential LN mapping).
Stage I: cancer confined to uterus
Stage II: cancer extends to cervix
Stage III: LN involvement/ovaries/tubes
Stage IV: distant mets (omentum, lungs)
Robotic/minimal invasive surgery has best outcomes (but NOT in cervical cancer). With robot, conversion to open only happens 3% of the time (whereas its 20% of the time with typical surgery). This is really important for patients with elevated BMI who have a much better/easier recovery with minimally invasive surgery and way less bad outcomes.
2) Immunotherapy may be indicated for Stage III or IV or recurrent endometrial cancer
Historically, chemo was used (Carboplatin and paclitaxil) but with new molecular studies, immunotherapy is showing increasing promise.
Fertility preservation in young women with endometrial cancer is important to many women! 14% are pre-menopausal at diagnosis and may not be done building their families. Low Grade (1) and non-invasive cancers (as determined by MRI) can sometimes be treated temporarily with high dose progesterone (either oral Megace 80mg BID or Mirena IUD). Informed consent is important. About 50% respond, but 20-30% will either progress or return. Some women hate the side effects of high dose progesterone, which include increased appetite, weight gain, and blood clots.
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On a final note, Dr. Delic recommends TWO passes with your EMB pipelle when doing an EMB to ensure you get a good amount of tissue. And without a tenaculum whenever possible.
Stay tuned for the spring for Part 2: Ovarian cancers
Functional Medicine: when the symptoms don't match the textbook (Walton 11/1/2023)
A recording of this presentation is available HERE.
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Many thanks to senior resident, Dr. Rebecca Walton, for a thought-provoking Grand Rounds presentation this week on Functional Disorders. Such an important and challenging topic!
What are functional disorders, you ask? As the name implies, functional disorders is not one entity; it is an umbrella term for a group of syndromes including functional GI disorders (e.g. IBS), fibromyalgia, interstitial cystitis, chronic pelvic pain, chronic headaches, and chronic fatigue.
Functional disorders are all disorders that do not have an identifiable disease label (at least not in our world of allopathic medicine) and feature "normal labs" but negatively impact the functioning of the body. They tend to be chronic and some are relapsing.
Functional disorders can be challenging to treat, cause patients and providers frustration and distress, and are steeped in bias. Functional disorders have their roots in psychiatric disorders: Freud's conversion disorder, substitution of a somatic symptoms for a mental one; hysteria, medically unexplained symptoms in multiple organ systems, often tied to the presence of a uterus; and somatic symptom disorder, a significant focus on physical symptoms that results in major distress or problems functioning.
Functional disorders are common in primary care and impose an impressive healthcare burden:
- Functional GI disorders represent 12% of the workload in primary care and 30% of outpatient GI consultations
- Fibromyalgia affects 2-4% of the population, and can lead to up to 10 outpatient visits per person per year
- Chronic headaches, one of the most common complains for neurological referral, are found in 4-5% of the population and results in, on average, 9 days of missed work per year
Patient groups who are already marginalized and at risk for poor outcomes are at highest risk for functional disorders; these include women, rural populations, less educated patients, lower SES, and those with a history of physical or sexual abuse.
There are much higher rates of functional disorders in female-identified persons than male-identified: interstitial cystitis (14x), fibromyalgia (6x), IBS (2x), chronic headache (2-3x), TMJ (1.5x). Healthcare provider bias plays a role in diagnosis and treatment.
Dr. Walton wants us to be careful not to tell patients that it is "all in their head". In fact, the second part of Dr. Walton's presentation was an effort to educate us on the many ways in which these functional disorders are not just in people's heads.
Chronic Pain and Central Sensitization
Central Sensitization is a state of persistent neuronal dysregulation that leads to allodynia (pain to non-painful stimuli), hyperalgesia (abnormally heightened pain), and widespread pain. These symptoms seem to occur due to increased responsiveness to stimuli by the CNS. This is super interesting!
Attributes of patients with central sensitization:
- no objective tissue or laboratory findings
- a genetic and/or environmental predisposition
- stress as triggering or exacerbating symptoms
- dysfunctional pain or sensory processing
- do not respond to therapies used for pain (e.g. acetaminophen)
See the image below for a description of how this plays out pathophysiologically in both the central and peripheral nervous systems:
IBS
Moving on to IBS. There are many theories as to how IBS comes about. Many have biologic plausibility and evolving understanding. These include post-infectious IBS (e.g. after a bad gastroenteritis with shigella, salmonella and e coli), autoimmune theories (including anti vinculin and anti-CdtB antibodies), and dysbiosis. Did you know, for example, that people with IBS tend to have higher levels of bacteroides in their guts compared to healthy controls who tend to have higher levels of prevotella?
SIBO, which is characterized by abnormal bacterial growth in the small intestine (most of our gut microbiome resides in our LARGE intestine), can occur due to IBS and other motility issues. Common symptoms include bloating, flatulence, abdominal pain, and diarrhea, weakness, and fatigue.
There is absolutely bidirectional communication between our gut and our CNS. Animal studies have shown the extreme stress leads to lifelong alterations in gut microbiome and the HPA access. Also CBT can not only increase serotonin levels in the gut but also decrease bacteroides (crazy cooL!!)
There is little argument that early trauma and adverse childhood events (ACEs) have a huge influence on IBS, and prevention of these events is key in preventing leaky gut, microbiome changes, and lifelong GI upset.
***
I will leave you with Dr. Walton's own takeaways
The brain matters, but it isn’t the whole picture
Those who are already facing healthcare discrimination are prone to having functional disorders and thus experience further neglect
There is ongoing research into these syndromes, and I hope that soon the “lack of biomedical markers” changes
Even without biomedical markers, these symptoms matter
Those who are already facing healthcare discrimination are prone to having functional disorders and thus experience further neglect
There is ongoing research into these syndromes, and I hope that soon the “lack of biomedical markers” changes
Even without biomedical markers, these symptoms matter
Here is a list of references and further reading provided by Dr. Walton:
https://pubmed.ncbi.nlm.nih.gov/32294476/
https://www.sciencedirect.com/science/article/abs/pii/S0049017222001111?via%3Dihub
https://www.sciencedirect.com/science/article/abs/pii/S0049017207001473?via%3Dihub
https://pubmed.ncbi.nlm.nih.gov/22180058/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10507713/
Wholesome Sleep for Healthcare Professionals (Deshpande, 10/25/2023)
A link to a recording of this presentation is available HERE.
So many pearls in this week's Grand Rounds by SMGR Sleep Medicine Dr. Abijit Desphande. Everyone sleeps, right? And almost everyone has trouble sleeping, right? Well, Dr. Deshpande has a myriad of suggestions for how you might sleep more and sleep better. . .Stay tuned for my notes coming soon.
Empiric Antibiotics and Antibiotic Stewardship (Green & Patel 10/18/2023)
LINK to a recording of the presentation is available HERE.
***
It is with deep gratitude and great joy that I can say proudly that we did Grand Rounds in a room together at SSRRH for the first time since February 2020! It has been over three years since we gathered today in Conference Rooms A/B at SSRRH, and while we have had some magnificent zoom talks together in the interim, it felt both deliciously indulgent and so very right to be sitting together fighting the AV equipment. Together. We had 22 esteemed live attendees, and another 31 online. And that was even without serving breakfast (which will be available starting next week). A guest appearance from our very own Dr. Rick Flinders was icing on the cake.
And I haven't even started talking about the presentation yet -- which was excellent.
Many thanks to our antibiotic experts, Dr. Gary Green and Pharmacist Omi Patel, for both inspiring the reunion and giving an excellent opening talk on Empiric Antibiotics and Antibiotic Stewardship at SSRRH. The recording will be available shortly and the empiric antibiotic guidelines and the antibiogram are both available on the SSRRH intranet.
As for my notes:
We are so lucky to have the camaraderie and support of our pharmacists at SSRRH for improved antibiotic management of hospitalized patients. They are truly partners and educators for our clinicians.
Antibiotic stewardship program includes several important pharmacy driven protocols. These evidence-based pharmacy driven protocols include:
- Renal adjustments of antibiotics
- Pharmacokinetic review of vancomycin and aminoglycoside (i.e. vancomycin dosing "per pharmacy protocol")
- Automatic stops for medications like azithromycin and oseltamivir (when indicated)
- Transitioning from IV to PO antibiotics
- Extended infusions of beta lactam antibiotics (meropenem, cefepime, cefazolin, and zosyn)
- Probiotics for floor patients at high risk for C Diff colitis
Omi Patel reviewed the importance of these protocols and gave us a preview of an upcoming QT monitoring protocol as well.
Then Dr. Gary Green then filled us in on highlights of the ASP 2022-2023 Empiric Antibiotic Guidelines
These include:
Skin and Soft Tissue Infections (SSTI): a review on clinical assessment of cellulitis, most commonly strep vs. staph infections, including a reminder that staph infections tend to have a more demarcated (i.e. easy to draw) line between infected and uninfected tissue compared to strep infections, which tend to have a more "feathered edge". Don't forget that strep is also famous for causing lymphangitis ("streaking and tenderness" above the level of the actual cellulitis).
When treating SSTI, remember, "Cefazolin is your friend." -Gary Green, MD
Bullae are common later in SSTI and should not be cultured or removed (creating a wound)
If there is concern for toxin-mediated cellulitis (e.g. early bullae, <24 hours from cellulitis onset), consider the addition of clindamycin as an anti-toxin medication. Reminder that clindamycin works on ribosomes, which gives it its anti-toxin properties.
Vancomycin, while bactericidal, is still a very slowwwwwwwwwwwww bactericidal drug, and Dr. Green reports lots of failures in treatment of SSTI. Don't use it if you don't need it.
In the setting of fluctuance (carbuncles or furuncles), you should definitely consider ca-MRSA as the likely culprit. Cultures are imperative, and consider Septra or doxy as first line oral outpatient abx. Dalbavancin ER is sometimes used in the ED for patients for whom compliance can be challenging.
 |
| slide c/o Dr. Green, Omi Patel, PharmD |
Diabetic foot infections are a totally different thing than cellulitis and should NOT be misdiagnosed. They are often characterized by a diabetic foot ulcer (and can include osteomyelitis). Outpatient treatment for diabetic foot infections first line are Augmentin and/or moxifloxacin. If you are concerned about MRSA, you could add septra or doxy to those first-line drugs. Inpatient treatment for diabetic foot infections are a start with vanc/zosyn, but culture quickly and drop vanc as soon as culture does not reveal MRSA. Remember the combination of v/z is nephrotoxic and should only be continued if clinically indicated.
Additionally, do not use abx to treat lower extremity venous stasis, which often presents with dependent rubor (redness). If you believe this is erythema of gravity, lift the legs above the level of the heart to see if rubor improves. Venous stasis is chronic and can present with some mild tenderness and even mild warmth. Do not treat in the absence of active infection.
Diverticulitis and intra-abdominal infections
outpatient empiric abx: Augmentin OR ciprofloxacin plus metronidazole
inpatient empiric abx: Pip/taz (i.e. Zosyn) or ceftriaxone plus metronidazole . The Zosyn should be delivered as an extended infusion whenever possible. Ceftriaxone plus metro does miss enterococcus, but, as Dr. Green said "enterococcus is generally the bridesmaid and never the bride" -- meaning, it may be present but is often not the cause of the infection.
Pancreatitis should NOT be treated with abx. Unless it is necrotizing. In rare cases of necrotizing pancreatitis, the drug of choice (with good evidence for improved outcomes) is meropenem.
UTI is where the largest system-wide change in empiric abx comes in.
First off, Asymptomatic bacteriuria (AB) is too often in appropriately treated with abx. Dr. Green said that 50% of inappropriate abx are attributed to treatment for asymptomatic bacteriuria. The bladder is transiently colonized and the presence of bacteria on culture does not indicate infection in the absence of symptoms. So, in other words, do NOT treat AB with antibiotics. The exceptions are: 1) pregnant patients and 2) transplant patients.
Based on our local antibiogram, nitrofurantoin (aka Macrobid) is the empiric antibiotic of choice for uncomplicated outpatient UTI. Additional options include TMP/SMX and ciprofloxacin, though there is more resistance to both of these abx than there is to Macrobid. The one downside to Macrobid, we al know, is that it does not have good renal penetration and should not be used for pyelonephritis.
In complicated UTI (defined as neurogenic bladder, Foley catheter present, suprapubic catheter, and/or recurrent UTI),
Okay, now for complicated UTI and/or pyelonephritis in hospitalized patients. The new drug of choice is Cefoxitin (2gm q6 hours). This is for two reasons: 1) Ceftriaxone has never been a great UTI drug, it is hepatically metabolize and not renally cleared). 2) Our local sensitivities for e coli are down to 88% at SSRRH. Once under 90%, it is no longer a reliable empiric abx.
Other drugs to consider for complicated UTI are aztreonam and cipro IV.
A note on ceftriaxone: While we should no longer be using ceftriaxone for pyelonephritis or complicated UTI in hospitalized patients for the above reasons, Ceftriaxone (2gm, per Dr. Green 1gm is a homeopathic dose) remains an excellent choice for both community acquired pneumonia and gonorrhea.
And finally,
Community acquired pneumonia. Empiric guidelines still recommend ceftriaxone plus either azithro or doxycycline. Both Dr. Green and I agree that doxycycline is probably a better choice in most patients due to the QT prolongation and increased CV mortality that occur with azithromycin.
Another reasonable option for CAP. is levofloxacin.
For Aspiration Pneumonia, SSRRH and Dr. Green's empiric guidelines differ slightly from the IDSA on aspiration pneumonia, recommending Zosyn, particularly in frail patients with teeth (pearl: if patients have no teeth, you don not have to worry about anaerobes). Hospital acquired and Ventilator associated PNA should get ID involved, abx include pip/tazo and/or cefepime.
Weight Stigma and Fatphobia (Erlanger - 10/11/23)
A recording of this presentation can be viewed HERE.
***
This is one of those Grand Rounds that should be seen and heard (not read), so I am going to keep my notes very short. Please watch the recording at the above link. Prepare to feel challenged.
Dr. Lisa Erlanger, a family physician at University of Washington, is an advocate for weight-inclusive care and a compelling speaker with plenty of evocative things to say, many of which challenge the way that we were taught to think about obesity.
Dr. Erlanger encouraged us to reconsider the (generally accepted) notion that obesity is a disease, and encouraged us, rather, to consider how "anti-fat bias" in healthcare providers and "weight stigma" are actually causing tremendous harm to patients -- so much harm, in fact, that they may be responsible for poor outcomes in this population.
Here are a few of Dr. Erlanger's talking points to ponder:
1) There is no evidence that increased adiposity causes increased morbidity and mortality.
2) "A starving fat person does not make a tiny person." In other words, patients at the higher end of the weight spectrum are not going get to "normal" weight or "normal BMI" by dieting, so asking them to do so is inappropriate.
3) Obese patients consistently experience inequities (and often harm) in their interactions with healthcare providers: less warmth and emotional rapport, less time, less eye contact, more patronizing, adn more assumptions made on health based on size.
4) Weight cycling -- restriction of calories or increased use of calories in order to lose weight -- is harmful. It leads to 5-10% decrease in body weight over a short period of time, but ultimately leads to disordered eating and even higher weight and BMI.
If anyone wants a copy of Dr. Erlanger's slides with references, please contact me (Veronica Jordan) at jordanv@sutterhealth.org.
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