This week we at report we discussed a case of unintentional fentanyl
overdose associated with cocaine ingestion.
Unfortunately this type of case has become all too common for us in San Francisco in recent days. A September 2019 Health Update from the San Francisco Department of Public Health shared that there were 89 fentanyl related deaths in San Francisco in 2018 – a marked increase from <10 in 2014. Fentanyl is a potent synthetic opioid – 50x more powerful than heroin and 100x more powerful than morphine – and has led to increased overdoses nationwide. Though most fentanyl related deaths in SF have happened in people who were aware they were using fentanyl, there are also more and more cases of stimulants that are contaminated with fentanyl as for our patient. From our anecdotal experiences caring for patients, we know that many deaths have also been prevented by prescriptions and distribution of naloxone throughout the city. A few pearls about fentanyl ingestion below.
In Hospital Testing: Keep in mind that fentanyl is often NOT included in a preliminary urine toxicology screen. At our hospitals, we have to send a “comprehensive” toxicology screen in order to detect it. If you’re concerned about fentanyl contamination, keep in mind that it may still have happened even if the utox itself just shows cocaine.
Harm Reduction: Naloxone is no longer just for people using opiates. You should consider prescribing naloxone to ALL of your patients who use street drugs given the recent patterns of contamination. You can also advise patients who are at high risk to test their drugs (using fentanyl test strips, sometimes available through public health depts), use very small test doses and never use alone.
Case: 32yo female with hypothyroidism who is 10 weeks postpartum, presents to your office with left breast swelling and pain.
As internists, we don’t see a lot of pregnancy-related complications, and have been known to phone an OBGYN friend at the sight of woman who is or has recently been pregnant. However, it’s important to have a basic understanding of lactation complications, since we often reassume primary responsibility for our patients a few weeks postpartum.
Let’s refresh on the differential diagnosis of breast pain and swelling in a lactating woman, roughly in order from least scary to scariest.
In a woman without systemic symptoms (malaise, fevers, etc), consider:
severe engorgement (this is interstitial edema that occurs with the accumulation of excess milk, and is usually, but not always, bilateral)
plugged duct (presents as a tender lump that is often wedge shaped)
galactocele (when a plugged duct progresses to become a milk-filled cyst)
In a woman with systemic symptoms, consider:
mastitis (caused by bacterial infection, characterized as firm, red , painful area of the breast accompanied by a fever >38.3)
breast abscess (generally presents as a tender fluctuant area in the setting of mastitis)
inflammatory breast cancer (should be considered if mastitis does not resolve with appropriate treatment and is differentiated by skin thickening and peau d’orange appearance)
Case continued: On further questioning, the patient reports malaise and subjective fevers in addition to the pain and swelling that has been persistent for the last three days. On vitals, her temperature is 39 and her breast looks like this:
You remember your differential and make the clinical diagnosis of mastitis, which occurs in 10% of women who are breastfeeding. She asks if she needs any additional tests. Turns out, a milk culture is not necessary except in cases where the infection is severe enough for the patient to need to be admitted.
Then she asks if should see her OBGYN. You say, “Don’t worry, I can treat that.”
The treatment strategy for mastitis involves:
Continuing breastfeeding: it is safe to continue (since infants are already colonized with the bacteria causing the infection) and helps avoid development of an abscess
One caveat: HIV positive mothers should avoid breastfeeding on the infected side as transmission is increased during this time
Cold compresses and adequate hydration
First line antibiotic therapy for mastitis is: dicloxacillin 500mg PO QID or cephalexin 500mg PO QID. Or, if the patient is at risk for MRSA infection, TMP-SMX 1 DS tab PO BID or clindamycin 300mg PO TID. There isn’t great data on length of therapy, but it is generally continued for 10-14 days.
On Wednesday, Wora shared with us a case of a patient with a history of pulmonary coccidioidomycosis who presented with an acute exacerbation of respiratory symptoms.
Our patient had imaging findings overnight consistent with
interstitial lung disease, and it was initially unclear how much of her
symptoms had been attributed to cocci and whether she had undergone evaluation
This discussion was a great reminder of clinical decision-making
heuristics such as anchoring bias, and an opportunity for a diagnostic time-out. The initial
diagnosis of pulmonary cocci can be a powerful anchor to which all of our
diagnostic information gets tied. We discussed the exercise of taking a
time-out to reframe the data that we have, to ensure that we considered other
We refreshed ourselves on how cocci might present!
Check out this pyramid with some rough numbers on the clinical presentation of cocci, courtesy of Dr. Harry Hollander:
When patients do present with symptomatic pulmonary disease, they
typically present 7-21 days after exposure. The presentation can be similar to
community acquired pneumonia – in fact in endemic regions, there have been
studies showing that ~30% presenting with CAP had serologic evidence of CAP
infection (link here)
Extrapulmonary symptoms are typically systemic (fevers, chills,
weight loss), dermatologic (erythema
nodosum and/or erythema multiforme) and rheumatologic (arthralgias).
findings of pulmonary cocci might include:
unilateral infiltrate, hilar adenopathy
diffuse reticulonodular disease
In our patient, the findings on CT (possible honeycombing and
traction bronchiectasis) were less consistent with a presentation of pulmonary
cocci, and prompted concern for IPF.
In our pyramid, there is a small percentage of patients who
develop severe or disseminated disease.
What factors influence risk for these complications? The following factors all increase the risk:
(Filipinos and African Americans at higher risk for dissemination than
Immunosuppression either due to medication administration (such as with organ
transplantation, treatment of rheumatological or other illness), acquired (such
as infection with human immunodeficiency virus)
Underlying illnesses (such as hematological malignancies or diabetes mellitus),
Finally, a quick reminder on how we
serology is most common methodology
at our hospital cocci immunodiffusion (IgM and IgG) is qualitative
complement fixation assay gives us a titer
this can correlate w disease activity (>1:16 correlates w aggressive or disseminated dz)
can be followed over time w treatment
– can also detect cocci on pathology (spherules w endospores), fungal cultures, and cocci antigen can be positive in urine/blood of patients w extrapulm disease and in CSF of pts w cocci meningitis (particularly useful in immunocompromised pts)
On Friday, Clayton shared with us a case of a patient who was s/p
liver transplant who presented with acute on subacute progressive altered
We reminded ourselves about the framework for a patient s/p solid
organ transplant who presents with a new symptom that Jack and Harry have
Complications of immunosuppression. This
includes infectious complications (e.g. viral, fungal etiologies) and malignant
complications (e.g. post transplant lymphoproliferative disorder)
Toxicity of immunosuppressive medications
Rejection of the transplanted organ
Worsening of underlying disease that led to
originally led to transplant
This patient ended up having a primary CNS post-transplant
lymphoproliferative disorder, with multiple masses causing his presentation of
progressive AMS. This is a lymphoid and/or plasmacytic malignancy that occurs
in the setting of solid organ or allogeneic hematopoietic cell transplantation
as a result of immunosuppression (see # 1 in our framework above!)
A couple of pertinent bits of info about PTLD:
The incidence in solid organ transplant recipients is ~ 1% at 10
Who is at highest risk?
patients with marked immunosuppression
EBV positive patients
80% of these malignancies occur in first year after transplant
(likely related to degree of immunosuppression)
half present with with extranodal masses – these can be in the CNS (as
in our patient), in the transplanted organ or elsewhere
Case Summary: Middle-aged man with history of decompensated cirrhosis (refractory ascites s/p TIPS, HE, and varices) who presented to primary care with progressively worsening R knee pain 6 weeks after a fall.
Acute knee injuries can lead to fractures, patellar dislocation, ligament ruptures, and meniscal tears, in addition to more benign tendon strains. The mechanism of injury can often narrow the differential.
Ask if the patient was able to bear weight immediately after the trauma. Specifically, if they were unable to take four steps, you cannot rule out fracture and should get an X-ray.
Locking (inability to flex knee) suggests a meniscal tear. A sensation of popping at time of onset of pain or giving way suggests ligamentous rupture.
Rapid development of effusion (< 2 hours) suggests fracture or ACL tear. Slower development of effusion (24 – 36 hours) suggests meniscal injury.
Look at both knees! If your patient is wearing pants, ask them to change into a gown so you can look for asymmetry including muscle atrophy, erythema, and effusions.
Check out this 2 min video for performing a targeted knee exam in primary care.
This AAFP review article is also a great resource (thanks to Max Kinet, rheum fellow, for sharing!).
Should I get an X-ray? Use the Ottawa Knee Rules to decide. If any of the criteria are met, get an X-ray to assess for fracture. If the X-ray shows periarticular erosions, consider osteomyelitis which may require a bone biopsy.
Any red and warm joint should be tapped to assess for septic arthritis. Most traumatic effusions will be hemarthroses and the tap will show thousands of RBCs.
If your exam is consistent with a meniscal or ligamentous tear (see video or article above), get an MRI to confirm the diagnosis.
This week we reviewed a lot of medicine…parapneumonic effusions, CNS lesions in HIV, ITP, poison ivy treatment! A highlight was intern report on Thursday thanks to the discussion and questions from our phenomenal interns!
We reviewed a case of an elderly lady with DM and hypothyroidism who presented with subacute progressive weakness and falls, was found to have upper motor neuron pattern weakness with sensory loss (vibration, proprioception and light touch) of her bilateral lower extremities as well as a profound macrocytic anemia – ultimately diagnosed with…Subacute Combined Degeneration due to B12 Deficiency caused by Pernicious Anemia.
This led us on a trip down memory lane back to our biochemistry
and neuroanatomy classes from medical school. Stay with us!
Flashback: Diagnostic Testing for B12 Deficiency
Remember that serum B12 is not a perfect test. When it’s
super low (<100 pg/mL) – you can feel confident your patient is deficient.
When it’s high (>300 pg/mL), you can be reassured they have enough B12. But
many of our patients fall in the middle “borderline zone” (100-300 pg/mL). In
that case two additional tests – MMA and homocysteine – can help you figure out
if B12 levels are adequate. MMA and homocysteine act as precursors in two of
the key reactions that B12 mediates. If B12 is low, these precursors build up –
so both MMA and homocysteine will be high in B12 deficiency! In contrast,
folate is only a co-factor in the reaction involving homocysteine (not the MMA reaction),
so in folate deficiency you have normal MMA but have a buildup in homocysteine.
Neuroanatomy Flashback: Subacute Combined Degeneration vs Tabes Dorsalis
Now B12 deficiency can manifest in a variety of ways – anemia, neuro-psychiatric symptoms, peripheral neuropathy, glossitis – but one of the most profound presentations is Subacute Combined Denegation. This disease of progressive weakness, spasticity, sensory loss and ataxia is caused by demyelination of TWO pathways in the spinal cord. The degeneration is “COMBINED” because you get patchy loss of both the (1) DORSAL COLUMNS (sensory/ascending: light touch, vibration and proprioception) and the (2) LATERAL CORTICOSPINAL TRACT (motor/descending: limb movement). This can result in both sensory loss in a dorsal column pattern associated with weakness with upper motor neuron features (spasticity, hyper-reflexia, upgoing Babinski). This differs from Tabes Dorsalis due to syphilis, which typically has dorsal column loss but preserved corticospinal tract function. Patients with dorsal column disease from either cause may have a sensory ataxia resulting from their impaired limb proprioception, but only patients with subacute combined degeneration will typically have motor loss too (unless syphillis is doing something else crazy to the nervous system!).
Yesterday we discussed a 30 year-old healthy man presenting for a new patient visit. He had no “complaints,” but as a longtime vegan, he wondered if he should have any blood tests.
Though at first it may have seemed like there wasn’t much to discuss about this case, or with the patient during his visit, we discovered that “healthcare maintenance” comprises much more than what appears in the Epic banner.
What to talk about when your patient has no complaints:
Ask your patient about the things he/she values. What is he proud of? What are her hobbies? Spend some time getting to know each other – this will pay off down the line!
Review the health-related behaviors that you don’t always get time to discuss: alcohol, tobacco, substance use, sexual history, contraception.
Spend some time on diet and exercise. We highlighted the importance of asking about soda, sweetened coffee beverages, and alcohol.
A recent cohort study in JAMA IM found that among 450k individuals from 10 European countries, consumption of soda was associated with higher all-cause mortality (artificially-sweetened beverages associated with higher risk of death from circulatory diseases; sugar-sweetened beverages associated with higher risk of death from digestive diseases).
Ask about safety: seatbelts, helmets, and firearms.
A vegan diet excludes all animal products, including milk, eggs, and milk products.
Vegans are at risk for vitamin B12 and vitamin D deficiency if they do not consume enough fortified food products.
Consider vitamin B12 and vitamin D supplementation for these patients.
Finally, let’s take a look back at our case of hematuria from last week. A recent microsimulation model published in JAMA IM highlighted some of the costs and benefits associated with various guidelines for the evaluation of hematuria. These guidelines range from a recommendation for risk stratification followed by ultrasonography and cystoscopy (Canadian Urological Association) to a recommendation for CT urography and cystoscopy for all patients >35yo (American Urological Association).
While the AUA guidelines missed the fewest number of cancers, this came at a significant cost in terms of dollars, radiation exposure, and other testing-related harms.
Something to consider in your initial evaluation of microscopic hematuria!
Case Summary: An elderly gentleman presented to clinic with his caregiver who expressed significant frustration because the patient had become more argumentative and confused over the preceding few months. The patient had several unwitnessed falls, was no longer completing his daily responsibilities like cleaning, and endorsed visual hallucinations. Objectively, he was oriented to self only, had no signs of parkinsonism on exam, had a normal gait and was unintentionally losing weight because he was no longer eating regularly. He was diagnosed with Lewy Body Dementia and eventually transitioned to a long-term care facility.
Tips on completing a history and physical for a patient with dementia:
Separate the caregiver and patient. Be direct and explain that you do this with all of your patients. Spend time 1:1 with both the patient and the caregiver. Discuss caregiver burnout and additional resources available in your community such as short-term respite. Even if the patient cannot answer many questions, you can ask them short, direct questions like “Is anyone hurting you?”
Assess function. Ask the patient to describe their morning routine to assess ADLs (ex. bathing, toileting, eating, grooming, etc) and then their afternoon routine to assess for IADLs (ex. cooking, shopping, paying bills, housework, etc). The get-up-and-go test is a good screening test for frailty.
Assess cognition. The mini-cog is a quick screening test for cognitive impairment and includes 3-item recall and clock drawing. If it’s positive, the MOCA can be a useful way to assess the severity of impairment. However, the MOCA was developed and studied in patients from Western cultures with high levels of education. For patients with limited English proficiency and low literacy, results may not accurately reflect the patient’s cognitive status.
Provide Support and Resources! Remember to utilize your clinic, health system, and community resources. Keep in mind that undocumented patients are not eligible for many government programs like SSI (Supplemental Security Income) and IHSS (In-Home Support Services). In California, consider referring elderly or disabled low-income patients who are undocumented to CAPI (Cash Assistance Program for Immigrants) for supplemental income.