Thank you to Vaibhav for making an appearance while on the lung consult service to present a diagnostic mystery! He presented the case of a middle aged man presenting with 4-6 weeks of HA, night sweats and cough who was found to have severe eosinophilia > 5,000!! We never did identify the cause of this patient’s elevated eos, however given recent travel he was treated with albendazole despite negative serology tests for parasitic infections. While on therapy and without steroids his eosinophilia gradually improved.
- The differential diagnosis for eosinophilia can be remembered with the pneumonic NAACP – Neoplasm, Addison’s disease, Allergy (includes medications), Collagen Vascular disease (GPA) and Parasitic infections (thanks Greg!!).
- The most common cause of eosinophilia worldwide is helminthic infections and most common cause in industrialized nations is atopic disease.
- The differential diagnosis narrows when one considers severe >(5,000k) eosinophilia:
- Primary hematologic disease (eosinophilic leukemia, systemic mastocytosis with eosinophilia)
- Paraneoplastic (Lymphoma)
- Infectious – thank you Jen for this ddx: lymphatic filiariasis, toxocara, trichinosis and strongyloides all cause eos > 5,000
- NOTE: giardia, malaria and babesia do NOT produce eosinophilia.
- Tissue damage is more likely at eosinophil counts >1500, but can also occur at lower levels!
For those who want to learn more about Eosinophilia!!
- Eosinophilia: Absolute eosinophil count > 500
- Hypereosinophilia: Severe eosinophilia >1500
- Hypereosinophilic syndrome (HES): Hypereosinophilia (1,500) lasting > than 6 months on at least 2 occasions with end-organ dysfunction due to eosinophilia.
- Recommended workup for unexplained eosinophilia:
– CBC, diff, blood smear
– Chem, u/a, LFTs
– Troponin (cardiac infiltration)
– Strongyloides serology (stool as we discussed not as helpful if patient is without diarrhea)
– Vit B12 (elevated in myeloproliferative neoplasm)
– Flow cytometry for lymphocyte subsets
– Chest Xray
– Serum tryptase (mastocytosis or hypereosinophilic syndrome)
Can also send if appropriate:
– Molecular testing for hematologic disorders
– Immunoglobulin levels (autoimmune disease or immunodeficiency)
– Morning cortisol
– Stool O&P
– Viral serologies (e.g. HIV, HTLV)
– Serologies for specific parasitic infections (e.g. schistosomiasis)
– CT, lymph node biopsy
iii. Specific organ involvement:
- Well’s syndrome (eos cellulitis),
- Shulman’s syndrome (eos fasciitis)
- Eosinophilic panniculitis
- Kimura’s disease- amgiolymphoid hyperplasia
- Pulmonary- interstitial lung disease, hypersensitivity pneumonitis,
- Loeffler’s (pulm infiltrates w/eos due to helminthic infxn)
- Eosinophilic gastroenteritis
- Cardiac- hypersensitivity myocarditis, endomyocardial fibrosis
See this article for much more on Evaluation and ddx of marked, persistent eosinophilia!
Thank you pre-Holiday ZSFG residents for presenting a great case of an elderly woman with fall with LOC coming in with facial bruising. In addition to talking about bradycardia, we had a great discussion about home supports for elderly patients.
Keeping Elders at Home: Social Supports at Home
- In-Home Supportive Services (IHSS) Program
- Administered through the California Department of Social Services
- Can help with domestic chores, laundry services, food shopping, other shopping/errands
- Maximum of 283 hours/month (9 hrs per day) for severe disability
- Maximum of 195 hours/month (5 hrs per day) for not severe disability
- Note that is can be very difficulty to get up to this max number of hours
- Home Health
- RN, PT, OT, SW, SLP, home health aide (“Skilled Needs”)
- Does not provide for “non-skilled” needs like custodial care
- Somewhat variable in the amount they can see a patient
- Requires a physician to complete a “face-to-face” evaluation and designate that a patient is essentially homebound
- Covered by Medicare/Medicaid for some amount of time
- Meals on Wheels
- Can provide 2 meals per day delivered to a patient
- Adult Day Health
- Typically privately paid for by patient’s families
- Typically provides 4-5 days/week of day time (think office hours) oversight
- Can be highly variable in the activities and services available ranging from including transportation to/from facility, meals, physical therapy, occupational therapy, exercise
- OnLok/PACE Programs
- Medicare funded model for wrap-around care
- When a patient enrolls, OnLok becomes the insurer and medical provider including the PCP
- OnLok is the model program for PACE programs across the country (started in SF)
- Revolves around a Day Program, where residents are picked up from their homes and brought to program
- Drop-in for physicians and can bring multiple services into site (including Ophtho, Dental, Podiatry, etc.)
- If you join OnLok, you cannot keep IHSS and this can be a barrier
Sorry for the late post. Catching up on some of those awesome peri-Holiday reports. Thanks for your patience team! Thank you to our ZSFG Team for presenting a case of “mucoid” Klebsiella (also called hypervirulent (hypermucoviscous) Klebsiella pneumoniae.
Thanks to Lekshmi Santhosh, whose prior pearls are integrate here
Hypermucoviscous Klebsiella pneumoniae:
- Originally from the Pacific Rim, but it’s here now, so brace yourselves
- Defining Clinical Features:
- Serious, life-threatening community acquired infections
- Often in younger, healthy hosts
- Metastatic Spread! (Remember that this is very unusual for Gram-negative bacilli – and essentially acts like STAPH)
- Liver abscess
- Klebsiella pneumonia is an encapsulated GNR and the K antigen is the capsular polysaccharide
- It has a mucoid appearance and one of the main determinants of virulence
- The hypermucoviscosity (HV) Phenotype is determined by the string teste. formation of viscous strings when a loop is used to stretch a colony from an agar tape https://www.youtube.com/watch?v=_LP5KoguPC0
- This hypermucoviscosity phenotype has been seen more commonly in patients from East Asia esp Taiwan – DM is also a very common risk factor
- It does not appear that there are clear clinical guidelines about a standard work-up (confirmed with local expert Lisa Winston)
- Work-up for metastatic disease should be guided by clinical suspicion
- Fortunately, most strains have been susceptible to antimicrobials, except Amoxicillin (sensitivity testing is important)
- Source control is essential, and since this can cause abscesses remember that those need to be drained
- Hypermucoviscous Klebsiella Pneumoniae:
- Shon AS, Bajwa RPS, Russo TA. Hypervirulent (hypermucoviscous) Klebsiella pneumoniae: A new and dangerous breed. Virulence. 2013;4(2):107-118. doi:10.4161/viru.22718.
Thanks to Arielle for presenting a fascinating case of a 65M with multiple prior stokes who presented with AMS, hypernatremia and then found to have new multifocal strokes.
- Head imaging [CT non-contrast] is not necessary in patients presenting with altered mental status [without trauma] after an obvious cause [e.g. hypernatremia] is uncovered on routine labs.
- Multiple trials have previously shown that PFO closure does not reduce the incidence of recurrent stroke(CLOSURE-I, PC, and RESPECT). However, two recent meta-analyses showed potential benefit in patients with recurrent cryptogenic strokes at the cost of an increases risk of Afib/flutter . Link 1 Link 2
- While a thrombosis on anti-coagulation raises concern for a number of hypercoaguable conditions [see below] the first step is to clarify whether the patient was receiving adequate anticoagulation [e.g. under-dosing].
Initial evaluation of a stoke
- Is this a stoke? [DDx: Seizure, hypoglycemia, syncope, other]
- Last known normal?
- NIH stroke scale?
- contraindications to tPA?
- <90 min —> NNT for functional independence = 3.6
- <180 min —> NNT = 4.3
- 6% of any bleed
- 1-2% of significant bleed
- More evidence to suggest benefit up to 24h
- NNT 2-3
- Aspirin 325 x1 —> 81
- Give in ED if no tPA
- Give 24h later if tPA given
- BP management
- Permissive HTN up to 220, usually < 1 week
- See above for tPA or embolectomy
Clotting on anticoagulation
- An important part of the management of VTE is the reversal of any underlying trigger.
- Easier when the DVT is provoked [e.g. surgery]
- In cases with unprovoked VTE either:
- provoking factor was not recognized OR
- There is a genetic disruption [e.g anti-thrombin 3] in the control of the coagulation cascade.
- These disruptions are usually related to a protein deficiency in the regulation of the cascade [e.g., protein C deficiency]
- The urge to uncover this disorder is tempered by the fact that it rarely changes management [life long anticoagulation]
- Down-regulation of the pro-coagulant factors [e.g. Factor 2] with lifelong anticoagulation is usually sufficient for these conditions.
- In some acquired causes, the driver for the hypercoaguability exists outside the coagulation cascade [e.g. heparin-induced thrombocytopenia].
- Syndrome specific features may offer clues to the Dx [e.g. recent receipt of heparin –> thrombocytopenia], but other features include
- Clotting in atypical locations – e.g. Budd Chiari/venous sinus thrombosis
- Multiple simultaneous thrombi
- Clotting while on full dose anticoagulation.
Here’s one approach to this scenario
Step 1: Is the patient taking/on the right dose of anticoagulation?
Step 2: Consider embolic disease
Step 3: Consider thrombotic disease
Thank you Monica for presenting the case of an elderly gentleman presenting with chronic fatigue, muscle aches, wrist and hand joint pain, and weight loss found to have PMR and RA.
- LT’s pearl: Many patients with PMR present with acute onset of symptoms
- Other lab findings that may be present in patients with PMR: mild normocytic anemia, elevated alk phos (although more common in patients with GCA)
- Patients with PMR only need temporal artery biopsy if they have symptoms of arteritis. About 5-30% of patients with PMR will have GCA
Polymyalgia Rheumatica Refresher
- Clinical Manifestations
- Proximal pain and morning stiffness
- Shoulder pain is the most common symptom
- LT’s pearl: Many patients report acute onset of symptoms
- Distal symptoms occur in ~50% of patients including peripheral arthritis, carpal tunnel, pitting edema of hands and feet)
- Systemic symptoms (fever, weight loss, malaise) are present in ~1/3 of patients
- Laboratory Findings
- Elevated inflammatory markers
- Non specific findings (not present in all patients)
- Mild normocytic anemia
- Elevated Alk Phos – although more common in patients with GCA
- No other systemic disease to explain symptoms
- Onset of symptoms after age 50
- Proximal aching and morning stiffness lasting >30 minutes for at least 2 weeks
- LT’s pearl: Many patients report acute onset of symptoms
- Shoulder pain is the most common presenting symptom
- ESR > 40
- Rapid resolution of symptoms with prednisone
- Lack of response strongly suggests another diagnosis
- There are no set diagnostic criteria, but the ACR/EULAR have proposed criteria to be used in research studies but do not recommend use for diagnosis in individual patients
- Atypical PMR
- Asymmetric symptoms
- Low ESR
- Some patients have normal or mildly elevated ESR (7-20% at time of diagnosis)
- Check CRP
- If both ESR and CRP are normal, much less likely to be PMR
- Does my patient with PMR have GCA?
- 50% of patients with GCA have PMR. Of those with PMR, 5-30% get GCA
- Clinical manifestations of GCA
- Only need to get temporal artery biopsy if the patient is having symptoms of temporal arteritis
- Goal of therapy: Improve symptoms
- Starting dose: 15-20 mg prednisone per day
- After a period of quiescence (2-4 weeks) then start a slow taper by 10-20% every 2-4 weeks
- 50% of patients will have recrudesce of their symptoms and need re-treatment with steroids or increase in their steroids
Evernote Link: https://www.evernote.com/l/AMr2DzbkfG9K56vgSepfENvXq9AhGchMp04
Here are some round-up pearls from 2 great cases this week!
Case summary 1: On Monday, Jill presented the case of an elderly man with a history of obstructive struvite stones and Proteus bacteremia s/p nephroureterostomy tube, who presented with septic shock from recurrent/persistent struvite stones.
- Interestingly, Proteus contributes to recurrent stone formation in 2 ways:
- Urease splitting bacteria generate high urinary pH levels
- The body can’t clear the urinary tract of the bacteria because they are embedded in the stones.
- Other reasons to have alkaline urine:
- (1) urinary tract infection (Proteus and others)
- (2) metabolic or respiratory alkalosis
- (3) failure of acidification (renal tubular acidosis)
- (4) ingestion (alkaline diet [a fad diet right now!], medications like sodium bicarbonate).
- This is important, as alkaline urine can precipitate struvite and calcium phosphate stone formation
- Acidify urine with cranberry juice or betaine
- In contrast uric acid, cystine and calcium oxalate [most common in adults] stones precipitate in acidic urine (prevent with alkalinzation of urine via dietary changes or calcium citrate/K citrate
Here’s a great review on nephrolithiasis: https://www.aafp.org/afp/2011/1201/p1234.html#afp20111201p1234-c1
- A nephroureterostomy tube has both internal (via ureter) and external (via nephrostomy tube) drainage, so lack of external drainage does not necessarily indicate tube dysfunction.
Here’s a diagram for the visual-minded:
Case summary 2: At intern report, we discussed a patient who was post-op day #1 s/p an ankle fusion who developed chest pain and was found to have diffuse ST depressions and STE in aVR. This got us to talking more broadly about ACS and “STEMI equivalents.”
- Moral of the story: new or presumed new LBBB may not predict ACS.
- 2 retrospective studies looked at ~900 and ~300 patients with new or presumed new LBBB and concluded
- Those patients with new or presumably new LBBB are a high-risk group (older, higher TIMI scores, more cardiomyopathy).
- However only ~1/3 had acute MI, while the remaining patients had other cardiac or non-cardiac diagnoses
Here’s a Medscape article summarizing the literature on LBBB as a STEMI equivalent: https://www.medscape.com/viewarticle/753695_1
Thank you Kapil for presenting the case of an elderly man born in China presenting w/ cough found to have a unilateral exudative pleural effusion. After inpatient work-up w/ ddx initially including TB and malignancy, it was felt that this effusion is likely a result of his recent CABG (the date was signed out to the team was years prior when in fact it was weeks prior).
- Always verify history, labs, medications and imaging for holdover patients as this can dramatically influence your approach and work-up. Trust, but verify!
- Light’s criteria (below) is positive when ONLY 1 out of the 3 criteria (below) are met. This test is extremely sensitive (98%) so as not to miss exudative effusions (see below).
- Pleural effusions are common after CABG with a reported prevalence of 40-75% 1 week after surgery. Most of these are asymptomatic, exudative, small, left-sided and resolve over several weeks.
- The cause of 15-20% of all plural effusions will remain unknown. See this article from Chest looking at non-malignant effusions. They found that bilateral, transudative effusions were associated with a one year mortality of 50%!
More on Effusions after CABG
- Bloody, exudative, effusions tend to occur to earlier ( < 4 weeks after surgery). These are usually easy to control with one to three therapeutic thoracenteses.
- Non-bloody effusions tend to occur later (> 4 weeks after surgery) and have a relatively low LDH and high percentage of lymphocytes. These effusions tend to be more difficult to control.
See this article for a review of pleural effusions and these figures!