ZSFG Morning Report Pearls 1/7-1/11

Monday, 1/7: Pulm/ICU Report

Thank you to Mike T. for presenting!

Man in his 20s w/ h/o atopy, smoke exposure p/w subacute progressive DOE & wheezing w/ inspiratory & expiratory wheezing on exam c/w obstructive airway disease.

  • Important exposure history: Pets, mold, hot tub, occupation or in Mike’s words “What do you breathe in that the average person doesn’t?”
  • Inhaled corticosteroids should be held 72h prior to PFTs. They shouldn’t influence results prior to 72h so OK to start patients on ICS and then hold them 72h before PFTs.
  • Rabih Geha’s obstructive airway disease schema here:

obstructivelungdiseaseschema_gehaTuesday, 1/8: HIV/ID Report

Thank you to Mike R. for presenting!

Middle-aged man with h/o IV drug use, HIV not yet in care p/w left shoulder pain, found to have left septic shoulder w/ strep viridans, microcytic anemia, and acute on chronic kidney injury.

  • You can page the PHAST team from any hospital to get people w/ HIV connected to care including ART as fast as possible.
  • The overall WBC count can be reduced in s/o acute illness, which can artificially lower the CD4 count. Use the percentage to help figure out if the CD4 count is accurate. A CD4 of 200 should correlate with a CD% of about 12-14%.
  • Septic joint is most likely 2/2 hematogenous spread. In this case, it was most likely 2/2 direct spread from an abscess containing strep viridans.
  • Licking needles or spitting to mix drugs can introduce strep viridans into the blood. Again, another mechanism of entry is suspected in this case.
  • When selecting initial ART for a patient, aim for a one pill regimen if possible, consider patient’s comorbidities like CKD, possible interactions with other medications like HCV treatment, as well as adherence and the regimen’s likelihood of becoming resistant. However, HIV/ID team wants to be involved as well to help you make these decisions!
  • Integrase inhibitors, like dolutegravir, are more likely than protease inhibitors to decrease the viral load quickly.

Wednesday, 1/9: Hospital Medicine Report

Thank you to Tash for presenting!

Man in his 60s w/ h/o 80 pack year smoking hx presenting with subacute shortness of breath and diffuse wheezing on exam.

  • Indications for noninvasive positive pressure ventilation (NIPPV) – BiPAP/CPAP:
    • Moderate-Severe COPD Exacerbation
    • Respiratory acidosis, pH generally 7.25-7.35
    • Cardiogenic pulmonary edema
    • Possibly – hypoxemic respiratory failure for immunocompromised individuals

Thursday, 1/10: Intern Report

Thank you to Tash for presenting twice in a week!

Young woman with h/o hydroxycut use p/w subacute progressive abdominal distension & jaundice 2/2 new dx cirrhosis, UMN & sensory deficits, thought to be possibly due to copper deficiency from excessive zinc ingestion from the zinc in hydroxycut.

Copper deficiency:

  • Causes: Gastric surgery is most common cause of acquired copper deficiency. Other causes include excessive zinc ingestion, dietary copper deficiency, malabsorption syndromes, and chelation therapy in Wilson disease.
  • Most common neurologic findings: Dorsal column disease (like Vitamin B12 deficiency) + spasticity & + Babinski, +/- peripheral small fiber neuropathy in stocking distribution
  • Most common heme manifestations: anemia (MCV could be anything) and leukopenia. Thrombocytopenia and pancytopenia are relatively rare.
  • One case series and a case report describe hepatic iron overload and/or cirrhosis in five patients with copper deficiency myeloneuropathy. Authors speculated this was caused by secondary deficiency of ceruloplasmin, which oxidizes iron for binding to transferrin, which facilitates iron mobilization.

https://www.uptodate.com/contents/copper-deficiency-myeloneuropathy?search=copper%20deficiency&source=search_result&selectedTitle=1~54&usage_type=default&display_rank=1

Thackeray EW, Sanderson SO, Fox JC, Kumar N. Hepatic iron overload or cirrhosis may occur in acquired copper deficiency and is likely mediated by hypoceruloplasminemia. J Clin Gastroenterol 2011; 45:153.

Videt-Gibou D, Belliard S, Bardou-Jacquet E, et al. Iron excess treatable by copper supplementation in acquired aceruloplasminemia: a new form of secondary human iron overload? Blood 2009; 114:2360.

Friday, 1/11: GI Report

Thank you to Zane, one of our awesome new clerkship students, for presenting!

Young woman w/ h/o former alcohol & IV drug use, HCV, cirrhosis presumed 2/2 alcohol p/w decompensation w/ encephalopathy & ascites likely 2/2 non-adherence to diuretics.

  • For diuresis, push the spironolactone until you see the UrineNa > UrineK.
  • She should be referred for evaluation of liver transplant!
  • This person should be treated for HCV to decrease the risk of progression of ESLD and HCC, though if she’s going for transplant, would do it afterward.

DDx for young adult with cirrhosis:

  • Tox: Alcohol (can also accelerate other processes like HCV and NASH)
    • 10 years of daily alcohol use of 80g for men and 30g for women can lead to cirrhosis, which is important to educate our patients about!
  • Infectious: HCV, HBV (vertical transmission)
  • Autoimmune: PBC, PSC, autoimmune hepatitis
  • Infiltrative: Wilson disease, NASH
  • Genetic: Wilson, glycogen & lysosomal storage diseases (like Gaucher’s), alpha-1 antitrypsin deficiency
  • Copied from a prior blog post on 3/8/17 (thanks, Sam!)
    • In a 1988 Indian studyof 63 young cirrhotic patients of mean age 22 years (Sarin SK, Gut 1988;29:101-107), the most common causes were HBV(50%), followed by alcohol (10%), cryptogenic (19%), and rarely, Wilson disease or alpha-1-antitrypsin deficiency (1% each). Notably, HCV was discovered in 1989 so would have been part of the cryptogenic group in this study.
    • 2014 U.S. study of 219 cirrhotic patients under the age of 40 (Sajja KC, J Investig Med 2014;62:920-926) showed that the most common causes of cirrhosis in patients <40 years old were alcohol(45%), HCV(33%), autoimmune (5%), cryptogenic/NASH (4%), HBV(4%), and PBC/PSC (2%). Notably, this study was single-hospital in Texas. The patients were 69% male, 41% Hispanic, 40% Caucasian, 14% African-American, and only 1% Asian/Pacific Islander, so the prevalence of vertically transmitted HBV is likely different than in the San Francisco population.
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ZSFG Morning Report Pearls 12/17-12/21

Monday, 12/17: Pulm/ICU Report

Thank you to Serge for presenting!

Man in his 60s h/o lithium use p/w AMS & seizure-like movements who developed acute hypernatremia upon admission in s/o SAH who then developed acute tachycardia and hypotension 2/2 acute GIB 2/2 large duodenal ulcer despite PPI therapy. Gastrin level of 700.

  • DDx of duodenal ulcer despite PPI: H. Pylori, Gastrinoma
  • 90% of isolated duodenal ulcers 2/2. H. Pylori
  • Massive transfusion protocol if expect to use > 4 units/1hr or > 6units/12hrs
  • PPI use leads to elevated gastrin levels in nearly all patients.
  • In the majority, gastrin levels are only moderately increased (<400 ng/l or <4 x ULN) and in most of these patients, gastrin levels quickly normalize after stopping PPI.
  • In some patients however gastrin levels during PPI therapy can increase to higher levels (400–4000 ng/l) and may show slower or incomplete normalization after PPI withdrawal. These people are more likely infected withH pyloriand have a high prevalence of atrophic gastritis of the gastric body mucosa.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1860013/

Tuesday, 12/18: HIV/ID Report

Thank you to Jack for presenting!

Man in his 60s h/o polycythemia vera s/p BMT p/w 7-10d dyspnea and cough initially improving but then acutely worse w/ hypoxia & high fevers on admission w/ CT showing multifocal dense consolidations with some cavitation and GGOs w/ MRSA on sputum cx, all though to be due to MRSA PNA +/- concomitant viral PNA.

  • If sputum gram stain shows one kind of bacteria, it’s likely true pathogen.
  • If a patient is taking vori (either prophylaxis or treatment), check a vori level to see if therapeutic.
  • Voriconazole-resistant molds on the rise due to use of vori for prophylaxis.
    • Mucormycosis
    • Rhizopus
    • Scedosporium
  • Think about chest CT findings in three categories: Consolidations, nodules, and GGOs. Consolidations and nodules can cavitate.
  • This CT description above was classic in many ways for MRSA PNA. GGOs are less likely the MRSA itself (though still possible) and may be due to viral PNA (more likely in this case) or hemorrhage (less likely in this case).

Wednesday, 12/19: Hospital Medicine Report

Thank you to Kendra M. for presenting!

45M with no significant PMH p/w 2 wks progressive dyspnea who quickly developed hypoxic respiratory failure & was found to have bilateral opacities on CT scan as well as numerous nodules throughout chest and abdomen. Diagnosis TBD, possibly T-cell lymphoma.

  • Lymphoma can present in many different ways.
  • Non-Hodgkin lymphoma often presents with diffuse or variable LAD, whereas Hodgkin lymphoma (HL) presents with contiguous LAD (ex cervical—> supraclavicular —> axillary).
  • HL presents as a painless mass in approximately 70% of cases.

Thursday, 12/20: Intern Report

Thank you to Justin for presenting!

Middle-aged man h/o HIV out of care for years p/w frontal headache and somnolence, serum Crag +, LP w/ + CSF Crag, diagnosed with cryptococcal meningitis.

  • Typical presentation: Immunocompromised person who develops headache, lethargy +/- personality changes and memory loss over two to four weeks. Rarely can occur in immunocompetent host.
  • Treatment:

1.Induction with Amphotericin & Flucytosine for at least 2 weeks, repeat LP @ 2 wks to send repeat fungal culture

2.Transition to consolidation therapy w/ fluconazole (400 to 800 mg po daily for eight weeks) when:

  • There’s a clear clinical response to treatment and favorable baseline CSF studies, such as a low starting fungal burden by quantitative CSF yeast counts (eg, <5 log10 colony-forming units [CFU]/mL) and/or CrAg titer (≤1:160)
  • For all others, wait until CSF fungal cultures from that repeat LP are negative at two weeks

3.Maintenance therapy with fluconazole (200 to 400 mg po daily) for usually one year after diagnosis.

Friday, 12/21: Caring for Vulnerable Patients Report

Thank you to Mike for putting together a great presentation and facilitating an awesome discussion!

Man in his 60s h/o schizophrenia, OUD on methadone maintenance with recent decompensation from his schizophrenia and resulting medical complications.

  • Uncertainty tolerance: We all fall on a spectrum. The culture of medicine manifests a deep-rooted unwillingness to acknowledge and embrace uncertainty. Uncertainty instills vulnerability and a lack of security. Higher intolerance of uncertainty has been linked to burnout in PCPs and EM doctors.
  • We can sit with uncertainty with resilience-building, community, and perspective-taking.
  • Resilience: positive attitudes and effective strategies that we employ in response to life stressors.
  • Perspective-taking:
  • Our patients are resilient.
  • We capture them in a moment in time and may not change their overall trajectory dramatically but we will have an impact.
  • We are one of many providers or people encountering our patients every day.
  • Resources: Mobile Crisis Unit for patients acutely decompensating from mental health issues, police wellness check (Phone #: 415-553-0123), Practice embedded mental health in BAART

Zion AM Report: Collection of Clinical Updates 12/2018

Thanks to our Zion residents’ feedback to add clinical guidelines to our AM reports! This month, we discussed many cardiology based topics – aspirin for primary prophylaxis, new guidelines for lipid management, and practice management for smoking cessation!  See below for pearls!

Aspirin for primary prevention of cardiovascular disease:

USPSTF current recommendation (2016):

  • Low dose ASA recommended for adults ages 50-59 if 10 year cardiovascular risk > 10% and not at excess risk of bleeding
  • Not enough evidence to recommend low dose ASA for adults older than age 60

Three recent trials: ARRIVE, ASCEND, ASPREE

RCT

Goal

Findings?

 

ARRIVE

(Lancet 2018)

 

 

100 mg daily ASA versus placebo in reducing cardiovascular conditions in patients deemed moderate risk (10-20% ASCVD 10y risk) No difference in primary endpoint (CVD event) in ASA v. placebo group.

 2x statistically significant increased rate of GI bleed (mostly mild) in ASA v. placebo group

 

ASCEND

(NEJM 2018)

 

Evaluate effect of ASA (100 mg daily) on serious vascular event in patients with diabetes Decreased risk of serious vascular events (8.5% v 9.6%, RR 0.88, p = 0.01) in ASA group, BUT statistically significant more major bleeding events (4.1% v 3.2%, RR 1.29).
ASPREE

(NEJM 2018)

 

Healthy elderly patients (65+) assigned to ASA 100 mg daily or placebo CVD events similar in ASA group v placebo.

Major hemorrhage occurred at higher rates in ASA group (HR 1.38, CI 1.18-1.62, p<0.001)

Key pearls for aspirin as primary prevention?

  • Decreased risk of cardiovascular events probably reflects a more low-risk population due to other risk modifying strategies (statin, HTN control, smoking cessation) – these methods of primary prevention appear SAFER and more BENEFICIAL than use of aspirin!
  • The bleeding risk with aspirin should be thoroughly discussed with your patients with diabetes, elevated ASCVD risk. The benefit in reduction of cardiovascular events is marginal.
  • For your elderly patients on aspirin for primary prevention, safe and recommended to discontinue use!

Shout out to the Curbsiders recent podcast on this very topic!

 

Clinical Guidelines Update: Lipid Management:

ACC and AHA released new guidelines this past month on management of hyperlipidemia:

  • ASCVD risk scores between 7.5 – 19.9% are now intermediate risk; these patients need lifestyle changes and consideration of moderate intensity statin
  • Patients with established ASCVD or those with elevated ASCVD risks (>20%)?
    • 1st line therapy: high intensity statin
    • Not at goal? Add ezetimibe to high intensity statin, followed by PCSK9 inhibitor
  • Primary prevention still focuses on lifestyle modifications! Don’t forget about other risk factors for ASCVD not traditionally included in calculators – FH, ethnicity, metabolic syndrome, coronary artery calcium score > 100. In these folks, consider initiation of statin therapy.
  • Now recommended to check repeat lipid panel 1-3 months after treatment initiation/change to monitor therapy effectiveness – goal is > 50% reduction in LDL!

 

Smoking Cessation Best Practices:

ACC also released consensus recommendations on management of smoking cessation this month! We discussed key pearls in managing our patients that currently smoke tobacco products:

  1. We do a great job of screening patients for tobacco use disorder, but we often struggle with the follow up! Current guidelines recommend close follow up in 2-4 weeks post-treatment to monitor response, adherence, and troubleshoot barriers to success! Utilize your clinic staff or make this part of your panel management efforts 🙂
  2. Varenicline NO LONGER has a blackbox warning as of 2016 – there is still some stigma and hesitancy to prescribe this medication due to prior blackbox risk of increased psychiatric adverse effects and suicidality. These events are NO more common than with other cessation tools.
  3. Pharmacotherapy and Counseling COMBINATION is most effective in helping patients reach their cessation goals.
  4. OK to combine nicotine replacement products to help with situational cravings, even in patients with known CVD!
  5. Use the APEX smartset for tobacco cessation to easily order smoking cessation medications, refer to tobacco quit line or Fontana center, and print AVS patient materials!!
  6. Other great resources to provide patients:

Zion AM report: New hypertension & nephrotic syndrome!

Thanks to Molly Heublein for presenting a fascinating case of a middle aged woman with metabolic syndrome and new hypertension, ultimately found to have nephrotic range proteinuria, and diagnosed with FSGS on renal biopsy!

What workup is recommended for the initial evaluation of the hypertensive patient?

basic testing for HTN

  • ACC recommends basic testing to identify those at risk of secondary causes of hypertension (see below), further risk stratify patients cardiovascular health, and to identify target organ damage that might warrant more aggressive BP control/goals.
  • Currently, the ACC recommends starting with urinalysis rather than spot microalbumin, although this might change in the future!

Who should be considered for secondary causes of hypertension?

screening for secondary hypertension

**Remember the long list of medications that can contribute to hypertension as well!

  • OCPs
  • NSAIDs
  • Stimulants
  • Steroids
  • Licorice
  • Decongestants
  • Diet/herbal teas
  • EPO

What should the PCP know about Nephrotic Syndrome?

Check out these prior Chief Blog posts for some other awesome information: Moffitt report, VA ambulatory report, and ZSFG report

  • Key features:
    • Proteinuria > 3.5g per day
    • Hypoalbuminemia (usually < 3 g/dL)
    • Peripheral Edema (2/2 to hypoalbuminemia and low oncotic pressure + sodium retention)
    • Hyperlipidemia (lipoprotein production stimulated by drop in oncotic pressure)
    • +/- Thrombotic events (due to loss of important clotting factors/proteins!)
    • +/- increased susceptibility to infections (particularly pneumonia due to loss of immunoglobulins)
  • Etiologies:

Nephrotic syndrome etiology

(stolen from Matt’s previous post with some additions!)

Primary renal disease

Extrinsic/systemic causes

Minimal change disease

(can be paraneoplastic or associated with NSAIDs in adult onset)

Membranoproliferative (SLE, subacute bacterial endocarditis, HCV/HBV/cryoglobulinemia)
Primary FSGS (usually more acute onset) Secondary FSGS (more chronic/insidious onset – secondary to HIV, obesity, drugs)
Primary membranous nephropathy Membranous nephropathy (SLE, HBV, thyroiditis, meds)
Deposition diseases (DM, amyloid)
  • Workup of Nephrotic Range Proteinuria:
    • Urine protein : creatinine ratio
    • A1C
    • TSH
    • HIV, RPR
    • HCV, HBV serologies
    • Lipid profile
    • SPEP/SFLC
    • Other tests routinely sent but should really be history driven: ANA, C3, C4, anti-dsDNA, cryoglobulins, ASO
    • Renal ultrasound: important in the outpatient setting if unexplained reason for proteinuria/CKD; helps to identify physical abnormalities (such as solitary kidney, multiple renal cysts, small kidneys) which would make renal biopsy contraindicated
    • Referral to renal for biopsy!! Usually warranted in adults if proteinuria persistent and etiology unclear!

Management of FSGS?

  • Immunosuppressive therapy (steroids, tacrolimus( usually trialed for those with primary/genetic FSGS
  • Prevention of disease progression and treatment of underlying cause warranted for secondary/chronic FSGS
  • All patients:
    • Treat proteinuria and HTN with ACE/ARB
    • Treat edema with loop diuretics and sodium restriction
    • Pneumococcal vaccine for all patients with nephrotic range proteinuria!
    • Statin therapy usually warranted for hyperlipidemia
    • Prophylactic anticoagulation controversial but if thrombosis, usually warfarin is agent of choice, duration for 6-12 months or as long as patient remains nephrotic.

Pearls:

  1. Pay attention to the urinalysis protein, especially if persistent and without symptoms of UTI/fever/illness.
  2. Remember that hypertensive patients should get some initial laboratory evaluation; starting with BMP and UA are totally appropriate! Remember to also further risk stratify for other cardiovascular diseases like diabetes, hyperlipidemia!
  3. Always ask your hypertensive patients at the very least about medications/OTCs (including NSAIDs, herbals), alcohol, and snoring!

References:

American College of Cardiology/American Heart Association Task Force on
Clinical Practice Guidelines. 2017 Guideline for the Prevention, Detection, Evaluation,
and Management of High Blood Pressure in Adults. J Am Coll Cardiol. Sep 2017, 23976.

Katakam, Brukamp, & Townsend. What is the proper workup of a patient with hypertension? Cleveland Clinic Journal of Medicine. 2008 September;75(9):663-672.

 

Evernote: https://www.evernote.com/l/AN00skM48fBDL7FbNzfUhlMqKGAAgPndae0/

 

 

Mt. Zion Report: Cold Urticaria!

Thanks Corynn for presenting the case of a young woman with urticaria induced by cold exposures (including eating icecream – eek!) ultimately diagnosed with cold urticaria syndrome. What a great opportunity for us to discuss key features for any patient coming in with a rash, and to learn more about this rare disorder!

Patient coming in with a rash – what are key questions/features to ALWAYS ask about?

  • Sexual history
  • Occupation
  • Other exposures (travel, pets, meds/drugs, sick persons)
  • Systemic symptoms
  • Distribution/mucus membrane involvement
  • Pruritis v. pain
  • TRIAGE! Airway/respiratory symptoms, extent of involvement, vital signs

Cold Urticaria – What is it?

  • Presentation: Inducible urticaria (pruritic hives) and/or angioedema AFTER cold exposures (contact with cold temperature, liquids/foods, air)
  • Pathophysiology: IgE mast cell activation in response to cold temperatures
  • Usually self-limited disease that can go into remission after a few years, but case reports show some association with Lyme disease, hepatitis, HIV, mononucleosis, chronic H pylori.
  • Subset of patients high risk of more severe systemic reactions such as angioedema and anaphylaxis, especially if significant time duration, extensive body involvement, and lower temperatures of cold exposure.
  • Workup: no specific labs usually needed, but can consider Cold Stimulation Test
    • Ice cube test – place ice cube in thin plastic bag with small amount of water, then place bag on forearm for 5 minutes. Remove the bag and reassess after 10 minutes. If wheal has developed, highly suggestive of cold urticaria (Sn 83-90%, Sp 100%)!
  • Management:
    • Avoidance of cold exposures (especially swimming, eating cold foods/liquids, surgery/ORs!)
    • Antihistamine therapy for prophylaxis (surprisingly, folks with cold urticaria often need higher than usual doses of nonsedating antihistamines, with some requiring 4x/day dosing!)

 

References:

  • UptoDate Cold Urticaria
  • Singleton & Halverstam. Diagnosis and Management of Cold Urticaria. Cutis: Vol 97, Jan 2016.

 

Evernote: https://www.evernote.com/l/AN1XT1ioYPtMCaAEe_JKY0itOcB0lV9RUNc/

Moffitt GI Report: Alcoholic Hepatitis

Thanks to Brendan for presenting a great case of a young man with EtOH use d/o who presented with confusion and was found to have a bilirubin over 30, ultimately diagnosed and treated for alcoholic hepatitis. Pearls below!

TLC (Tim and Laura, your Chiefs)

Top pearls:

  • ALF = 1) Encephalopathy 2) Synthetic dysfunction (INR>1.5) 3) No pre-existing liver disease
  • Give NAC in ALF even if APAP is negative
  • MRI can pick up iron deposits in the liver, so can use it if any question of hemochromatosis
  • Give prednisolone instead of prednisone on alc hep, because it bypasses liver metabolism

Alcoholic Hepatitis (thanks to former chief Grant for much of this content!)

Etiology:

  • Most patients who develop alcoholic hepatitis have a history of heavy alcohol use for at least a decade, but it can occur with intermittent heavy drinking and over much shorter periods in some patients

Evaluation:

  • Symptoms: RUQ pain, anorexia, jaundice
  • Elevated INR and T bili, only moderate elevations of AST and ALT, and ratio of 2:1 or higher. Leukocytosis
  • Imaging: Fatty change in the liver, may have underlying cirrhosis or ascites
  • Diagnosis is based on clinical features above and ruling out other common causes of acute hepatitis, including infectious, obstructive, autoimmune, etc.

Treatment:

  • Severity is calculated using the Maddreys’ discriminant function. Easiest to plug the T Bili and PT into MedCalc, but here is the formula for your reference:
    • DF = 4.6 x (patient prothrombin time – control) + T bili
  • Treatment with steroids has been shown to improve mortality for those with severe alc hep, though steroids may be contraindicated if there is concern for GI bleeding, infection, or renal failure.
    • Recommended steroid treatment is with prednisolone, since the liver usually metabolizes prednisone to the active prednisolone!
  • For severe alc hep with contraindications to steroids, pentoxifylline is an alternative, though data is weaker than for steroids and it has not been definitely shown to improve mortality (STOPAH trial from NEJM below)
    • Supportive care with nutrition, PPI and abstinence from alcohol are also important
  • If there is no improvement in the DF after 1 week of therapy, ongoing treatment is not recommended and thought to have little benefit (calculate the Lille score).
  • For patients with severe alc hep (DF ≥32) who do not receive treatment, mortality at 1 month is over 25%, primarily due to sepsis, GI bleeding and liver failure.

Lille Model for Alcoholic Hepatitis:

The Lille Model risk stratified patients already receiving steroids for alcoholic hepatitis for 7 days to predict which patients will not improve and should be considered for other management strategies.

  • 6 Factors in model: age, renal insufficiency (Cr >1.3 or CrCl <40), albumin, PT, initial bilirubin, and bilirubin at day 7)
  • Score greater than 0.45 correlates to a marked decrease in survival compared to others 25% vs 85%.
  • This model identified about 75% of the deaths in the cohort
  • Validates in additional study, which used a cut off of >=0.56
  • Patients who are failing to response to therapy may need to be referred to liver transplant
  • Of note, liver transplant for alcoholic hepatitis is controversial at this time and should be discussed with local experts.

Liver transplant in Alc hep (thanks to Jake for bringing this up!)

  • 26 patients were included. They had severe alc hep and high Lille scores after treatment with steroids and pentoxyfilline. They had supportive family members and a commitment to alcohol abstinence, but no requirement for a minimum period of sobriety.
  • 6 month survival rate was 77% for those who received early transplant vs. 23% for those who did not, and this benefit continued to 2 years. Three patients resumed drinking alcohol, all at 2+ years after transplantation.

Evernote: https://www.evernote.com/shard/s582/sh/726ada50-a04a-4351-8e3d-d4bacefbe018/8ad449715247d53366909a45f57e3791

 

 

Mt. Zion report: Tinnitus

Thanks to Dan Minter for presenting an intriguing case of a middle aged man with prior MVA and mild TBI presenting with subacute pulsatile tinnitus, ultimately diagnosed with small aneurysm of the carotid near the petrous aspect of the temporal bone (remember all that anatomy!??!)!

Keywords for ‘sounds in the ear’:

  • Tinnitus (usually represents inner ear etiology) – buzzing, ringing
    • Pulsatile (more worrisome for vascular pathology) – “heartbeat in my ear”, “drumbeat”, “subwoofer”, “pulsing”. Often gets louder in a quiet environment.
    • Venous hums – soft, low-pitched humming,  “whooshing”; Associated with systemic hypertension or elevated intracranial pressure
    • Changes in tinnitus with head movement, change in position, or activity suggestive of vascular etiology!

Important history to ALWAYS ask in patients with tinnitus:

  • Unilateral versus bilateral symptoms?
  • Constant versus episodic?
  • Headaches?
  • Hearing loss?
  • Vertigo?
  • History of head trauma?
  • History of occupational noise exposure?
  • History of sinus or allergic disease?
  • Thorough medication and OTC review
  • Depression/anxiety? (high prevalence of depression/anxiety in patients with tinnitus, possibly due to lower threshold to be affected by symptoms of tinnitus)

DDx for tinnitus:

  • Vascular disorders (think pulsatile tinnitus!):
    • Arterial bruit (turbulent blood flow near temporal bone) or aneurysm
    • AVMs
    • AV fistulas (usually secondary to head trauma, surgery, infection, or tumor)
    • Dissection
    • Aneurysm
    • Venous hum (secondary to ICH, pseudotumor cerebri, systemic hypertension)
  • Neurological disorders
    • Vestibular migraine
    • Multiple sclerosis
    • CNS vasculitis
    • Spasm of middle ear muscles
  • Otologic disorders
    • Menieres disease
    • Sensorineural hearing loss (tinnitus can be an early sign of presbycusis)
    • Vestibular schwannoma
    • Otosclerosis
  • Medications (> 130 meds that can cause tinnitus/otologic complaints!)
    • NSAIDs, aminoglycosides, loop diuretics, hydroxychloroquine, and many more!!
  • Others:
    • TMJ dysfunction (nonpulsatile)
    • Eustachian tube dysfunction

Pearls for Tinnitus Workup:

  1. Observation of those with short duration, infrequent episodes of tinnitus is acceptable initial management!
  2. CONSTANT or FREQUENT PULSATILE tinnitus always requires evaluation by ENT and audiology testing.
  3. Imaging includes angiography such as MRA/CTA (many patients require both CT and MR imaging due to the vast etiologies that can cause pulsatile tinnitus).
  4. Patients with unilateral findings on audiology testing usually warrant head imaging to r/o acoustic neuroma.

**From American Academy of Otolaryngology: Clinicians should not obtain imaging studies of the head and neck in patients with tinnitus specifically to evaluate the tinnitus UNLESS they have 1 of the following: tinnitus localized to one ear, pulsatile tinnitus, focal neurological deficits, or asymmetric hearing loss.

References:

AAFP Diagnostic Approach to Patients with Tinnitus (2014)

American Academy of Otolaryngology Clinical Practice Guideline Tinnitus Executive Summary (2014)

Evernote:

https://www.evernote.com/l/AN1IJhqrGSxLA4sEDQc4odjN2opUlcNm0ic/