All posts by alp37

VA AM report 8.14.17: Hyponatremia hiding mediastinitis

Case summary: Kelly Sydell paid us a visit this morning to tell us about a great case– a 74M with PMH aortic stenosis s/p recent aortic valve replacement, who presented with mild hyponatremia with a difficult volume exam, as well as mild incisional erythema and was found to have post-operative Salmonella mediastinitis.

Top pearls:

  1. The most common cause of mediastinitis in the modern era is a post-operative complication of thoracic or cardiac surgery; the majority are monomicrobial and nosocomial.
  2. Chest CT scan with contrast is the radiologic test of choice in diagnosing mediastinitis, as symptoms and exam findings can be subtle (as in this patient), and mediastinal widening on CXR is not sensitive in post-operative mediastinitis (but interestingly IS more sensitive in mediastinitis from other causes!).
  3. LT and Goop reminded us that during the AIDS epidemic, we learned that non-typhoidal Salmonella has a predilection for aortitis and mycotic aneurysm, particularly in the setting of atherosclerosis.

Post-operative mediastinitis

  • In the olden days, most mediastinitis arose from esophageal perforation, contiguous spread of oropharyngeal infection, penetrating trauma or hematogenous spread
  • Now, most cases are the consequence of cardiac or thoracic surgery
  • Incidence post-operatively ranges from 0.5-4% and depends on both patient factors (e.g. DM, obesity) and operative characteristics (e.g. how long the sterum is open)
  • Bacteriology (majority nosocomial and mono microbial):


  • More atypical causes: fungi, Legionella, Mycoplasma hominis, or Nocardia and Mycobacterium tuberculosis
  • Presentation can be fulminant and acute or mild and subacute-to-chronic
  • Patients present with:
    • fever
    • tachycardia
    • chest pain
    • sternal instability
    • signs of sternal wound infection
    • purulent discharge
    • majority with leukocytosis and 50% with +BCx
  • Physical exam findings can be subtle; if suspicious, mediastinal widening on CXR is insensitive for post-operative mediastinitis (more sensitive for non-post-op causes), so radiologic test of choice is CT chest with contrast
  • Treatment:
    • surgical debridement with either primary or secondary closure
    • antibiotics for 2-6 weeks (vanc/zosyn–> narrow pending intra-operative cultures)


Dubert M, Pourbaix A, Alkhoder S, Mabileau G, Lescure F-X, Ghodhbane W, et al. (2015) Sternal Wound Infection after Cardiac Surgery: Management and Outcome. PLoS ONE 10(9): e0139122.

Salmonella and the vasculature

  • Vascular infections due to Salmonella can involve the thoracic and abdominal aorta, as well as coronary arteries, peripheral arteries, or vascular grafts and prosthetic valves.
  • Aortic infections are much more frequent, and the majority of these involve the abdominal aorta.
  • Nearly all cases of aortitis due to Salmonella result in formation of an aneurysm or, less commonly, in enlargement of a previously existing aneurysm
  • Most patients with aortitis due to Salmonella have preexisting atherosclerotic disease at the site of the subse- quently infected aneurysm
  • Mediastinitis due to Salmonella is rare and morbid, as it is strongly associated with concomitant aortitis, mycotic aneurysm, and rupture.


Soravia-Dunand, VA et al. Aortitis Due to Salmonella: Report of 10 Cases and Comprehensive Review of the Literature. Clinical Infectious Diseases 1999;29:862–8.


Fernández-Ayala M1, Nan D, Gutierrez JA, Fariñas MC. Postoperative mediastinitis due to Salmonella. Scand J Infect Dis. 2003;35(1):67-8.

Approach to hyponatremia

Just a reminder that until robots take over medicine and improve our volume exams, there exists a very nifty volume-independent hyponatremia algorithm found here (Rabih version) and here (Rachel Stern version)!


VA Morning report 8.7.17: Anabolic steroids and staph bacteremia

Case summary: Thank you to Kelly, who brought us the case of a 49F bodybuilder who injects anabolic steroids and presented with AMS and was found to have ALI and Staph bacteremia.

Top pearls:

  1. Bonus pearl from the daily ditty: the timing of deep brain stimulation is important! Patients who are just starting to have functional limitations are the best candidates, as those with more significant disability are unlikely to benefit.
  2. Since 2006, the CDC has recognized a new category of staphylococcus aureus: vancomycin intermediate staph aureus (VISA). VISA is more common in those exposed to vancomycin, on HD, or with CVC/prostheses and corresponds to an MIC of 4-8 .
  3. The complications of anabolic steroids are myriad but (pertinent to this patient) include both hepatocellular and cholestatic LFT abnormalities, hypercoagulability, and an increased infectious risk.

VISA: so much more than a credit card

  • Although less relevant to this patient, we discussed that there exists a category of staph aureus that is neither sensitive nor resistant to vancomycin: vancomycin intermediate staph aureus.
  • What is the “MIC”?:
    • Measure of an organism’s susceptibility to an antibiotic
    • Accomplished by plating bacteria with serial dilutions of antibiotic and measuring growth
    • It is the minimum concentration of an antibiotic that prevents bacterial growth, so lower numbers indicate greater susceptibility
  • Vanc intermediate staph aureus (VISA):
    • MIC<2= susceptible
    • MIC>16= resistant
    • MIC 4-8= intermediate
    • Pathophysiology: related to mutations in cell wall
    • Risk factors: prior vancomycin exposure, HD, central venous catheters/prostheses
    • Treatment: 
    • Uncomplicated (e.g. no metastatic focus): monotherapy with ceftaroline, linezolid or telavancin
    • Complicated: combo therapy with daptomycin and ceftaroline (note: some studies show that using daptomycin increases resistance)


Fridkin SK. Vancomycin-intermediate and -resistant Staphylococcus aureus: what the infectious disease specialist needs to know. Clin Infect Dis 2001;32:108-115

Gardete S, Tomasz A. Mechanisms of vancomycin resistance in Staphylococcus aureusThe Journal of Clinical Investigation. 2014;124(7):2836-2840.

Complications of anabolic steroid abuse:

  • Lance Armstrong, listen up!
  • Athletes and nonathlete weightlifters take steroids orally, transdermally, or by IM injection; however, the most popular mode is the IM route.
    • In this patient, she injected steroids intravenously, making her risk profile similar to that of an IVDU
  • Purported benefits for athletes: increases muscle mass and oxygen delivery, improves neuromuscular transmission leading to reduced reaction time, and potentially improves mood and motivation

  • Adverse effects:
  • Neuropsychiatric: Mood d/o, aggressive behavior
  • Cardiovascular:  Left ventricular hypertrophy or myocarditis; hyperlipidemia
  • Endocrine:
    • In women: hirsutism, hair recession, deepening of the voice, oligomenorrhea/amenhorrhea, breast atrophy
    • In men: hypogonadism and infertility, gynecomastia
  • Hepatic: ALI, cholestasis, hemorrhagic hepatic cysts (peliosis hepatis), hepatomas
  • ID: increased risk of infection
  • Heme: erythropoiesis, hypercoagulability
  • MSK: Tendon rupture, epiphyseal closure delay
  • GU: Prostatomegaly/prostate CA

Pope HG, Wood RI, Rogol A, Nyberg F, Bowers L, Bhasin S. Adverse Health Consequences of Performance-Enhancing Drugs: An Endocrine Society Scientific Statement. Endocrine Reviews. 2014;35(3):341-375. doi:10.1210/er.2013-1058.

VA ICU Report 7.28.17: The myth of metformin & lactic acidosis

Case summary: Our outgoing ICU team presented a whammy of a case today– a 62M with PMH DMT2 on insulin/glipizide/metformin, who presented with several hours of malaise and diffuse abdominal pain, and was found to have acute liver injury and severe lactic acidosis.

Top Pearls:

  1. The most common and most important to rule out eiologies of lactic acidosis are type A, which is due to anaerobic metabolism, including both diffuse (e.g. shock) and focal problems (e.g. intraabdominal catastrophe).
  2. The precursor to metformin, phenformin, was associated with an increased risk of lactic acidosis and was taken off of the market, but the perception of metformin leading to lactic acidosis persists.
  3. More recent data does NOT support an association between metformin and lactic acidosis in GFR>30, but nevertheless, ongoing concern have altered practice patterns such that it is only prescribed to 50% of patients who would benefit.

A systematic approach to lactic acidosis: 

  • Summary of all the biochemistry you remember from med school– lactate is produced to generate ATP when there isn’t enough O2 around OR oxidative phosphorylation isn’t working
  • First rule out Type A causes, and if these seem unlikely, then consider Type B causes


Type A: anaerobic metabolism

  • Diffuse
    • Insufficient oxygen delivery to tissues
      • Low BP: Cardiogenic, hypovolemic, septic shock (NB: sepsis also interferes with oxidative phosphorylation)
      • Low O2 content: hypoxemia, severe anemia, carbon monoxide poisoning (NB: also interferes with oxidative phosphorylation)
      • Transiently increased O2 demand: seizures, trauma, extreme exercise, shivering
  • Focal
    • Driven by exam and labs
      • intraabdominal catastrophe
      • critical limb ischemia
      • massive MI, etc.

Type B: aerobic metabolism

  • Increased lactate production via problems with oxidative phosphorylation
    • Warburg effect: in advanced cancer (NB: can also have local tumor tissue hypoxia)
    • Meds: metformin, beta agonists, NRTIs, propofol
    • Toxins: cocaine, cyanide, salicylates, toxic alcohols
    • Thiamine deficiency: needed to transport pyruvate inside mitochondria
  • Decreased lactate clearance: liver disease (cirrhosis, acute liver injury, diffuse liver mets, etc.)
  • Diabetes: mechanism UNKNOWN!

Fantastic NEJM review: Kraut  JA, Madias  NE.  Lactic acidosis.  N Engl J Med. 2014;371(24):2309-2319.

Metformin and lactic acidosis:

  • Likely overstated!
  • As Goop and LT pointed out, our association of metformin with lactic acidosis is in part historical because its precursor in the 1970s, phenformin, did have a strong association and was taken off of the market. (CONLAY LA, LOEWENSTEIN JE. Phenformin and Hyperamylasemia in Lactic Acidosis. Ann Intern Med. 1977;87:312-313. doi: 10.7326/0003-4819-87-3-312)
  • More recent data suggest that metformin may not confer an elevated risk, but the perception is preventing patients who would benefit from metformin from receiving it:
    • A 2014 systematic review in JAMA showed that the incidence of lactic acidosis in patients with DMT2 and CKD (GFR 30-60) was equivalent among those on metformin and those not on metformin.
      • (Inzucchi SE, Lipska KJ, Mayo H, Bailey CJ, McGuire DK. Metformin in Patients With Type 2 Diabetes and Kidney Disease: A Systematic Review. JAMA. 2014;312(24):2668-2675.)
    • A 2015 research letter in JAMA IM showed that metformin is significantly underprescribed due to an FDA warning against use in patients with Cr >1.5 in men and >1.4 in women, which is in conflict with society guidelines recommending use if GFR>30. Specifically, the rate of metformin use in patients with a GFR >90 was 90.4%, at GFR 60 to 90 the rate was 80.6%, and at GFR 30 to 60, at which metformin use is usually formally contraindicated but professional guidelines support cautious use, rates were 48.6% to 57.4%
      • (Flory JH, Hennessy S. Metformin Use Reduction in Mild to Moderate Renal ImpairmentPossible Inappropriate Curbing of Use Based on Food and Drug Administration ContraindicationsJAMA Intern Med.2015;175(3):458-459.)



VA ICU report 7.21.17: Hypertriglyceridemia and pancreatitis

Case summary: Thanks to the ICU team for presenting a great case of a 61M HIV on ARVs (CD4 >400), abdominal gunshot wound c/b SBO, HCV without cirrhosis, HFpEF, PSA including EtOH abuse who presented with acute onset abdominal pain, nausea/vomiting, who was found to have severe acute pancreatitis and hypertriglyceridemia to the 1000s.
Top pearls:
  1. Why are the labs taking forever to come back!? Recall that there are both endogenous (hemolysis, lipids, proteins, antibodies, bilirubin) and exogenous substances (drugs, poisons, herbals, IV fluids, IVIg, digibind, and collection tube/sample additives/clotting in the tube) that can interfere with lab tests.
  2. Hypertriglyceridemia can be congenital (due to familiar hyperlipiemias) or acquired (usually due to obesity, EtOH, pregnancy or DMT2). Levels >1000 are associated with pancreatitis.
  3. There is debate whether hypertriglyceridemia is a cause or a consequence of pancreatitis. Nevertheless, the key features of management are: hydration!, pheresis, IV insulin +/- heparin.

Why are the labs taking forever to come back!? Aka Causes of lab interference
  • Endogenous interference- originates from substances found naturally in the patient sample.
    • hemolysis (haemoglobin and other substances)
    • bilirubin
    • lipids
    • proteins
    • antibodies (autoantibodies, heterophile antibodies)
    • excessive analyte concentration (e.g. the lab doesn’t dilute the sample enough)
    • cross-reacting substances (e.g. bicarb can react with some of the lab machinery)
  • Exogenous interference– results from substances not naturally found in the patient’s specimen
    • drugs (parent drug, metabolites, and additives)
    • poisons
    • herbal products
    • IV fluids
    • substances used as therapy (e.g. monoclonal antibodies, IVIg, digi-bind)
    • collection tube components, test sample additives, processes affecting the sample (e.g. transport, storage, centrifugation), clots (post-refrigeration in heparin plasma, slow-clotting serum)

Hypertriglyeridemia: a brief review
  • Defined as:
    • Normal – <150 mg/dL (1.7 mmol/L)
    • Borderline high – 150 to 199 mg/dL (1.7 to 2.2 mmol/L)
    • High – 200 to 499 mg/dL (2.3 to 5.6 mmol/L)
    • Very high – ≥500 mg/dL (≥5.6 mmol/L)
    • important to test fasting levels
  • Causes:
    • congenital:

Screen Shot 2017-07-21 at 9.54.04 AM

    • acquired: obesity, diabetes, alcohol, nephrotic syndrome, hypothyroidism, pregnancy, medications (estrogen, tamoxifen, beta blockers except carvedilol, immunosuppressive medications (steroids, cyclosporine), ARVs, retinoids
  • Findings:
    • limited data linking hypertriglyceridemia to cardiovascular outcomes
    • patients with congenital etiologies can have xanthomas and xanthelasmas
    • greatest risk is of pancreatitis at levels >1000
    • some clinicians will treat outpatients with fasting levels >886 because this is associated with postprandial levels that can cause pancreatitis, but there are limited data to guide this decision
      • Non-pharmacological therapy includes lifestyle modification (weight loss, exercise, and restricting fat and simple sugars)
      • Fibrates are first-line therapy, niacin and omega 3 fatty acids are second line. These drugs can be used alone or in combination with statins.
  • Hypertriglyceridemia and pancreatitis:
    • The incidence of AP in patients with TG > 1,000 is 5%, which increases to 10-20% with levels > 2,000
    • Elevated TG are associated with more severe end-organ complications of pancreatitis and increased mortality
    • Treatment:
      • Hydration!
      • Pheresis
      • IV insulin (increases the activity of lipoprotein lipase, which breaks down TG-rich chylomicrons)
      • +/- heparin (contraversial)
Chaudhary A, Iqbal U, Anwar H, Siddiqui HU, Alvi M. Acute Pancreatitis Secondary to Severe Hypertriglyceridemia: Management of Severe Hypertriglyceridemia in Emergency Setting. Gastroenterology Research. 2017;10(3):190-192.
Berglung L, et al. Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2012 Sep;97(9):2969-89.
Brunzell JD. Hypertriglyceridemia. N Engl J Med 2007;357:1009-1017

VA Morning report 7.18.17: Acute liver injury and aortic dissection deep cuts

Case summary: Huge thanks to Jin Ge for presenting a fascinoma: 33M with PMH cocaine abuse, who was admitted to the liver transplant unit with acute liver injury and was found to have an aortic dissection extending from the aortic root to the iliac arteries leading to multi organ ischemic injury.
Top pearls:
  1. Northern California had an outbreak of amanita mushroom poisoning this year, which starts with GI symptoms 9 hours after ingestion and can progress to fulminant hepatic failure. There is an ongoing RCT testing a new antidote called silibinin.
  2. Many of us are familiar with the triumvirate of acute liver failure: toxin, viral hepatitis, ischemia; consider using an anatomic approach the includes more rare causes.
  3. Aortic dissection is due to weakening of the vessel wall. This is most commonly caused by HTN but can result from any aortopathy, either acquired (infection, inflammation) or genetic (collagen/vascular disease, bicuspid valve, familial TAAD).

Amanita “deathcap” mushroom poisoning
  • Paul Blanc (international expert in toxicology/occupational health) and Jody Garber (international expert in the VA ED, beer, and Northern California in general) gave us some great deep cuts on amanita mushroom poisoning.
  • Amanita phalloides is responsible for most mushroom-related deaths worldwide.
  • The toxin is activated in the GI tract and is “heat stable,” meaning that cooking doesn’t dilute their potency.
  • They taste good!
  • They’re found under trees after heavy rainfall.
  • Northern California experienced an outbreak this year because of our wet weather; the CDC released a report on 14 cases in 2016-2017 (as compared to the typical 1-2 cases/year).
    • all patients developed severe GI symptoms (abdominal pain, diarrhea) 9 hours after eating the mushrooms
    • Eleven patients recovered, although three required liver transplants
    • One of those patients, a child, developed cerebral edema despite liver transplant and suffered permanent neurologic sequelae
  • Ask a mycologist (mushroom expert) to examine your mushrooms before eating!
  • There’s an ongoing clinical trial testing an antidote that is licensed in Europe called silibinin (the cases described above received it empirically)

Anatomic approach to acute liver injury
  • Courtesy of Rabih Geha:

Causes of aortopathy
  • This patient had dissection of the almost the entire length of his aorta, and the presumed etiology is cocaine/HTN.
  • It’s important to remember, particularly in a young patient, the spectrum of diseases that can cause aortopathy.
  • Dissection develops due to a weak aortic wall leading to a tear of the intima.F2.large
    • Acquired
      • HTN- vessel wall degeneration over time; by far the most common cause
      • Infection- septic embolism, bacterial inoculation (e.g. syphilis!) or contiguous infection (e.g. extension of perivalvular abscess) of vessel wall
      • Inflammation- giant cell arteritis, Takayasu arteritis, rheumatoid arthritis, ankylosing spondylitis, Wegener’s granulomatosis, reactive arthritis, and Behcet syndrome cause inflammation of vessel wall
    • Genetic
      • Abnormal collagen/vasculature- Marfan syndrome, vascular Ehlers Danlos syndrome, Loeys-Dietz syndrome, and Turner syndrome
      • Familial thoracic aortic aneurysm and dissection (TAAD)-patients with a family history of aneurysmal disease who don’t have a connective tissue disorder
      • Bicuspid aortic valve- independent association with aortopathy; most commonly recognized congenital abnormality in adulthood, and 25 percent require intervention on aortic valve, aorta, or both
  • Note that these risk factors also increase the risk of aortic aneurysm, which can lead to dissection as well as rupture.

Mussa FF, Horton JD, Moridzadeh R, Nicholson J, Trimarchi S, Eagle KA. Acute Aortic Dissection and Intramural HematomaA Systematic ReviewJAMA. 2016;316(7):754-763.

Thrumurthy Sri GKarthikesalingam AlanPatterson Benjamin OHolt Peter J EThompsonMatt MThe diagnosis and management of aortic dissection 

VA ICU report: Peritoneal dialysis peritonitis and PEA arrest

Case summary:  Thanks to the ICU team for presenting the difficult case of a 69M with HTN, HLD, ESRD on peritoneal dialysis, who was transferred from an OSH with a diagnosis of peritonitis, severe nausea/vomiting/abdominal pain, and found to have an inferior STEMI. He had an unfortunate hospital course– including severe metabolic acidosis, multiple PEA arrests in the cath lab– and ultimately passed away.
Top pearls:
  1. The diagnostic criteria for peritonitis in peritoneal dialysis patients is different than classic SBP: diagnostic paracentesis with WBC >100 and >50% PMNs.
  2. Recall that EKG changes in inferior MI come in 2 flavors. This is because in 20% of patients, the L circumflex supplies the inferior wall, resulting in STE in II=III, V5, V6 and STD in aVR.
  3. The LUCAS mechanical CPR device is in the ED, ICU and cath lab at the VA; an RCT showed improved neurologic outcomes in patients who received mechanical CPR compared to standard CPR.

Peritonitis in peritoneal dialysis
  • Peritoneal dialysis (PD) primer
– In peritoneal dialysis, there is exchange of solutes and fluid between the peritoneal capillary blood and the dialysis solution in the peritoneal cavity across the peritoneal membrane
– PD entails a closed system in which fluid is initially instilled by gravity into the peritoneal cavity via a catheter and then drained out after several hours
– Equivalent outcomes to HD, cheaper, but not used as frequently in the US (for multiple reasons, including higher reimbursement for HD)

Screen Shot 2017-07-14 at 10.58.06 AM

  • Peritonitis in PD: has several key features that distinguish it from peritonitis from other causes (e.g. cirrhosis)
Clinical syndrome
Spontaneous bacterial peritonitis
– due to contamination during PD process from skin flora or catheter-related inoculation
– more subtle symptoms (abdominal pain, fever, cloudy effluent)
– better prognosis
– WBC count >100 and >50% PMNs (or >50% alone in patients on automated PD)
– can have artificially low WBC count for technical reasons (e.g. timing of para in relation to PD session, type of effluent), so symptoms alone enough to treat if high clinical suspicion
– 80-95% have positive bacterial culture
– antibiotics: gram negative and gram positive coverage (e.g. vanc/cefepime)
– add anti-fungal if Gram stain shows or culture grows fungus (usually empiric fluconazole)
– remove PD catheter IF: 1) recurrent peritonitis with same organism within 4 weeks, 2) refractory peritonitis that doesn’t respond within 5 days, 3) fungal or mycobacterial peritonitis
Secondary bacterial peritonitis
– due to intraabdominal process causing perforation or bacterial translocation
– rarely due to hematogenous spread
– more severe symptoms (abdominal pain, fever, cloudy effluent)
– worse prognosis, but less common (~5%)
– same diagnostic criteria
– Runyon’s criteria (NOT validated in PD patients): at least 2 of total protein >1, glucose <50, LDH >serum ULN
– polymicrobial culture
– repeat diagnostic para with rising WBC count despite ABX
– antibiotics as above, sometimes with empiric anti-fungal coverage
– should get abdominal CT
– +/- surgery depending on pathology
– remove catheter
Gokal, R, Mallick, NP. Peritoneal dialysis. Lancet, 353 (1999), pp. 823-828
Davies, SJ. Peritoneal dialysis—current status and future challenges. Nature Reviews Nephrology 9, 399-408 (July 2013)

Defining features of inferior MI
  • Symptoms: abdominal pain, nausea/vomiting predominant
  • RV infarct (40%): get R-sided leads (look for STE in V4R)
  • Hypotension: 2/2 RV infarct and exacerbated by nitrates and responsive to fluids
  • Posterior infarct (more rare):  V1-V3 horizontal STD, tall/broad R waves, upright T waves, R/S>1 in V2; get posterior leads (look for STE (0.5mm is sufficient!) in V7-V9)
  • Bradycardia (20%): 2/2 AVB (AV nodal artery emerges from RCA) and/or sinus node dysfunction (SA nodal artery is supplied by the RCA in 60% of people). Can also be from vagal tone induced by ischemia
  • EKG:
    • 80% RCA- STE III>II, aVF, and STD in aVL
    • 20% LCx- STE II=III, STE in V5, V6, and STD in aVR
  • At the VA, we have a device called “The LUCAS” that delivers mechanical CPR during codes.
  • LUCASes (sp?) are located in the Emergency Room, ICU, and cardiac cath lab
  • Why use the Lucas? 2011 RCT showed survival with a favorable neurologic outcome was higher in patients receiving CPR with a mechanical device compared with manual CPR
  • Some questions as to whether it is associated with higher incidence of CPR-related injury
Aufderheide, TP, Frascone, RJ, Wayne, MA, Mahoney, BD, Swor, RA, Domeier, RM, Olinger, ML, Holcomb, RG, Tupper, DE, Yannopoulos, D, Lurie, KG Standard cardiopulmonary resuscitation versus active compression-decompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: A randomised trial.. Lancet. (2011). 377 301–11

VA Ambulatory report 7.12.17: Tremor and dementia for internists

Case summary: Thanks to our clinic immersion all-star intern Santo Ricceri for presenting a fantastic outpatient case today. The patient is a 64M with prior EtOH use disorder in remission, MDD, who presented to clinic with subacute tremor, word-finding difficulty, and memory problems, found to have a MOCA of 12/30.

Top pearls:
  1. LT and Goop emphasized the old adage: the physical exam starts as soon as the patient walks in the room. In particular, noticing a patient’s tremor while taking the history allows you to observe it “in the wild,” rather then while it’s under scrutiny.
  2. The 3 most common tremors to present in primary care are: enhanced physiologic tremor, essential tremor and parkinsonian tremor.
  3. Work-up for “reversible causes of dementia,” while still recommended by most major society guidelines, is low-yield diagnostically and not cost-effective.
  4. The American Geriatrics Society and most other society guidelines NO LONGER recommend routine neuroimaging in patients with dementia.
Tremor for internists:
  • Tremor, an involuntary, rhythmic, oscillatory movement of a body part, is the most common movement disorder encountered in clinical practice.
  • The 3 most common tremors to present in primary care are: enhanced physiologic tremor, essential tremor and parkinsonian tremor.
  • Goop and LT reminded us to note the tremor while taking the history in order to observe it “in the wild,” rather than under scrutiny (in particular, this can help identify psychogenic tremor, which disappears with distraction)
  • The classic taxonomy of tremor has always seemed a little cumbersome to us.
  • The AAFP has a great review article that simplifies the diagnostic algorithm!
  • First, some definitions:
    • rest (occurs at rest, worsened by mental stress or movement of another body part and improved by movement of the hands)
    • action (occurs with voluntary contraction of a muscle)
      • postural (occurs while maintaining a position against gravity)
      • isometric (occurs with muscle contraction against a rigid stationary object)
      • kinetic (occurs with any voluntary movement)
  • Then, move on to this algorithms

Screen Shot 2017-07-12 at 10.53.54 AM

  • Followed by this algorithm

Screen Shot 2017-07-12 at 10.59.00 AM

Crawford, P, Zimmerman, EE. Differentiation and Diagnosis of Tremor. Am Fam Physician. 2011 Mar 15;83(6):697-702.

Evaluation of dementia in the clinic:
  • Work-up for “reversible causes of dementia,” while still recommended by most major society guidelines, is widely considered to be low-yield diagnostically and not cost-effective.
  • The proportion of dementia cases thought to be due to potentially reversible causes is about 9%.
  • Entails B12, TSH, HIV, RPR (+/- PHQ9, LP and MRI)
  • This is especially true with the aging of the US population, as the proportion of patients with organic, irreversible dementia has risen, and the prevalence of reversible dementia has fallen.
  • This testing is more relevant for young patients (<60) and those with rapid (<2 years) progression of symptoms.
Neuroimaging in dementia: no longer recommended by most society guidelines EXCEPT American Academy of Neurology (AAN)
    • NCHCT: typically to exclude subdural, large tumor, normal pressure hydrocephalus
    • MRI: pattern can give clues to sub-type of dementia in addition to more detailed imaging of the above diagnoses
    • the AAN notes that Neurologists typically only evaluate patients once in clinic and thus do not have a longitudinal relationship that might reveal more chronic symptoms and obviate the usefulness of NCHCT/MRI
    • again, for young patients (<60) and those with rapid (<2 years) progression of symptoms, neuroimaging is still recommended
Langa KM, Levine DA. The Diagnosis and Management of Mild Cognitive Impairment: A Clinical Review. JAMA. 2014;312(23):2551-2561.
Robinson Louise, Tang Eugene, Taylor John-Paul. Dementia: timely diagnosis and early intervention BMJ 2015; 350 :h3029