All posts by cssoran

VA Ambulatory Report 2.7.18 – Double case – Facial numbness and Arm Swelling

Morning report today was like a regular primary care clinic day – one daily ditty and two patients all in one hour no problem!  Thanks Lily for presenting two awesome cases.

Case 1: A young woman on OCPs with right sided facial numbness and facial droop sparing the forehead found to have MS.

Unilateral Facial Paralysis:

  • The key to evaluation is determining if the lesion is central vs. peripheral
    • The forehead is spared in a central process due to bilateral innervation
    • There are possible peripheral causes that spare the forehead BUT forehead sparing should raise your suspicion for a central process
    • Pearl from Jody is that forehead weakness can be subtle as patients try to overcome it with muscles of the scalp. In addition to having the patient raise their eyebrows, have them maintain raised eyebrows against your force.
    • Central
      • Stroke
      • Malignancy
      • Demyelinating diseases
      • Migraines
    • Peripheral – Facial nerve palsy
      • Infections: Herpes zoster, otitis media, lyme, HIV
      • Immune-mediated: GBS
      • Autoimmune: sarcoid, Sjogrens
      • Idiopathic (Bell’s palsy)

 

Case 2: A 45 yo G1P0 female with recent spontaneous abortion and RUE DVT with chronic right arm pain and skin changes found to have complex regional pain syndrome.

  • We reviewed indications for thrombophilia work-up.
    • We should not test every individual with an unprovoked VTE because for most people it will not change management.
    • Who does it change management in?
      • Women planning conception
      • Possible need to treatment with pro-thrombotic agents such as estrogen
    • In general we should consider testing in the following populations:
      • Young patients (<50) with weak provoking factors or strong family history
      • Arterial clots
      • Unusual locations: Splanchnic veins, cerebral veins
    • Check out this awesome NEJM review article.
  • And remember the Budapest criteria when considering the diagnosis of complex regional pain syndrome
    • Continuing pain, which is disproportionate to any inciting event

    • Must must report at least one symptom in three of the following four categories:

    • 1 – Sensory: hyperaesthesia (an abnormal increase in sensitivity) and/or allodynia (pain caused by usually non-painful stimuli);

    • 2 – Vasomotor: skin colour changes or temperature and/or skin colour changes between the limbs;
    • 3 – Sudomotor/oedema: oedema (swelling) and/or sweating changes and/or sweating differences between the limbs.
    • 4 – Motor/trophic: decreased range of motion and/or motor dysfunction (weakness, tremor, muscular spasm (dystonia)) and/or trophic changes (changes to the hair and/or nail and/or skin on the limb).
    • There is no other diagnosis that better explains the signs and symptoms

Advertisements

VA Ambulatory Report 1.10.18 – Aches and Pains all over – PMR and RA

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.

Learning Peals  Screen Shot 2017-10-11 at 12.58.11 PM

  1. LT’s pearl: Many patients with PMR present with acute onset of symptoms
  2. Other lab findings that may be present in patients with PMR: mild normocytic anemia, elevated alk phos (although more common in patients with GCA)
  3. 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
  • Diagnosis
    • 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
  • Treatment
    • 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

VA Ambulatory Report 12.20.17 – Night Sweats for a Decade and the Million Dollar work-up

Thank you Dan for presenting this great ambulatory care.  We discussed a young male with a decade of night sweats with unremarkable work-up whose symptoms improved  after starting an alpha-blocker.  We had an interesting discussion of psychological disorders such as PTSD and anxiety as a cause of night sweats.

Night sweats

  • Pathologic =  drenching sweats that require changing pajamas or sheets
  • LT pearl Pathologic night sweats occur as result of the exaggeration of the normal diurnal temperature changes.
    • Max temperature occurs at 10pm
    • Sweating occurs in the following 2-4 hours. Therefore pathologic night sweats almost always occur after midnight

Approach to a patient with night sweats

  • A similar approach can be used with a patient with flushing or diffuse hyperhidrosis)
  • Break down by organ system
    • Malignancy
      • Lymphoma
      • Solid tumors: germ cell, medullary thyroid, RCC, prostate
    • Infections
      • Mycobacterial
      • Bacterial: Abscess, brucellosis, endocarditis, osteomyelitis
      • Fungal:
      • Viral: HIV, HCV
    • Endocrine
      • Carcinoid
      • DI
      • hyperthyroid
      • Pheo
      • Post-orchiectomy
      • Ovarian Failure
    • Medications: The list is extensive.  Some are more likely to cause flushing vs. night sweats
    • Substance withdrawal
      • Alcohol, cocaine, opiates
    • Neuro
      • Autoimic dysreflexia, autonomic neuropathy, stroke
    • Other/Mimickers
      • Hot flashes from Menopause
      • Overbundling
      • Hypoglycemia
      • OSA
      • PTSD
      • Panic disorder
      • Chronic fatigue syndrome
      • Food additives
      • GERD
        • There is an association between GERD and night sweats and some evidence patient’s symptoms improve after treatment with antireflux meds
      • Mastocytosis
      • Temporal arteritis
      • Takayasu’s arteritis
      • Idiopathic hyperhidrosis
      • Roseacea

How can we evaluate this non-specific compliant in a cost-effective manner?

  • Key is a focused history and physical to help target your diagnostic work-up
  • Always review the medication list
  • If no clear localized signs or symptoms the AAFP suggests a step-wise approach
    • Step 1: CBC, ppd, TSH, CXR
    • Step 2: HIV, ESR
    • Step 3: Trial of anti-reflux meds
    • Step 4: Diary of noctural temperature
    • Step 5: Blood cultures specifically looking for HACEK organisms
    • Step 6: Consider CT abdomen, CT chest, and/or Bone Marrow biopsy
    • Step 7: Reassurance and monitoring for new symptoms
  • Check out the full article here: AAFP Article on the Diagnosis of night sweats.

Link to Evernote: https://www.evernote.com/l/AMrvxcLdXUlN9o7pqVhD0L4WkiTAh67vgRk

VA Ambulatory Report 12.13.17 – Flatulence!

Thanks to Vaibhav who presented his patient’s case of bothersome flatulence found to have positive celiac serologies, but negative EGD now being treated for H. Pylori.  This case allowed us to have an excellent discussion about approaching a less common chief complaint such as flatulence and how we diagnose celiac disease and IBS.

Learning Pearls    Screen Shot 2017-10-11 at 12.58.11 PM

  • Patients may experience belching (also called eructation), flatulence, or abdominal bloating due to decreased intestinal motility or increased sensitivity to normal gas production.  Reference the Rome IV criteria for diagnostic criteria of functional gastrointestinal disorders.
  • Healthy individuals are not able to completely digest some carbohydrates which leads to increased H2 production.  This is the basis for the H2 breath test for carbohydrate malabsorption
  • A low FODMAPs diet has good evidence for symptom reduction in patients with IBS. Some studies have shown benefit in other functional gastrointestinal disorders and in patients with IBD with symptoms such as bloating not explained by their inflammatory disease
  • Anti-TTG is testing for IgA antibodies and may be falsely negative in individuals with IgA deficency.  Consider co-testing with IgA levels or testing for Gliaden.  No test is perfect and the gold standard is small bowel biopsy.

 

More than you want to know about Intestinal gas

  • There is about 200 mL of gas in the intestinal system
  • The main elements in gas are nitrogen, oxygen, carbon dioxide, hydrogen, and methane
  • The odor in gas comes from minor elements such as methanethiol, dimethyl sulfide, hydrogen sulfide, short-chain fatty acids, skatoles, indoles, volatile amines, and ammonia.
  • Where does intestinal gas come from?
    • 1 – Swallowed air
    • 2 – Digestion of fat and protein leads to production of CO2 in the small bowel
    • 3 – Bacterial fermentation leads to production of Hydrogen and Methane
      • Hydrogen
        • Normal in the colon
        • Produced in the small bowel in SIBO
      • Methane
    • 4 – Carbohydrate malabsorption
      • In healthy individuals, foods with high concentrations of oligosaccharides (such as wheat, oats, potatoes, and corn, legumes) cannot be completely digested by enzymes within the normal small bowel, leading to increased H2 production
        • This increased colonic H2 production from carbohydrate ingestion is why we perform the H2 breath test for carbohydrate malabsorption
      • Fructose malabsorption may be an underappreciated cause of gastrointestinal symptoms. Up to one-half of the population cannot completely absorb the load of fructose consumed in the average diet
    • 5 – Diffusion from the blood
  • Gas Disorders (Look to the Rome IV criteria for diagnosing these conditions)
    • Belching (also called Eructition)
      • Involuntary belching occurs after meals
      • Can be increased by foods that decrease LES tone such as chocolate, fats, mints
      • Chronic, repetitive belching due to habitual air swallowing
    • Flatulence
      • May patients reporting bothersome flatulence produce a normal amount of gas but may be experiencing symptoms from it due to: alteration in intestinal motility or bacteria, dietary factors, or physiologic factors that heighten awareness of gas
    • Functional Abdominal Bloating and Distention
      • Correlation between symptoms of bloating and amount of gas production is inconsiente
      • Similar underlying contributors as flatulence: decreased gut motility, increased sensitivity to gas,
      • Rome IV criteria for diagnosis: recurrent bloating or distention at least on day/week and insufficient criteria for diagnosis of IBS, functional constipation, functional diarrhea, or postprandial distress syndrome

 

What is up with the FODMAPs diet?

  • FODMAPs = Fermentable, Oligo, Di, Monosaccharides and polyols
  • Studies have consistently shown improvement in symptoms on a low FODMAPs diet for patients with IBS including this recent RCT conducted in the US demonstrated a low FODMAP diet reduced IBS symptoms reduced symptoms
    • There is evidence it can be helpful in symptom reduction for other functional gastrointestinal disorders and in patients with IBD but symptoms such as bloating or discomfort that are not related to inflammatory disease
    • There is some evidence
  • Key concepts to teach to your patients
    • Elimination or limiting of all FODMAPs (not just one component)
    • FODMAPs foods are not the cause of the symptoms, but help reduce symptoms related to visceral hypersensitivity or decreased gut motility
  • Here is an excellent review article on FODMAPs

 

Diagnosing Celiac disease – why are Celiac Serologies so confusing?

  • When we check anti-TTG this is traditionally testing for IgA antibodies
  • Given the co-occurence with IgA deficiency, you may also want to test for IgA to ensure there is also not IgA deficiency leading to a false negative TTG
  • Gliaden is an IgG test and therefore avoids the problem with IgA testing
  • Gold standard is duodenal biopsy looking for
  • HLA testing is helpful in very specific instances (possibly in high probability population and discordance on serology and biopsy)
  • Remember, patients should be on a gluten-rich diet (yum!) when these tests are performed

 

What are the recommendations for “screening labs”

  • HIV: Screen in adults age 15-65 or at other ages if increased risk or pregnant
  • Screening for diabetes: USPSTF recommends screening in adults age 40-75 who are obese or overweight
  • Lipids: USPSTF recommends calculating ASCVD risk in all people 40-75
  • HBV, HCV: Screen in high risk individuals
  • No recommendations to get screening CBC, metabolic panel, or UA

Evernote link: https://www.evernote.com/l/AMrAvmVoGvRAdYlVY8T3cXx5RJIktWhm-Nw

VA Ambulatory Report 11.28.17 – When your patient is seeing double – Diplopia and Stroke Pearls

Thanks Amanda for sharing your case of a middle aged male with a past history of diabetes and HTN presenting with diplopia found to have a sixth nerve palsy due to a pontine infarct.

Diplopia Pearls   Screen Shot 2017-10-11 at 12.58.11 PM

  • Your approach to diplopia should be the same as we approach any neurologic deficit –  Localize the lesion along the anatomic pathway
    • Central
    • Peripheral cranial nerve
      • Both a mononeuropathy or external compression of the cranial nerve
    • Extraocular muscles
    • neuromuscular junction
    • Globe (retina, cornea, lens)
  • Monocular diplopia vs. binocular diplopia
    • Binocular diplopia: If the diplopia is present only when both eyes are open then the diplopia is due to ocular misalignment
    • Monocular: Most often due to diseasse of the cornea or lens, less commonly the retina or cerebral lesion
  • Extraoccular muscle weakness can be subtle. LT pearl: when testing EOM, move your finger fast as this will be more likely to demonstrate subtle weakness than slow movements.
  • Cranial nerve palsies
    • 3rd nerve: longest cranial nerve after exiting the brainstem, more commonly affected by compression from an aneurysm or tumor.  When a third nerve palsy is due to microinfarction from diabetes it typically spares the pupil.  Therefore pupillary defects should raise your suspicion for intracranial lesion
    • 4th nerve: Most prone to injury from trauma and more rarely affected by microinfarction
    • 6th nerve: Most commonly affected

Check out this excellent chart from EB Medicine reviewing CN III, IV, and VI palsies.

Screen Shot 2017-11-30 at 1.49.47 PM

Stroke Pearls    Screen Shot 2017-10-11 at 12.58.11 PM

  • Code stroke: time sensitive interventions may be changing in the future
    • The latest trials are showing benefit to endovascular intervention in patients with large vessel occlusion within 6 hours of symptoms onset even after tPA administration.
    • Newer trials are investigating endovascular intervention up to 24 hours after symptom onset
  • Risk of future stroke after TIA: Use the ABCD2 score
    • This helps estimate the risk of stroke within the next 2 days after TIA
    • In patients with a risk < 1%, outpatient work-up may be appropriate
      • Goal is to get work=up completed within 24 hours

Evernote link: https://www.evernote.com/l/AMphZJl3GedO_Zz0p6Mjya3DIEWYfNB-uB8

Mt. Zion Ambulatory Report 11.21.17 – Clot vs. Bleeding: Recurrent PEs in a patient with abnormal uterine bleeding

Thanks Bennett for presenting a case of a young female with history of PE x2, DVT off anticoagulation with subacute dyspnea on exertion found to have recurrent PE.  The management was complicated by heavy uterine bleeding and patient limitations for close follow-up after starting anticoagulation.

Which patients should we work-up for thrombophilia after a VTE?

  • Do not test in the acute setting or if the patient is on anticoagulation
  • Do not test in patients with provoked VTE
  • Consider testing in: young patients with weak provoking factors or who have strong family history and in patients with recurrent VTE
  • Why test?
    • Determine prophylactic treatment for future VTE
    • Inform risk in family members (especially female family members considering hormonal contraceptives or pregnancy)
    • Determine cause of VTE (especially if unusual location or severe VTE)
  • Why do we not test everyone with VTE?
    • Results should not affect initial management
    • Results rarely effect clinical outcomes
    • Test results should not affect the duration of anticoagulation treatment because there is no data suggesting patients with or without thrombophilia should be treated differently after VTE.
  • See this excellent NEJM review article on thrombophilia testing.

 

Utility of D-dimer

  • Only validated in outpatients or patients in the ED. It is used for its negative predictive value in low risk patients.  A negative d-dimer in a low risk patient can effectively rule out PE without further testing.
  • There is debate about the utility of d-dimer in intermediate risk patients.
  • D-dimer increases with age.  The ADJUST-PE study demonstrated using an age-based d-dimer cutoff in combination with pre-test probability allows for a higher cut off value of d-dimer in older patients and more patients to be safely ruled out for PE without a CT
  • D-dimer in chronic thromboembolic disease? One study undertook a retrospective chart review found poor test characteristics for the use of d-dimer in the diagnosis of chronic thromboembolic pulmonary hypertension (sensitivity 37% and specificity 46%).
  • D-dimer may be helpful in deciding who can stop anticoagulation after an initial unprovoked VTE, but this area is still controversial (stay tuned as there is currently a prospective cohort study being conducted trying to answer this very question)

Long term management of patients with Pulmonary Embolism

Flashback to Anna Park’s awesome pearls from a prior morning report.

  • How long should the patient be treated with anticoagulation?
    • Should be an individualized decision with the patient based on risk of recurrent VTE and the increased risk of bleeding from anticoagulation
      • After first unprovoked VTE the risk of recurrence is ~10% in the first year and 5%/year after
      • There are several prediction rules for assessing risk of recurrent VTE but none of these have been clinically validated
    • Most patients will need lifelong anticoagulation after a first episode of unprovoked VTE
  • Assess for signs of CTPHE
    •  In patients with persistent symptoms of dyspnea after acute PE and 3 months of anticoagulation, CTEPH should be ruled out.  There is no indication for routine screening for CTEPH if the patient in asymptomatic patients after an acute PE.

 

Abnormal Uterine Bleeding

  • Treatment options
    • Acute bleeding: High dose hormones including estrogens, combo OCPs, or progestin
    • Prevention of recurrent bleeding
      • Non-hormonal options: NSAIDs, tranexamic acid
      • Hormonal: OCPS, high dose progestin, Mirena IUD
    • If the cause of bleeding is due to fibroids
      • Many surgical options including: hysterectomy, myomectomy, uterine artery embolization,
      • See this NEJM review article on the Management of Uterine Fibroids.
  • Reminder about the pathophysiology of leuprolide
    • GnRH agonist in women –> Initial surge in LH and FSH –> chronic use will lead to suppressed LH and FSH  –> ovarian suppression –> Induce amenorrhea and reduce uterine size
    • Can be used for treatment of abnormal uterine bleeding but given ovarian suppression the patient will experience symptoms of menopause.  Mainly used for short-term treatment such as pre-operative or in a perimenopausal woman.

Evernote Link Click Here.

VA Ambulatory Report 11.8.17 – Low back pain and spondylolisthesis

Thank you Kelly for presenting your patient with subacute worsening of chronic low back pain without red flag signs or symptoms found to have surprising findings on MRI of L3-L4 instability with spondylolithesis and edema causing mass effect on the spinal cord.

Screen Shot 2017-10-11 at 12.58.11 PM  Learning Pearls   Screen Shot 2017-10-11 at 12.58.11 PM

  • Don’t forget your physical exam maneuvers to assess for radiculopathy: straight leg raise (L4-S1); opposite straight leg raise (L5-S1); and reverse straight leg raise (L3-L4).
  • Order spinal MRI for patients with red flag signs or symptoms, pain that is progressive, or when it will change treatment (including referral for spinal injections or surgery)
  • Inflammatory markers may be helpful in determining who needs an urgent MRI

 

 

Screen Shot 2017-11-08 at 9.55.37 AM

The Physical Exam Maneuvers for the evaluation of Low Back Pain

  • Straight leg raise:
    • How to do: Patient supine, examiner raises affected side leg keeping it straight up to 60 degrees
      • Positive test: reproduces pain on side of leg raised
      • Suggests L4-S1 nerve root pain if radiates below the knee
      • Sensitivity = 80%, specificity = 40%
  • Reverse Straight Leg Raise (femoral stretch test)
    • How to do: Patient lying prone passively extending the hip and leg straight up off the plane of the table
    • Suggests L3 nerve root pathology if pain radiates into the anterior thigh
  • Opposite Straight leg raise
    • How to do: Patient supine, raise opposite side leg, keeping it straight
    • Positive if pain reproduced on the affected side
    • More specific test for L5-S1 radiculopathy
    • An L5-S1 radiculopathy is 95% sensitive for lumbar disk herniation (thus, the absence of radiculopathy almost rules-out a herniated disk)
  • FABERE (Flexion, Abduction, External Rotation, and Extension)
    • Consider performing if evaluating for hip or SI joint as cause of pain
    • How to do: Hip is externally rotated with the ipsilateral knee flexed at 90 degrees and placed on the opposite knee. Then apply downward pressure on the leg towards the examine table. Goal of getting leg parallel to exam table
      • If pain: indicates SI joint disease
      • If limited ROM: indicates hip, SI, or iliopsoas spasm

 

When to get imaging for low back pain?

  • Red flag signs or symptoms
  • If low back pain is not improving after conservative management and the patient is a candidate for surgery or epidural spinal injections
  • Imaging choice
    • MRI is ideal
    • Can consider a CT if a patient cannot get an MRI
    • Xrays may be helpful to evaluate for compression fracture and degenerative changes

 

When should I order inflammatory markers?

  • Consider ordering if you are concerning about do not miss diagnoses including seronegative spondyloarthropathies, malignancy, or infection.
  • Check out this article on the use of a clinical decision support tool utilizing risk factors and ESR/CRP to evaluate for spinal epidural abscess
    • The bottom line: The use of a clinical decision guideline for patients presenting to the ED with low back pain involving risk factors and ESR/CRP to determine who should receive urgent MRI decreased the time to diagnosis of spinal epidural abscess and decreased the incidence of neurologic deficits at the time of diagnosis.

 

Check out the ACP guidelines on the treatments for chronic low back pain.

Click here for an Evernote on Low Back Pain