VZV Meningitis 3/21/16

Teaching Pearls – Thanks to Dr. Sharma for joining us!

  • Viral Meningitis Differential: Viral causes of meningitis includes EBV, WNV, HSV2, HSV-1, enterovirus, VZV, mumps
    • The most common viral meningitis cause is enterovirus which includes Cocksackie virus. Usually presents in the summer and fall, fecal-oral transmission, often mild and self-resolving.
    • Remember that HSV1 usually causes encephalitis while HSV2 causes a recurrent self-limited meningitis (Mollarets meningitis)
    • West Nile Virus can present with asymmetric flacid paralysis
    • VZV meningitis usually causes a more severe meningitis than HSV, make sure to check skin for dermatomal rash (particularly on the back where the patient may not be aware)
  • Other non-viral causes of aseptic meningitis includes drug induced (Ibuprofen is classic, ranitidine), rheumatologic (SLE, Behcets), sarcoidosis.
  • Ramsay Hunt Syndrome is VZV reactivation causing ipsilateral facial paralysis, ear pain, and vesicles in the auditory canal and auricle
  • VZV meningitis causes CSF pleocytosis and elevated protein level
  • VZV CNS infections can cause strokes via infection of the cerebral arteries
  • Causes of hypoglycorrhachia: Bacterial, TB, Rheumatologic
  • Very elevated CSF protein is associated with hydrocephalus

Neurosarcoidosis 3/15/16

  • Illness Script for Sarcoidosis: Young AA female with cough and bilateral LAD
  • Sarcoid Lofgren’s Syndrome: Hilar LAD, arthralgia, erythema nodosum
  • Sarcoid Heerfordt’s Syndrome: uevitis, parotitis, chronic fever, facial nerve palsy
  • Neurosarcoidosis complicates 5-10% of systemic sarcoidosis, cranial nerve palsies are the most common manifestations of neurosarcodosis. Optic neuropathies, headache, HPA axis/endocrine abnormalities are also reported.
  • Treatment for neurosarcoidosis is corticosteroids.

Ocular Syphilis

NON-TREPONEMAL TESTS Syphilis infection leads to production of non-specific antibodies that react to cardiolipin. There can be a lot of false positives (cross react with other things).  You can also have the prozone/hook effect (which is a false negative due to very high titers).  Non-treponemal tests can be reported as a titer. RPR

VDRL (ONLY ONE USED for CSF fluid)

TREPONEMAL TESTS Looking for SYPHILIS ANTIBODIES specific for the spirochete.  NOT reported as a titer. It is Reactive or Non-reactive. These REMAIN positive usually lifelong. FTA-Abs

TPPA

EIA Testing – this is what we do

The prior testing algorithm was a NON-TREPONEMAL TEST followed by a TREPONEMAL TEST.  This changed a few years ago due to a study from New York City in which they found it to be more cost-effective to do a TREPONEMAL TEST followed by NON-TREPONEMAL TEST in high prevalence areas. This is why we at VALLEY switched the way we test for syphilis.

SYPHILIS TESTING AT VALLEY:

  • Syphilis EIA Antibody (TREPONEMAL) à If Positive go to Number 2
  • RPR with Quantification (NON-TREPONEMAL)

Other pearls:

  • Some Patients remain Serofast (low titers such as 1:2) even after treatment
  • Remember that the Treponemal Tests STAY positive lifelong, so it is important to ask if they have had syphilis before, what their titers were, and whether they were treated. Then you go by the RPR titers and compare to see if the RPR titers were higher than before.
  • LP results for syphilis usually show a lymphocytic pleocytosis (<100 total cells, > 5 Lymphocytes), Elevated protein > 45 mg/dl)
  • We only send the VDRL for the CSF fluid (occasionally you can do a treponemal test as well, but not routinely done)
  • Neurosyphilis can occur at any stage
  • Ocular syphilis can cause anterior uveitis, posterior uveitis, or panuveitis
  Clinical Features Treatment
Primary Syphilis Painless Chancre which appears at the site of inoculation, infectious Penicillin G 2.4 million Units IM x 1 DOSE
Secondary Syphilis Generalized non-pruritic rash involving palms/soles, infectious, also systemic symptoms including fatigue, diffuse LAD, fever Penicillin G 2.4 million Units IM x 1 DOSE
Latent Syphilis

 

Early Latent (seroconverted within past 12 mo) Penicillin G 2.4 million Units IM x 1 DOSE
Late Latent

 

Penicillin G 2.4 million Units IM x 3 Doses qweek
Tertiary Syphilis Gummas (granulomatous lesions)

Tabes Dorsalis

Ocular Syphilis

Aortitis

Neurosyphilis

24 million units of Penicillin daily for 2 weeks (continuous pump) for neurosyphilis, otherwise 3 doses of weekly PCN G

Morning Report 3/10/16 Cushing’s

  • Cushing’s Disease refers to ACTH secreting pituitary adenomas
  • Signs of Cushing’s Syndrome/Disease include: Centripetal obesity, facial plethora, glucose intolerance, proximal weakness, hypertension, psychiatric changes, easy bruising, menstrual changes, acne, oily skin, impotence, abdominal striae, polydipsia/polyuria, hyperpigmentation, headache, osteoporosis, abdominal pain
  • The hyperpigmentation is due to increased POMC production as precursor for ACTH and Melanocyte stimulating factor as a by-product
  • Initial work-up for Cushing’s disease is 24 hour urine cortisol, dexamethasone suppression test, or pm salivary cortisol testing
  • Use the high dose dexamethasone suppression test to distinguish between ectopic ACTH production versus pituitary ACTH production
  • Pituitary Adenomas prevalence from most common to least common is: Lactototrophs, Nonfunctions, Somatotrophs, Corticotrophs
  • For ACTH depending Cushing’s syndrome, the differential includes ACTH adenoma (68%), Ectopic ACTH (12%), ectopic CRH (<1%)
  • Treatment for ACTH Adenomas is SURGICAL
  • Must monitor very closely for Diabetes Insipidus after transphenoidal resection (there is a triphasic pattern of DI, SIADH, and DI – thanks Kefu for this pearl!)

3/8/16 Morning Report

Teaching Pearls: 

Four Clinical Manifestations of Meningococcal Disease (Mandells page 2321):

  1. Bacteremia without Sepsis: Present with upper respiratory illness or viral exanthem. Often recover without specific antibiotic therapy, and then blood cultures result positive for N. Meningitidis.
  2. Meningococcemia without meningitis: In these cases, patients are septic and often have skin rash, malaise, weakness, headache, and hypotension.
  3. Meningitis with or without meningococcemia: In these patients, headache, fever, and meningeal signs are present with a cloudy spinal fluid.
  4. Meningoencephalitic Manifestation: These patients are profoundly obtunded with meningeal signs and septic spinal fluid. Deep tendon reflexes are altered.

Meningococcal disease is carried in the nasopharynx of otherwise healthy people. It is spread via aerosolized secretions

Risk factors for disease include smoking, recent URIs, crowded places (dorms, military recruits, complement deficiency)

Treatment is with 3rd generation cephalosporins. Prophylaxis for close contacts usually consists of a single dose of ciprofloxacin.

The initial rash of Meningococcemia/meningitis can appear maculopapular resembling a viral exanthem.

The typical initial presentation is acute onset of fever, N/V, headache, decreased ability to concentrate, and severe myalgias

Major complications of meningococcemia include DIC, purpural fulminans, adrenal hemorrhage.

Resident Report 3/2 – Transaminitis

Teaching Points:

  • LFT abnormalities may manifest itself in a cholestatic or hepatocellular pattern
    • Cholestatic pattern
      • elevation of bilirubin, high alk phos in relation to AS and ALT elevation
    • Hepatocellular pattern
      • Elevation of AST and ALT in relation to alk phos and bilirubin levels
  • Pattern can determine initial imaging work-up
    • Clear cholestatic pattern
      • May proceed to EUS, MRCP or ERCP since these studies would be indicated despite getting abdominal ultrasound
    • Clear hepatocellular pattern
      • May proceed to CT initially
    • If picture is mixed:
      • Can start off with abdominal ultrasound
  • Differentials of cholestatic LFTs in IBD patients
    • Primary sclerosing cholangitis – occurs in about 10-15% of IBD patients (more associated with ulcerative colitis)
    • Primary biliary cirrhosis – associated with anti-mitochondrial antibody
      • Seen in middle aged female with chronic onset, manifesting with pruritis and gradual jaundice
    • Viral hepatitis
    • Autoimmune hepatitis
    • Post-obstructive etiologies including pancreatic CA, cholangio, gallstone, etc.
    • Alcoholic hepatitis
  • Patients on 6-MP or azathioprine for their IBD need to have their enzymatic TPMT levels checked.
    • Metabolites of 6-MP can cause cytopenia and also hepatotoxicity.