ZSFG Report Pearls: HA’s, Hyperinfection Syndrome w/ Strongyloides, Derm of Uremia

Alright alright alright (cue Matthew McConaughey’s voice 🙂 team, prepare yourselves for pearl explosion as we combine today’s report clinical bombs with Katie’s GI report knowledge nuggets from Friday below…

Today, Caroline Ong presented and Elvin from ID helped us discuss the case of an older woman w/ headache, neck stiffness, and confusion. Her LP was concerning for bacterial meningitis with CSF gram stain initially growing GNR, then GPR on repeat LP, and ultimately GNR of unclear speciation (what?!).

First, let’s start by reviewing the HEADACHE RED FLAGS from this fancy AFP table

red flags HA

***some would add:
1) HA initiated by Valsalva maneuver/bending/cough to the papilledema/increased ICP category above
2) A change in characteristic symptoms or response to previous treatments of HA



A few pearls from Elvin Geng, ID specialist extraordinaire:

  • In early bacterial meningitis, you can have a CSF w/o WBC’s but generally the gram stain will be positive
  • If you find yourself admitting an older person with confusion, HA, focal neuro deficit: consider Listeria as it can cause brainstem encephalitis.
  • Have someone with a fever, neck stiffness, and clean CSF: consider cervical epidural abscess as meningitis mimicker
  • Skin finding pathognomonic for Strongyloides stercoralis infection: Thumbprint sign which is periumbilical purpura (see article and photo below)
  • In chronic infection with Strongyloides, there is generally peripheral eosinophilia. This goes away in hyperinfection syndrome

thumb 2

So what is HYPERINFECTION SYNDROME, anyway?!?!

  • The autoinfection cycle of Strongyloides (see below) leads to hyperinfection syndrome as the parasite load is greatly increased
  • MKSAP or the boards may describe a patient who has traveled to or was born in a developing country and who is given high dose steroids (the typical trigger) and develops pulmonary infiltrates, meningitis, or GNR sepsis
  • Autoinfection within the GI tract occurs when rhabditiform larvae transform into filariform larvae and then penetrate the intestinal wall to enter the bloodstream
  • Massive dissemination of filariform larvae to the lungs, liver, heart, CNS, endo glands induces inflammationàsymptomatic dysfunction of these organs/septic shock
  • Sx’s: fever, N/V/D, anorexia, abd pn, wheezing, dyspnea, hemoptysis, cough
  • Tx: if present, tx bacteremia. Reduce immunosuppression if possible. Ivermectin is drug of choice (but limited data) usually 200mcg/kg PO daily for 14d after stool clear of inxn
  • Mortality rates of 10-85% have been reported


life cycle strongy.jpg

-Maher, N et al. Periumbilical thumbprint parasitic purpura: A highly fatal sign in disseminated Strongyloides infection that may mimic vasculitis clinically. Journal of American Academy of Dermatology. 2015 May; 72 (5): AB129. DOI: http://dx.doi.org/10.1016/j.jaad.2015.02.532

-Clinch, R et al. Evaluation of acute headaches in adults. Am Fam Physician. 2001 Feb 15; 63 (4): 685-92. 11237083


-Weiser, J et al. Periumbilical parasitic thumbprint purpura: Strongyloides hyperinfection syndrome acquired from a cadaveric renal transplant. Transpl Infect Dis 2011: 13: 58–62. DOI: 10.1111/j.1399-3062.2010.00516.x


**********From KATIE**********

And from last Friday, Katie Raffel joined ZSFG for GI morning report and wrote amazing pearls below…

Big thank you to Scott Goldberg for the fascinating case of an older woman w/ CKD and nephrotic syndrome 2/2 DM/HTN who presented w/ abd pn, ultimately found to have nodular pruritic skin lesions on legs and back and cholestatic pattern to LFT’s.

Both of these manifestations were 2/2 her CKD and nephrotic syndrome. Her skin lesions were prurigo nodularis, a cutaneous manifestation of uremia, and her cholestatic LFT’s were due to CBD obstruction from cholesterol stone (2/2 HL in setting of nephrotic syndrome). Amazing!

Dermatologic manifestations of uremia; just a few highlights… – Pruritis -> prurigo nodularis (pictured below):

  • Caused by metabolic disequilibrium NOS (uremiea/cholestasis/etc)
  • Nodules often begin at hair follicles and are generally pruritic, hyperpigmented, symmetric and firm
  • Generally found on the arms and legs, more typically on the extensor surfaces.
  • Chronic scratching then contributes to lichenification, hyperkeratosis and thickening
  • Tx the underlying cause, topical steroids, antihistamines and in diffuse cases consider UV-B light tx

purpura uremia

– Kyrle’s disease: Actually associated with DM (which is then often associated with CKD). Pruritic, located on extremities and buttocks and are typically papules with keratotic plug or occasionally coalescing plaques. May be follicular or extrafollicular; linear arranagement is common

– Nephrogenic systemic fibrosis: Estimated risk is 2.5-5% among those with ESRD exposed to gadolinium although very difficult to measure. Tissue deposition of gadolinium is thought to stimulate local tissue fibrosis. Skin fibrosis occurs in all patients and some also experience systemic fibrosis involving myocardium/pericardium, diaphragm, etc. Eek! Generally, we avoid gadolinium if eGFR <30ml/min

Medscape article! http://emedicine.medscape.com/article/1094846-overview#a3

Fistulous tracts with gallstones
Cholecystoenteric fistula:

  • Uncommon variant/complication of biliary disease
  • Within the cholecystoenteric fistulas, cholecystoduodenal is the most common (often presents with gallstone ileus) and cholecystocolonic fistulas are second most common (often present more vaguely)
  • This is typically treated with cholecystectomy, fistula resection and common bile duct exploration.
  • These patients are at high risk for biliary sepsis as there is direct contact between gut bacteria and biliary system

Mirizzi’s syndrome: Hepatic duct obstruction caused by an extrinsic compression from an impacted stone in the cystic duct.

Nephrotic syndrome
Definition: >3.5gm/day proteinuria, edema, hypoalbuminemia, hypercholesterolemia (LDL 900+ in this case!!)
Etiology: Glomerular disease: Minimal change, FSGS, Membranous, Membranoproliferative (rarely), IgA nephropathy. Systemic disease: DM, SLE.
Management: Tx underlying etiology. Treat BP/proteinuria with ACE-i, diuretics. Utilize anticoagulation if evidence of thrombus.


Evernote: https://www.evernote.com/shard/s354/sh/3b288dc3-9693-407a-b8d9-bead13c8db42/b80533bcf8bec4ab0714e93103563825











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