Pneumatosis Intestinalis

Dr. Haraga presented a case of a man with vascular disease and end-stage renal disease (ESRD) who recieved sodium-polysytrene-sulfonate for hyperkalemia. One day later he developed fever, hypotension and acute on chronic RLQ pain without diarrhea or hematochezia. CT showed pneumatosis coli. The differential included colonic necrosis from sodium-polystyrene sulfonate vs ischemic colitis given his comorbidities. At this point, the etiology remains unclear, but the patient improved with antibiotics for sepsis of unclear (but suspected abdominal) source.

Pneumatosis Intestinalis: It literally means gas in the wall of the small or large intestine. The differential for pneumatosis intestinalis is vast. To quote the an article from the American Journal of Roentgenology, etiologies range from "benign to life-threatening." History and risk factors are the key to discerning cause and need for acute workup.


Pneumatosis Intestinalis can be seen on abdominal x-ray or CT and is characterized by “thumbprinting.” On exams, it is classically associated with pseudomembranous colitis. Here are some actual photos of thumb-printing (the example from noon report was incorrect).

A note about sodium-polystyrene-sulfonate:

Intestinal necrosis is a rare side effect of SPS, but the risk is not zero. Many studies associate the SPS + sorbitol formulation as having the highest risk, and the FDA has removed sorbitol from SPS formulations. However, it is unclear if sorbitol alone was the clear culprit. At this point it is wise to avoid SPS in patients with altered gut motility (see below).

There is one small case series of patients with ESRD showing no development of colonic necrosis with daily low-dose sorbitol-free SPS. However, this is not standard of care, and hemodialysis is still the best way to normalize potassium in patients with ESRD.

As a general rule, AVOID sodium-polystyrene-sulfonate (SPS) in:

  • post-operative patients

  • patients with ileus or receiving chronic opioids

  • patients with large or small bowel obstruction

  • patients with underlying bowel disease (UC, crohn’s, C diff)

  • patients with ESRD where iHD is readily available.

"Spells"- a clue in elderly patients

Dr. Manley presented a case of an elderly man with history of dementia and visual hallucinations (small children running around) who was admitted for “spells”. These spells were short lived, characterized by sudden staring off, occasional atonia, occasional urinary incontinence, some extremity jerking and absence of post-ictal state.

…. Does this illness script jog anyone’s memory?

What if I told you that this was his orthostatic vitals:

  • Lying: 107/64, HR 82

  • Standing 1 min: 97/50, HR 84

  • Standing 3 min: 79/42, HR 86

…Anything strike you about the heart rate?


Now what's on your differential for neurodegenerative disease + autonomic failure?

  • PARKINSON’S DISEASE: motor symptoms predominate, 20-60% patients will develop autonomic failure

  • LEWY BODY DEMENTIA: next slide

  • MULTIPLE SYSTEMS ATROPHY: dysautonomia, motor symptoms, oculomotor issues, and urinary incontinence- challenging to differentiate from Parkinson’s. Preserved cognitive function + minimal response to Levodopa are clues

  • PURE AUTONOMIC FAILURE: isolated dysautonomia without other symptoms, good prognosis

This patient had likely LEWY BODY DEMENTIA! We characterized these “spells” as “cognitive fluctuations”.

“like” this post if you got the diagnosis right!


Agranulocytosis and a word on Bronchiectasis

Dr. Kiefer presented a thought provoking case of a patient with chronic saccular bronchiectasis who presented with agranulocytosis and fevers! Let’s review:

What’s agranulocytosis? I remember learning that in med school…

It’s when neutrophilia gets bad:

  • Mild: Absolute neutrophil count (ANC) <1500

  • Moderate: ANC 500-1000

  • Severe: ANC <500 *

  • Agranulocytosis: ANC<200 **

* ANC <500 + fever (T>38.2 OR >38 degrees for greater than an hour) is neutropenic fever

** Agranulocytosis is caused by medications up to 70% of the time (most commonly: sulfasalazine, TMP-SMX, methimazole (these three are responsible for up to 42% of cases). Other ones on the list include NSAIDs, macrolides, vancomycin (Commonly USED ones just to keep in mind).


Figure 1: Algorithm for the evaluation and treatment of adult patients with neutropenia ( Gibson, C., & Berliner, N. (2014). How we evaluate and treat neutropenia in adults. Blood, 124(8), 1251-1258. Accessed August 11, 2019.

Ok, now how do I think about etiologies of bronchiectasis?

Very briefly, we can categorize conditions associated with bronchiectasis into the following categories: Post-infectious, congenital conditions, immunodeficiencies, sequelae of toxic inhalation/aspiration, rheumatologic conditions.

Please refer to this review article by our very own Alan Barker, MD for details!

Barker, A. (2002). Bronchiectasis. N Engl J Med, 346:1383-1393


Ruling out Fournier's Gangrene!

Dr. Spencer presents a case of a young man with untreated diabetes who presented with acute, progressive scrotal pain and swelling.

Our astute residents quickly raised concern for Fournier Gangrene which is an essential "rule out" diagnosis. However, Fournier Gangrene is challenging to diagnose and can only be definitively diagnosed with surgical evaluation.

Fournier Gangrene is a necrotizing fasciitis of the male genitalia (usually the scrotum and perineum but can involve the abdominal wall and penis). Though exceedingly rare, it should be considered in diabetic patients with scrotal cellulitis. SGLT-2 inhibitors have been associated with rare cases of Fournier Gangrene.

Physical Exam finding that raise concern for Necrotizing Fasciitis:

  • necrosis (maybe that's obvious)
  • pain out of proportion to exam
  • crepitus
  • subcutaneous air
  • bullae/blistering

Necrotizing skin and soft tissue infections can be polymicrobial (type I) or monomicrobial (type II, most likely Group A strep or Staph). Type I (polymicrobial) infections are more common in diabetics, patients who are immunocompromised, or patients who have recently had surgery.

We discussed the initial promise of the LRINEC score in diagnosing nec fasc, but highlighted that retrospective studies show inadequate sensitivity to rule out the diagnosis. LRINEC score includes CRP, WBC, sodium, glucose, creatinine, and hemoglobin. Despite its issues with sensitivity, it may help build your case when you call surgery for an urgent consultation!

A meta-analysis entitled "What is the Accuracy of Physical Examination, Imaging and the LRINEC Score for the Diagnosis of Necrotizing Soft Tissue Infection?" in the Annals of Emergency Medicine reviewed sensitivity, specificity, and positive and negative liklihood ratios of the following variables.

Treatment for Necrotizing Fasciitis:

1) surgical debridement!

1) empiric antibiotics

should cover gram positive, gram negative, anaerobic + clindamycin for antitoxin effect (inhibits protein synthesis)


  1. vancomycin + pipercillin/tazobactam + clindamycin

  2. vancomycin + ertapenem + clindamycin

  3. vancomycin + meropenem + clindamycin (if HC-associated)

Approach to Sensory Loss & Abdominal Reflexes

Dr. Wells presented an interesting case of a man who presented with bilateral, symmetric, progressive, ascending lower extremity numbness that turned out to be secondary to compressive myelopathy from a benign lipomatous growth.

Step one: Localize the lesion:

  • Examine their sensation to light touch, sharp stimuli, proprioception, vibration and temperature

  • Vibration and proprioception live in the DORSAL COLUMN

  • Temperature and pain sensation live in the SPINOTHALAMIC TRACT

Step two: Determine the pattern of sensory loss:

  • If it’s one limb: think peripheral nerves/mononeuropathy, nerve plexus or a spinal root

  • If it’s bilateral or symmetric, think polyneuropathy or spinal cord lesion

  • If only one side is affected, think higher up (ie brainstem and above) and on the contralateral side.


Our patient here ended up having compressive myelopathy of T7-T10 which can be very difficult to localize. Dr. Sullivan gave us a pearl about how to test thoracic reflexes #Sullivanpearls: Superficial abdominal reflexes! Here’s a video:



Dr. Oppegard presented a case of a young man who presented with hypertensive emergency with vision changes, headache, and vomiting. He was found to have a blood pressure of 230/150 and severe AKI (BUN 122, sCr 19)!.

We reviewed the initial work up for hypertensive emergency, BP target goals based on clinical picture, and what IV medications to use acutely. This article from The American Academy of Clinical Pharmacy's Critical Care Self-Assessment Program provides a nice review.

“Hypertensive Emergencies” by: Scott Benken, PharmD found in CCSAP 2018, Book 1

“Hypertensive Emergencies” by: Scott Benken, PharmD found in CCSAP 2018, Book 1

Conditions Requiring Different BP Goals in Hypertensive Emergency:

  • Aortic dissection: the goal SBP is less than 120 or as low as clinically tolerated.

  • Acute ischemic stroke: permissive hypertension due to potentially elevated ICP. Acute treatment is indicated if:

(1) use of thrombolytic therapy

(2) other target-organ damage (dissection, MI, etc)

(3)"severe" elevations in BP SBP >220 and/or DBP >120.

  • Acute hemorrhagic stroke: Complicated data but likely SBP <160 (per UTD).

From “Hypertensive Emergencies” by: Scott Benken, PharmD found in CCSAP 2018, Book 1)

Derived from UptoDate “Drugs used for the treatment of hypertensive emergencies” and “Hypertensive Emergencies” by: Scott Benken, PharmD found in CCSAP 2018, Book 1

Derived from UptoDate “Drugs used for the treatment of hypertensive emergencies” and “Hypertensive Emergencies” by: Scott Benken, PharmD found in CCSAP 2018, Book 1

Dr. Oppegard brought up an excellent teaching point!

All patients that present with hypertensive emergency should have a work up for secondary causes of hypertension.

See below for an excellent framework for thinking about secondary hypertension from the book Frameworks for Internal Medicine which was written by one of our OHSU attendings, Dr. Andre Mansoor.

It should also be noted that the work up for endocrinologic causes of secondary hypertension can be inaccurate in the setting of acute illness and increased sympathetic drive. For example, plasma metanphrines may be falsely positive in the hospital. Thus this work up is best suited for the outpatient setting.

From  Frameworks for Internal Medicine  By: Andre Mansoor (OHSU Faculty)

From Frameworks for Internal Medicine By: Andre Mansoor (OHSU Faculty)


Dr. Doan presented an intersting and complex case of fever and malaise in a recently returned traveler. She talked us through some "don't miss" diagnoses, including malaria and enteric fever, and we discussed frameworks for travel-related illness, with a focus on predominant symptoms, geographic location, and incubation periods. Here are some takeaways:


Below is a sample approach from a NEJM article: "Approach to Fever in the Returning Traveler". You should memorize this algorithm. Just kidding! But do know that resources are available on the CDC website (or in articles like this one), if you find yourself grappling with fever in a returned traveler.


Lastly...A Word on Leptospirosis

Reminder-a zoonosis (mammal urine-remember from Step 1?) that causes a nonspecific febrile illness. Dr. Obley dropped some knowledge bombs for us on leptospirosis.


-Frequently see conjunctival suffusion (redness)

-Weil's disease: leptospirosis complicated by jaundice and renal failure

-Serology: timing of testing matters! antibodies appear in ~5-7 days then can be missed. Need both acute and convalescent samples for diagnosis.    


Intermittent Lymphadenopathy! Kikuchi Disease!

Dr. Collins presented a fascinating case of a young woman with 2 months of intermittent cervical lymphadenopathy, intermittent fevers, malaise, and mylagias who was found to have Kikuchi Disease after a lymph node biopsy.

Kikuchi disease is a rare disease that mostly affects women. Dr. Collins's case is a classic presentation. Associated lab findings can include leukopenia with elevated CRP and LDH. It is diagnosed on excisional lymph node biopsy. It is also known as histiocytic necrotizing lymphadenitis based on pathology findings.

Kikuchi disease is benign and self-limited but typically leads to an extensive work up to rule out more sinister diagnoses (lymphoma, TB lymphadenitis, and other infections). Some people treat Kikushi disease with steroids though there is no data on if this improves outcomes.

Interestingly, Kikuchi disease is associated with SLE for unclear reasons. There have been numerous case reports on this association in which SLE followed a prior diagnosis of Kikuchi disease. Some advocate for close follow up for clinical and serologic evidence of developing SLE after a diagnosis of Kikuchi disease.

Intermittent lymphadenopathy should trigger a short differential.

  • T cell lymphoma
    • Illness script: middle aged man with generalized lymphadenopathy
  • Kikuchi Disease
    • Illness script: young previously healthy Asian woman with regional (usually cervical) lymphadenopathy
  • Recurrent infections/immunodeficiency
  • Incompletely treated infectious
derived from AAFP differential for lymphadenopathy and neck mass.

derived from AAFP differential for lymphadenopathy and neck mass.