All posts by alp37

VA ICU Report 3.23.18: Boerhaave’s syndrome

Case summary: Thanks to our multi-disciplinary ICU team for showering us with pearls today on a 55M with a PMH of esophagitis complicated by ulcerations and stricture s/p multiple dilations, EtOH abuse, who initially presented after a fall while intoxicated and symptoms of UGIB and was found to have esophageal rupture (Boerhaave’s syndrome!) and bilateral Candida empyema!

Top pearls:

1. This patient got a CT scan after presenting with signs of UGIB, which is not routinely part of the diagnostic work-up. Importantly, patients with prior stricture/dilations and other esophageal instrumentation and/or anatomic abnormality are at increased risk of Boerhaave’s and thus warrant a CT scan if any suggestive symptoms.

2. UGIB is not a classic symptom of Boerhaave’s; more common are retrosternal chest pain after wretching, creptius of chest wall due to pneumomediastinum, odynophagia, dyspnea and shock.

3. When you rupture your esophagus, caustic pharyngeal and gastric contents leak everywhere and can cause mediastinitis, pleural effusion, pericarditis/tamponade, ARDS and shock.

4. Management of Boerhaave’s is a great mix of medicine and surgery and involves: 1) pharyngeal decompression, 2) gastric decompression, 3) endoscopic stenting, 4) drainage or debridement of mediastinal/pleural/pericardial fluid collections or areas of necrosis, 5) lung protective ventilation given high incidence of ARDS, and 6) esophageal surgical reconstruction 4-6 weeks later.

Crash course in Boerhaave’s syndrome/Effort rupture of the esophagus

  • We were so lucky to have the fantastic Dr. Jan Horn (part-time VA ICU attending, part-time ZSFG trauma surgeon!) to teach us about Boerhaave’s from the surgical perspective.
  • Interesting factoids:
    • We learned today that Boerhaave’s is really hard to spell on the board in front of a crowd! In true old-school-doctor-fashion, Hermann Boerhaave, Professor of Medicine at Leiden University, named it after himself. The case he described was of  Baron Jan van Wassenaer, a Dutch admiral, who liked to vomit after feasting so that he could feast more, ruptured his esophagus, and lived less than a day afterward.
    • It can happen with a normal esophagus and after intense vomiting/wretching or anything else that causes a sudden increase in intraesophageal pressure (childbirth, seizure, prolonged coughing, weightlifting).
    • History of stricture/ulcerations/dilations, as well as eosinophilic esophagitis, medication-induced esophagitis, Barrett’s esophagus, caustic ingestions, or infectious ulcers can also predispose.
    • Usually the L posterolateral aspect of the distal intrathoracic esophagus (near the G-E jxn) but can be in the neck or sub-diaphragmatic.
  • Presentation:
    • Classic: excruciating retrosternal chest pain (can be superior or inferior depending on location of rupture)
    • 25 to 45% of patients have no history of vomiting
    • May have crepitus on palpation of the chest wall due to subcutaneous emphysema.
      • mediastinal crackling with each heartbeat may be heard on auscultation (Hamman’s sign)!
    • can develop odynophagia, dyspnea, and sepsis
  •  Complications:
    • pneumomediastinum
    • mediastinitis
    • pleural effusion
    • pericardial effusion and tamponade
    • ARDS
    • sepsis/multi-organ failure
  • Diagnosis: established by contrast esophagram or computed tomography (CT) scan.
  • Treatment:
    • Extremely high mortality (25-50% in some series)
    • The mainstay of treatment is to bypass the rupture such that pharyngeal and gastric contents can’t contaminate the thorax and treat any pre-existing sites of leakage. This involves:
      • NPO, sometimes a tube-like device that drains the pharynx
      • NG tube (very complex to place!) and ultimately G-tube
      • Endoscopic stenting
      • Source control +/- antibiotics for sites of contamination like the pleura (in this case, the patient had bilateral pleural effusions and yeast on a gram stain and got bilateral chest tubes), pericardium, mediastinum
      • Given the high incidence of ARDS, many patients require lung protective ventilation.
      • Esophageal surgical reconstruction 4-6 weeks later.
        • Thanks to the fantastic Dr. Horn for describing how difficult/impossible it is to operate on these patients immediately given the necrosis and friability of their thoracic tissues
  • Here are some fun pictures!

Mediastinal_air_Boerhaaves                                       Esophageal_perforation_CT

(1) Pneumomediastinum                                 2) Mediastinal widening, air, pleural effusions




VA ICU Report 3.16.18: To pUF or not to pUF

Case summary: Thanks to our stellar ICU team for presenting the case of a 64M with PMH CAD, single-lead PM and HFrEF, who presented in cardiogenic shock complicated by cardiorenal syndrome and was started on CRRT as a bridge to dual-lead PM (e.g. cardiac resynchronization therapy (CRT)). Amazing renal fellow Chris Carlos was there dropping pearls alongside our regular cast of ICU attendings.
Top pearls:
1. Patients with advanced heart failure and AKI who need CRRT have high in-hospital (~60%) and overall mortality (OS =10 months). As such, CRRT is generally reserved as a “bridge” therapy– i.e. for patients headed for LVAD, transplant, or (in this case) CRT.
2. Patients with advanced heart failure have a substantial symptom burden and survival rates on par with stage IV lung cancer, and patients randomized to early palliative care had improved quality of life scores and lower rates of anxiety and depression.
3. In a 2012 NEJM RCT comparing early ultrafiltration (pUF) to step diuretics for heart failure, there was no difference in weight loss between the two groups, and patients who got pUF had worse AKI and more serious events.

Palliative care in HF

  • Population: 150 patients with advanced HF were randomized to usual care (n = 75) versus usual care plus a longitudinal palliative care intervention (n= 75) at a single center (Duke)
  • Results:
    • Patients randomized to usual care + pall care had clinically and statistically significant improvement on 2 validated quality of life scoring systems.
    • They also had fewer symptoms of anxiety and depression
    • They also reported higher levels of spiritual well-being
    • There was no difference in rehospitalization or mortality

      Screenshot 2018-03-18 at 6.20.54 PM

  • Limitations: single-center, high drop-out rate
Reference: Rogers, JG, et al. Palliative Care in Heart Failure. 

Early pUF versus regular, old diuresis in heart failure
  • Thanks to Chris for passing this paper along!
  • CARRESS-HF trial published in the NEJM in 2012
    • Population: 188 patients at 22 sites in the US and Canada admitted with acute decompensated heart failure, AKI and volume overload were randomized to early ultrafiltration (-200cc/h) vs step diuretics (3-5L UOP/d).
    • Results:
      • No difference in weight loss between the two groups ( 5.5±5.1 kg vs 5.7±3.9 kg; P=0.58)
      • Early UF group had higher sCr @96h and more serious events, usually related to catheter use (bleeding and clotting.
      • Thus, no difference between the two therapies based on their bivariate endpoint (weight loss + SCr)Screenshot 2018-03-18 at 6.06.12 PM
        • Limitations: Unblinded and decision of when to stop diuretics or adjust UF was left to the caring physicians.


VA AM Report 3.13.18: A cat named Leo

Case summary: Thanks to Rand and Akshai for presenting a great case– an 84M with a history of gout who presented with RUE cellulitis complicated by GNR bacteremia after being bitten by his cat, Leo, who then developed olioarticular arthritis of the R DIP and PIP joints due to gout that improved on anakinra.

Top pearls:

  1. In contrast to Staph bacteremia, GNR bacteremia should trigger you to think of: a shorter duration of therapy  (7-14 days depending on clinical response), faster switch to oral therapy (48-72H afebrile and hemodynamically stable), and no need for surveillance blood cultures.
  2. Non-purulent cellulitis can take 48-72H to show clinical improvement (downtrending WBC count, afebrile, erythema/edema receding), so hold off on escalation of antibiotics!
  3. The pattern of joint involvement is useful in determining your pre-test probability for septic arthritis– it typically causes monoarticular or at least contiguous arthritis in larger joints, rather than the oligoarthritis in the small joints seen in this patient.
  4.  Anakinra (an IL-1 agent) is an option for patients with gout who have contraindications to traditional therapies (e.g. steroids, NSAIDs)

Gram-negative rod bacteremia pearls c/o Andrew Kerkhoff

  • Earlier in the year, Dr. Kerkhoff– ID fellow extraordinaire– gave us some fantastic pearls about GNR bacteremia during an M+M
  •  Source:
    • Community: GU>>>GI>respiratory tract
    • Hospital: GU>>central lines/wound infections>GI>respiratory tract
  • Risk factors:
    • Immunocompromised hosts (stem cell transplant/hematologic malignancy, solid organ transplant, diabetes, HIV, steroids, elderly)
    • Other organ dysfunction (ESLD, ESRD on HD, chronic pulmonary infection)
  • Microbiology:  Klebsiella, Pseudomonas, Enterobacteriacae, SPACE organisms
    • High mortality rate (12-38%)
    • Increasing drug resistance (to CTX/Zosyn)
  •  Therapy:
    • Duration: few RCTs and driven by site/severity of infection/response to treatment, but generally 7-14 days
    • Switch to oral: within 48-72H of normothermia and normal VS
    • Follow-up blood cultures: bacteremia is usually transient and clears quickly with therapy, and the value of repeat blood cultures is unclear given they are rarely positive

Cellulitis pearls c/o Jen Babik

  • In general, we expand antibiotics too soon in cellulitis, as clinical response (e.g. reduction in edema/erythema, decrease in WBC count, defervesence) can take 48-72 hours.Screenshot 2018-03-15 at 7.24.25 PM
  • For patients who are not improving by 72H, in addition to “wrong bug/wrong drug” that would support switching antibiotics, also consider the following:
    • lack of source control (e.g. abscess, osteomyelitis)
    • bacteremia
    • vascular insufficiency (venous stasis or arterial insufficiency + inadequate elevation)
    • alternative diagnosis (e.g. venous stasis, drug reaction, etc.)


VA Morning Report 3.6.18: Sailors’ malady

Case summary: Thanks to Arvind for presenting the fascinating case of a 72F with remote PMH of breast cancer s/p lumpectomy, lymph node dissection and XRT, who presented with 2-3 weeks of progressive DOE, anemia/thrombocytopenia, AKI and rash. Although there was initial concern for vasculitis, a dietary review by Nutrition led to the correct diagnosis: scurvy (severe vitamin C deficiency)!


1. Before bee-lining for a Rheum consult, recall the specific dermatologic manifestations of vasculitis: palpable purpura, petechiae, vesicles, pustules, urticaria, & splinter hemorrhages, livedo reticularis, subcutaneous nodules, ulcers, digital infarcts, and papulonecrotic lesions. Biopsy should show cellular infiltrates and fibrinoid necrosis within and around the vessel wall, referred to as leukocytoclastic vasculitis.

2. This patient got a CT chest/abdomen/pelvis to look for recurrence of her breast cancer. We reviewed that although these imaging modalities are great for picking up metastatic disease, they may miss locoregional recurrence, which accounts for 15 to 40% of recurrences, or contralateral breast cancer. The test of choice for evaluation of locoregional recurrence is 1) diagnostic mammography, 2) breast MRI if mammography is inconclusive.

3. Think about scurvy in patients who are institutionalized, have restricted diets or poor food access and present with 1) neurologic symptoms (lethargy, arthralgias, irritability), 2) dermatologic manifestations (especially easy bruising, gingival hemorrhage, poor wound healing) and 3) anemia (seen in 75% of patients).

Cutaneous manifestations of vasculitis

  • This patient’s multi-system findings– particularly skin rash and AKI with hematuria–initially raised concern for vasculitis. Goop reminded us of the specific dermatologic findings of vasculitis.
  • On biopsy: “leukocytoclastic vascultis,” which is characterized by cellular infiltrates and fibrinoid necrosis within and around the vessel wall.
  • Small vessel (Henoch–Schönlein purpura, urticarial vasculitis, cryoglobulinemic vasculitis, and cutaneous small-vessel vasculitis)
    • Palpable purpura is the hallmark
    • Other findings: Petechiae, vesicles, pustules, urticaria, & splinter hemorrhages
  • Medium vessel (PAN and Kawasaki disease)
    • Livedo reticularis, subcutaneous nodules, ulcers, digital infarcts, and papulonecrotic lesions
  • Mixed-vessel vasculitis (microscopic polyangiitis (MPA), eosinophilic granulomatosis with polyangiitis (eGPA), and granulomatosis with polyangiitis (GPA)
    • Combination of small/medium vessel skin findings
  • Large vessel (Takayasu arteritis or giant-cell (temporal) arteritis)
    • Typically no skin findings
    • Nondermatologic findings such as limb or jaw claudication, bruits, pulse defects, and new onset of headache.


Reference: Xu et al. Cutaneous Manifestations of Vasculitis. Semin Arthritis Rheum. 2009 Apr;38(5):348-60.

Scurvy 101

  • Historical interlude:
    • Between 1500 and 1800 BC, scurvy killed more sailors than all other diseases and disasters combined.
    • In 1747, Scottish surgeon James Lind conducted what is considered to be the first controlled trial in medicine and determined that citrus fruits were curative of the disease
    • Daily provision of lemon juice to sailors on long voyages was not implemented until the late 18th century.
    • Scurvy was effectively eradicated at sea but reemerged among the pediatric population during the 19th century, when heated milk and processed foods became staples in the diet of infants.
    • Now, this diagnosis is infrequently encountered in industrialized nations, and diagnosis is often delayed. Think about it in:
      • those with poor nutrition or extreme dietary restrictions (including picky toddlers!)
      • the isolated elderly
      • the institutionalized.
  • Vitamin C is required for biosynthesis and hydroxylation of hormones, neurotransmitters, and mature collagen–> prominent clinical features:
    • Generalized symptoms- fatigue, myalgias, arthralgias, weakness, anorexia, weight loss, and irritability.

    • Dermatologic manifestations- follicular hyperkeratosis with perifollicular hemorrhage surrounding twisted, brittle hairs (corkscrew hairs), ecchymoses, poor wound healing, and swelling in the legs.

    • Gingival swelling and hemorrhage

    • Soft-tissue or subperiosteal hemorrhage, most commonly affecting the legs, may cause pain so severe that affected persons are unwilling to walk.

    • Anemia occurs in 75% of patients with scurvy and is the only routine laboratory abnormality. Mechanisms: blood loss into tissues or from the gastrointestinal tract, intravascular hemolysis, and coexisting folate and iron deficiencies.

    • Left untreated, scurvy may result in cardiorespiratory failure and death, the mechanisms of which are incompletely understood.
  • Diagnosis and treatment:
    • Test early! Levels will rapidly normalize, so false negatives can occur if a patient is tested after he/she starts eating vitamin C as part of a hospital diet!
    • Treatment is with high-dose vitamin C, and symptoms should improve within days to weeks.

Reference: a great NEJM case with a review of scurvy! Hafez, D. et al. A Deficient Diagnosis. N Engl J Med 2016; 374:1369-1374

VA AM Report 2.13.18: Sepsis in the Psych ICU, OH MY!

Case summary: Thanks to Manoj, Lily and Matt Schwede in abstention for presenting the case of a 60M with schizoaffective disorder who was admitted to the Psychiatric ICU (PICU) for psychosis and transferred to Medicine after he developed LLE pain/erythema and sepsis physiology, with concern for necrotizing fasciitis.


1. In the setting of SSTI and sepsis physiology, consider: necrotizing fasciitis, toxin-producing beta-hemolytic Strep (e.g. toxic shock syndrome), abscess (lack of source control) and bacteremia.

2. Goop reminded us that the world of bullae is wide, and venous stasis ulcers + overlying cellulitis is a common diagnosis! Life threatening diagnoses include: toxic epidermal necrolysis, staph scalded skin syndrome, necrotizing fasciitis, disseminated HSV or VZV and purpura fulminans. See below for a comprehensive DDx.

3. See Grant Smith’s awesome post on necrotizing fasciitis (with his Evernote integrating all the Chiefs’ blog posts on nec fasc ever!), with a major takeaway a (small, single-center) study from the Archives of Surgery showing that CT is extremely sensitive for necrotizing soft tissue infection (Sensitivity was 100%, Specificity 81%, PPV 76%, NPV 100%).

The wide world of bullae



Grant’s blog post (with Evernote summarizing all the prior Chiefs’ blog posts on nec fasc):

Fantastic NEJM review on necrotizing SSTIs: Stevens  DL Bryant  AENecrotizing soft-tissue infectionsN Engl J Med 2017;377:225365.

VA Morning Report 2.12.18: Urinary obstruction– not all BPH

Case summary: Thanks to Scott “Red bone” Goldberg for presenting the fascinating case of an 85M with PMH well-controlled HIV, who presented requesting additional home services and was found to be in acute renal failure from obstructive uropathy.

Top pearls:

  1. The differential diagnosis for bilateral hydronephrosis is: lower urinary tract obstruction (bladder, urethra) OR bilateral upper urinary tract obstruction (bilateral ureters or kidneys).
  2. Renal ultrasound in AKI to evaluate for obstruction is most useful in: 1) older patients, 2) those with a history of obstruction, 3) those with a history of intra-abdominal malignancy.
  3. FeNa and FeUrea were validated in oliguric patients (e.g. UOP <500cc/day), so use caution interpreting results in the non-oliguric setting.
  4. The main clinical presentations of tenofovir nephrotoxicity are (a) proximal tubular dysfunction with preserved renal function and (b) proximal tubular dysfunction associated with decreased renal function. Decreased renal function may be classified as AKI, CKD, or a glomerular filtration rate (GFR) that is decreased when compared with baseline values, albeit within normal limits.

Sites of urinary obstruction

  • Manoj brought up a great question: Are there any non-obstructive causes of hydronephrosis?
    • Massive diuresis can cause mild hydronephrosis on imaging that is not clinically obstructive
    • Pregnancy can also cause hydronephrosis on imaging that is not clinically obstructive
  • Pearls on signs/symptoms:
    • Spontaneous urination does NOT rule out obstruction, as tubular injury can impair urinary concentration and urethral obstruction can lead to bladder distention and overflow incontinence, both of which can cause polyuria.
    • Hydronephrosis is almost always asymptomatic, and pain should prompt a consideration of additional diagnoses such as stones, papillary necrosis, or infection.
  • Is all obstruction BPH?! Can seem like it at the VA, but obstruction can occur anywhere along the urinary tract.
    • Remember that foley placement will not relieve obstruction of the upper urinary tract (proximal to the bladder)!
      • Even if foley placement produces a gush of urine or reduction in PVR, renal impairment and hydronephrosis will persist.
      • This typically requires either ureteral stent or nephrostomy tube depending on the site of obstruction.
    • Bilateral hydronephrosis Ddx:
      • lower urinary tract obstruction (bladder, urethra)
      • OR bilateral upper urinary tract obstruction (bilateral ureteral or kidney)
    • Age can be an epidemiologic clue:
      • kids- anatomic abnormalities (including urethral valves or stricture and stenosis at the ureterovesical or ureteropelvic junction) account for the majority of cases in children.
      • young adults- calculi
      • older adults- prostatic hypertrophy or carcinoma, retroperitoneal or pelvic neoplasms, and calculi
    • Recovery:
      • Prognosis depends on severity and duration of obstruction.
        • With total ureteral obstruction, for example, there is evidence that relatively complete recovery of glomerular filtration rate (GFR) can be achieved if obstruction is relieved within one week, while little or no recovery occurs after 12 weeks
      • If recovery occurs, it is dramatic and rapid, with a return to baseline renal function within 7-10 days (and often even more quickly).

Screenshot 2018-02-12 at 10.14.52 AM - Edited

Tenofovir and renal injury

  • TDF is a prodrug of tenofovir that can cause AKI, proximal tubular dysfunction, or both in combination.

    • Proximal tubular dysfunction=Fanconi’s syndrome=hypophosphatemia, renal glucosuria (glucosuria with a normal serum glucose concentration), hypouricemia, and/or aminoaciduria
    • Side note: Sjogren’s, MM and a host of other systemic diseases can also cause Fanconi’s!
  • TDF is also associated with increased risk of chronic kidney disease in large observational studies

  • Risk of renal injury overall ranges from 2-10%.
  • TDF should be avoided, if: 1) GFR<60 at baseline, 2) >25% decline to GFR<60 after starting

  • TAF (a new prodrug) was approved in 2015 based on studies showing significantly smaller decline in eGFR and similar reductions in VL.
  • The VA’s own Mike Schlipak (Chief of General Medicine and creator of cystatin-C!) published much of the seminal work on tenofovir and renal injury.

Reference: Scherzer R, Estrella M, Li Y, Choi AI, Deeks SGGrunfeld CShlipak MG. Association of tenofovir exposure with kidney disease risk in HIV infection. AIDS. 2012 Apr 24; 26(7):867-75.

VA AM Report 2.5.18: Hypercalcemia of malignancy

Case summary: Thanks to Max for presenting the case of a 64M with PMH squamous cell carcinoma of the lung s/p LUL lobectomy, who presented with several months of weight loss, fatigue, and mental “fuzziness.” He was found to have hypercalcemia with elevated PTHrp AND 1,25OH vit D, as well as new liver lesions and colonic narrowing on CT A/P.

Top pearls:

  1. Gerald Hsu pearl: in patients with prior cancer, especially lung, who have had only local therapy, the most likely site of recurrence is metastatic. Thus, in working up recurrence, these patients should get more extensive imaging (e.g. CT A/P and brain MRI–especially if ANY neurologic symptoms– in addition to local imaging like CT chest).
  2. Recall that there are multiple mechanisms of hypercalcemia in malignancy:  PTHrp (~80%, squamous cell cancers), bone osteolysis (~20%, extensive bone mets, especially multiple myeloma and breast), extrarenal 1,25(OH)2D (~1%, mostly lymphomas). Patients can have multiple mechanisms at once and can have non-malignant etiologies as well.
  3. Denosumab– a RANKL monoclonal antibody– is the new(ish) kid on the block for hypercalcemia, especially for patients with hypercalcemia refractory to bisphosphonates.

Hypercalcemia of malignancy: deep cuts

  • 1/3 of cancer patients develop hypercalcemia
    • 4x more common in stage IV cancer.
  • The most common malignancies associated with hypercalcemia are:
    • lung cancer
    • multiple myeloma
    • renal cell carcinoma.
    • breast
    • colorectal cancers
    • lowest rates are in prostate cancer
  • Hypercalcemia is associated with a very poor prognosis
    • Thirty-day mortality 50%
    • In-hospital mortality rate 6.8%
  • Lab patterns in malignancy-associated hypercalcemia (NB: this patient had BOTH mildly positive PTHrP and very elevated 1,25OH vit D– a rare combination):


Denosumab: the new(ish) kid on the block

  • Overarching schema for treating hypercalcemia: recall that treating the underlying driver (e.g. the malignancy) is also an important component in addition to calcium-targeted therapies.


  • Denosumab mechanism of action:
    • Tumors produce cytokines that impair the RANK/RANKL interaction and promote excess osteoclast activation and enhanced bone resorption
    • Denosumab is a human monoclonal antibody to RANKL; hence it will reduce the osteoclast activity and bone resorption.
  • Denosumab is more effective than zoledronic acid in delaying or preventing hypercalcemia of malignancy in patients with advanced cancer
  • It is also effective in hypercalcemia refractory to bisphosphonates.
  • It is dosed SQ and given ~1-2 weeks and then monthly
  • Unlike bisphosphonates, it’s safe to use in renal failure, as it’s not renally cleared, but should be dose-reduced to prevent hypocalcemia