All posts by gsmith003

ZSFG AM Report 8/21/2017: Oxygen Delivery Systems and Use of PA Catheters in Undifferentiated Shock

Thank you to Megan Lockwood and the ICU team for presenting an interesting case of a women with a history of HFrEF who presented with undifferentiated shock who where a mixed picture of septic and cardiogenic shock developed into a management challenge.

Top Pearls:

  1. There are diminishing returns on FiO2 above 6L NC, and you should switch to a different delivery device at that point.
  2. Think about checking Co-ox to rule out Met-Hemoglobinemia or Carbon Monoxide poisoning in refractory hypoxemia
  3. Pulmonary arterial catheterizations, although never linked with outcomes in large studies, may be helpful in cases of mixed shock or undifferentiated shock (although this remains an area of HOT debate)


Oxygen Delivery Systems and Approximate FiO2:

Supplemental O2

Notes on High-Flow Oxygen (Courtesy of Teja Kompala):

  • What is it? Heated and humidified air that allows for comfortable delivery of higher flow oxygen
  • No specific threshold that absolutely warrants ICU level care (institution dependent) but an escalating requirement is worrisome and should prompt ICU evaluation
  • Liters per minute (LPM) and FiO2 are the two variables that can be manipulated, again this is institution dependent
  • High flow oxygen also provides a small amount of positive pressure. Also found to have decreased 90-day mortality in pts with nonhypercapnic acute hypoxemic respiratory failure.


Pulmonary Arterial Catheterization – Use and Interpretation:

  • Pulmonary arterial catheterization (PAC) has never been shown to improve patient-important outcomes.
  • However, when the diagnosis or the type of shock remains undetermined or mixed, hemodynamic measurements obtained by PAC can be helpful
  • Additional patients that may benefit from PAC are those with unknown volume status despite adequate fluid resuscitation, those with severe cardiogenic shock (eg, acute valvular disease), or those suspected to have severe underlying pulmonary artery hypertension or cardiac tamponade.
  • The major hemodynamic indices measured on PAC are
    • cardiac output (ie, cardiac index)
    • systemic vascular resistance
    • pulmonary artery occlusion pressure (ie, pulmonary capillary wedge pressure)
    • right atrial pressure
    • mixed venous oxyhemoglobin saturation (SvO2).
  • These measurements are most useful diagnostically but can also be used to guide fluid resuscitation, titrate vasopressors, and assess the hemodynamic effects of changes in mechanical ventilator settings

Interpreting PA Catheter

aThere is significant patient-to-patient variation. Pressure may be normalized if cardiac output is low.

bForrester et al classified nonreperfused MI patients into four hemodynamic subsets. (From JS Forrester et al: N Engl J Med 295:1356, 1976.) PCW pressure and CI in clinically stable subset 1 patients are shown. Values in parentheses represent range.

c”Isolated” or predominant RV failure.

dPCW and pulmonary artery pressures may rise in RV failure after volume loading due to RV dilation and right-to-left shift of the interventricular septum, resulting in impaired LV filling. When biventricular failure is present, the patterns are similar to those shown for LV failure.

Abbreviations: CI, cardiac index; MI, myocardial infarction; P/SBF, pulmonary/systemic blood flow; PAS/D, pulmonary artery systolic/diastolic; PCW, pulmonary capillary wedge; RA, right atrium; RVS/D, right ventricular systolic/diastolic; SVR, systemic vascular resistance.

  • Hochman JS, Ingbar DH. Cardiogenic Shock and Pulmonary Edema. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 19e New York, NY: McGraw-Hill; 2014. Accessed August 21, 2017.
  • Mimoz et al. (1994). Pulmonary artery catheterization in critically ill patients: a prospective analysis of outcome changes associated with catheter-prompted changes in therapy. Crit Care Med. 22(4): 573.
  • Frat et al. (2015). High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. NEJM. 372:2185-2196.


  • Supplemental Oxygen & Oxygen Delivery:
  • Pulmonary Arterial Catheterization:

ZSFG AM Report Pearls 8/16/2017 – Acute Polyarthritis and Fevers

Thank you to Lev Malecanchik for presenting a very interesting, and mysterious case of a young woman with acute, progressive symmetric polyarticular arthritis whose underlying diagnosis remains shrouded in mystery and intrigue.

Top Pearls:

  1. The presence of synovitis is key in diagnosis an arthritis vs. arthralgia
  2. Acute etiologies of polyarthritis include infectious (viral, bacterial especially) as well as reactive
  3. Choosing Wisely campaign recommends a ANA prior to sub-serologies (including antibodies to double-stranded DNA, Smith, RNP, SSA, SSB, Scl-70, centromere)


“Perhaps no disease is more painful than acute polyarthritis. The inability to change the posture without agonizing pain, the drenching sweats, the prostration and utter helplessness, combine to make it one of the most distressing of febrile afflictions. A special feature of the disease is the tendency of the inflammation to subside in one joint, while developing with great intensity in another.”

-Sir William Osler, the Principles and Practice of Medicine

Approach to Polyarthritis:

  • The Differential is BROAD, but thinking about a few factors can help you narrow
  • Acute presentations should raise concern for infectious etiologies (especially bacterial and viral) as well as a reactive arthritis
  • Confirming the presence of synovitis helps you identify an arthritis vs. arthralgia.
  • “Inflammatory pain” (i.e. AM stiffness lasting than more than 1 hour) can also help you get to the right category of diseases as well


  • Assess the number of joints involved
    • Consider whether there is a presence of systemic symptoms
    • Systemic symptoms makes Rheum etiology much more likely
  • Presence of synovitis is also important in moving along algorithm
  • Don’t forget to think about subacute bacterial endocarditis


Discriminating Factor
Possible Diagnoses
Temperature >40.0 C
Still’s disease, bacterial arthritis, SLE
Fever preceding arthritis
viral arthritis, lyme disease, reactive arthritis, Still’s disease, endocarditis
Migratory arthritis
Rheumatic fever, gonococcus, meningococcus, viral arthritis, SLE, acute leukemia, Whipple’s disease
Effusion disproportionate to pain
TB arthritis, endocarditis, IBD, GCA, lyme disease
Pain disproportionate to effusion
Rheumatic fever, FMF, acute leukemia, AIDS
Positive RF
RA, viral arthritis, TB arthritis, endocarditis, SLE, sarcoidosis, systemic vasculitis
Morning stiffness
RA, PMR, Still’s disease, some viral and reactive arthritis
Symmetric small joint
RA, SLE, viral arthritis
Leukocytosis (>15K)
Bacterial arthritis, endocarditis, Still’s disease, systemic vasculitis, acute leukemia
SLE, viral arthritis
Episodic recurrences
Lyme disease, crystal-induced arthropathy, IBD, Whipple’s disease, FMF, Still’s disease, SLE




  • Polyarthritis:


ZSFG AM Report 8/14/2017: Management of Severe ARDS

Thank you to Josh Shak and Jesse Fitzpatrick for presenting a case of severe ARDS. Also thank you to Vincent and Alison, our pulm/crit care fellows for dropping knowledge bombs left and right in report. Amazing!

Top Pearls:

  1. Proning and paralysis are the two interventions in severe ARDS that have been consistently linked with improved mortality.
  2. Consider 4 parameters when considering whether you can give diuretics in a patient with severe ARDS (cardiac output, urine output, need for pressors, and volume status)
  3. Remember that high-flow can be used in hypoxemic respiratory failure.


  • Onset within one week of known insult
    • Direct injury: PNA, aspiration, pulmonary contusion, fat emboli, near drowning, post lung transplantation
    • Indirect injury: Sepsis, severe trauma, shock, drug overdose, DIC, pancreatitis, TRALI
  • Bilateral infiltrates on CXR not fully explained by effusions, nodules, or lung collapse
  • Resp failure not fully explained by heart failure or volume overload (PCWP <18)
  • Hypoxemia:
Severity: (PaO2/FiO2 ratio)
  • Mild: ratio 200-300
  • Mod: ratio 100-200
  • Severe: <100
  • Ventilation w/ ARDSNet Protocol: Less lung compliance, so goal is to reduce barotrauma, allow permissive hypercapnia
    • Volume/pressure limited ventilation: NEJM 2000- Small tidal volumes (6mL/kg ideal body weight) are associated with reduced mortality of 31% compared to conventional VT patients (12mL/kg) that have a mortality of 40%. Plateau pressure goal <30 cmH2O. If plateau pressure higher, decrease VT in 1ml/kg increments
    • Oxygenation: Goal PaO2 55-80 mmHg or O2 sat 88-95%. Two grids – low PEEG (ARMA trial) vs. high PEEP (ALVEOLI, LOV, Express trials). Chose strategy based on clinical scenario to avoid oxygen toxicity but if poor cardiac squeeze / chest tube / other reason to want lower PEEP keep that in mind
    • Minimize acidosis: pH >7.30. Adjust respiratory rate (max 35), consider bicarb to keep pH at goal
    • I:E ratio: Goal 1:1-1:3. Adjust flow rate and inspiratory flow to achieve this goal
  • Refractory hypoxemia on ARDSNet protocol
    • Neuromuscular blockade: NEJM 2010, single RTC showed mortality benefit of cisatracurium – decreases O2 consumption and improves synchrony (when given upfront)
    • Recruitment maneuvers: Transiently increase PEEP to recruit atelectatic lung – MD at bedside bc can become transiently hypotensive bc decreased preload, also increased risk barotrauma
    • Conservative fluid management: NEJM 2007- FACTT RCT showed that conservative fluid strategy with diuresis (goal CVP <4, PCWP <8) resulted in better oxygenation, fewer days on vent (of note, trial excluded patients with hypotension, on pressors, with oliguric renal failure, or on HD). So general concept is to maintain MAP >65 and avoid hypoperfusion, but better to be dry than wet in ARDS – fluid restrict and use diuretics
    • Inhaled epoprostenol (flolan) / inhaled nitric oxide: Vasodilation- temporarily improves oxygenation, but no mortality benefit
    • Tham/Bicarb: Minimizes acidosis, but no mortality benefit
    • Proning: NEJM 2013, PROSEVA group- French trial showed reduction in mortality if proning done early
    • ECMO: Lung replacement therapy with extracorporeal membrane oxygenation (ECMO)



  • Thank you to Laura Huppert for sharing this outline/Summary for ARDS including references for many of the trials!


  • ARDS:

ZSFG AM Report Pearls 8/11/17: Localizing the Lesion in Cirrhosis

Thank you to Scott Goldberg for presenting a case of a patient with new onset ascites who was found to have cirrhosis on ultrasound with questions about the utility of liver biopsy

Top Pearls:

  • Consider pre-sinusoidal, sinusoidal, and post-sinusoidal approach to a differential for elevated portal pressures in patients with new ascites
  • Other etiologies of ascites outside of elevated portal HTN, include peritoneal disease and hypoalbuminemia


A Framework for New Ascites:

  • There are many approaches and frameworks for ascites. One approach is thinking about elevated portal HTN versus other causes of ascites not due to portal hypertension
    • Other approaches include thinking about alterations in hydrostatic vs. oncotic pressures
  • Within elevated portal pressures, there is a separate differential that can be broken down into:
    • Pre-sinusoidal
    • Sinusoidal
    • Post-sinusoidal
  • Non-elevated portal pressure ascites can also be broken down into:
    • Generalized hypoalbuminemia
    • Peritoneal disease

Portal HTN

Elevated Portal Pressure Ascites:

  • Pre-Sinusoidal: Portal vein thrombosis, Splenic vein thrombosis (complication of pancreatitis, pancreatic tumor), Developmental abnormalities (polycystic liver disease, AV fistulas), Biliary disease (biliary cirrhosis, PSC), Neoplastic occlusion of intrahepatic portal vein (lymphoma, CLL, epithelial malignancy), Granulomatous processes (schistosomiasis, sarcoidosis)
  • Sinusoidal: Infiltrative disease into the space of Disse (amyloid, light chain deposition, ,mastocytosis), Fibrosis of space of Disse (NASH, viral hepatitis, CMV, schisto, toxins), compression of space of Disse (hypertrophied hepatocytes)
  • Post-Sinusoidal: Budd-Chiari, vascular malignancies, Cardiac causes (constrictive pericarditis, restrictive cardiomyopathy)

Space of Disse

Non-Elevated Portal Pressure Ascites:

  • Hypoalbuminemia: Nephrotic syndrome, Protein-losing enteropathy, Severe malnutrition
  • Peritoneal Disease: malignant ascites, infectious peritonitis, eosinophilic gastroenteritis, starch granulomatous peritonitis, peritoneal dialysis



ZSFG AM Report Pearls 8.8.17 – Epidural Abscess and Pitfalls to Avoid

Thank you to Claire DeBolt for presenting an interesting and perhaps confusing case of man with low back pain, RLE radiculopathy, and bilateral hand swelling found to have a large epidural phlegmon and septic emboli into the bilateral hands.

Top Pearls:

  • Early stages of epidural abscess can present with clinical picture similar to radiculopathy
  • Trial of back pain, fever, and neuro deficits is RARELY present
  • HIV patients are especially vulnerable to encapsulated organisms


Epidural Abscess:

Pathophysiology Pearls:

  • Bacteria gain access to the epidural space through contiguous spread (1/3 of cases) or hematogenous dissemination (1/2 of cases). The remainder of cases the source is not identified.
  • Staph aureus is the organism in approximately 2/3 of cases
  • Less common bugs include coag negative staph, Staph epidermidis, E. coli, and Pseudomonas

Clinical Pearls:

  • Stage 1: Back pain at level of affected spine
  • Stage 2: Nerve-root pain radiating from the involved spinal area
  • Stage 3: Motor weakness, sensory deficit and bladder/bowel dysfunction
  • Stage 4: Paralysis

Note that classic triad: Fever, Back Pain, Neuro deficit is only present in a MINORITY of patients

Lab Pearls:

  • Leukocytosis (only in 2/3rds of patients)
  • Elevated ESR/CRP (nearly 100%)
  • Bacteremia (~60% of patients)
  • CSF analysis should NOT be performed when suspected given risk of causing meningitis or subdural infection if the needle transverses the epidural abscess

Treatments Pearls:

  • Surgical Drainage (decompressive laminectomy and debridement of infected tissues) + Systemic Antibiotics

Outcome Pearls:

  • Irreversible paralysis is the worst complication and affects 4-22% of patients, typically thought ot be 2/2 delayed diagnosis and suboptimal management
  • 11-75% of cases are initially misdiagnosed

Pitfalls in Epidural Abscess


  • Darouiche, RO. (2006). Spinal epidural abscess. NEJM. 355: 2012-2020.



ZSFG AM Report Pearls 7/28/2017: Burn Baby Burn, Gastrin Inferno!

Thank you to Michelle Matzko for presenting an interesting case of a woman with hematemesis and melena who was found to have a large number of gastric and duodenal ulcers concerning for Zollinger-Ellison syndrome.

Top Pearls:

  1. The most common causes of multiple ulcers in the stomach and duodenum are NSAID use and H. pylori infection.
  2. Work-up should include careful history (smoking, meds, substance use), h. pylori testing, EGD w/ biopsy, serum gastrin level.
  3. Zollinger-Ellison Syndrome can be diagnosed with a gastric pH and serum gastrin level, and distinguished from other causes of hypergastrinemia with a secretin stimulation test.


DDx Multiple Gastric/Duodenal Ulcers:

Most Common:

  • NSAIDs
  • H. pylori
  • Multifactorial (NSAIDs + Alcohol + H. pylori)
  • H. pylori
  • HSV
  • CMV
  • Heliobacter heulmannii
  • Rare conditions (TB, syphilis, mucmormycosis)
Drug Exposure
  • NSAIDS and Aspirin
  • Bisphophonates (combined with NSAIDs)
  • Clopidogrel (when compined with NSAIDs)
  • Corticosteroids (when combined with NSAIDs)
  • Sirolimus
  • Spirinoloactone
  • Myocphenolate mofetil
  • KCl
Hormonal/Acid Hypersecretion
  • Gastrinoma (Zollinger-Ellison Syndrome)
  • Systemic Mastocytosis
  • Basophilia
  • Antral G cell hyperfunction
Post Surgical
  • Antral exclusion
  • Post-gastric bypass
  • Vascular insufficiency (esp with crack/cocaine use)
  • Duodenal obstruction
Radiation therapy
Infiltrative Disease:
  • Sarcoidosism
  • Crohn’s disease

Gastric ulcers

Zollinger-Ellison Syndrome

Pathophysiology: excessive gastrin secretion from a gastrinoma results in high gastruc acud output due to the trophic action of gastrin on parietal cells and histamin secreting enterochormaffin-like cells ECL cells. Gastrin also stimulates parietal cells largely via the release of histamine
Clinical Findings:
  • Multiple ulcers
  • Peptic ulvers in H. pylori-negative, NSAID-negative subjects
  • Ulcers beyond the duodenal bulb
  • Increased gastric folds on upper GI series or endoscopy
  • Findings suggestive of MEN type 1 (hyperparathyroidism, prolactinoma)
  • Fasting Serum Gastrin Level
    • If >10x normal limit + gastric pH <2 = diagnostic of ZES
    • Note that people on PPIs can also have elevated gastrin levels
    • Gastric pH helps differentiate people with other causes of secondary hypergastrinemia
  • Secretin Stimulation Test
    • Differentiates patients with gastrinomans from other causes of hypergastrinemia
    • Secretin stimulates release of gastrinoma cells and INCREASE in gastrin, while normal gastric G cells are INHIBITED by secretin
    • Note: False negative in 6-20% of patients and 15-39% false positive when patinets have achlorrydria induced by PPIs or chornic atrophic gastritis.
    • Note: Stim test should not be done in patients with severe manifestations of ZES (i.e. severe abdominal pain, vomiting, diarrhea, or specific EGD findings).


  • Vakil NB. (2017). Unusual causes of peptic ulcer disease. UpToDate. May 22, 2017.
  • Gisbert JP & Calvet X/ (2009). Heliobacter pylori-negative duodenal ulcer disease, Alimentary Pharm & Therapeutics.30: 791-815.
  • Wolfe MM & Jensen RT. (1987). Zollinger-Ellison syndrome current concepts in diagnosis and management . NEJM. 317:1200-1209.



ZSFG AM Report Pearls 7/25/2017: Glow-in-the-Dark Babies? – Radiology Studies in Pregnancy

Thank you to Jacqueline To for presenting the case of a 17-week pregnant woman who presented with an asthma exacerbation that brought up a lot of questions about how to best take care of our patients who are pregnant.


Top Pearls:

  • If admitting a pregnant woman and there are questions about what is safe to do diagnostically and therapeutically, there are lots of people to call and including obstetrics, radiology, and pharmacy.
  • When calling Obstetrics, consider framing your question as “what are the physiologic parameters/goals for the fetus? (i.e. is there a SaO2 that is optimal, how aggressive to be about correcting acidosis, etc..).
  • Pregnant women can get radiology studies. Up to 5 rad = 0.05gray = 50mSv = 5000mrem is thought to be safe across the course of a pregnancy.


Exposure to Radiation in Pregnancy:

  • The absorbed dose of radiation is the amount of energy deposited per kilogram of tissue and is measured in “rads.”
  • One rad is the energy transfer of 100 ergs per gram of any absorbing material. The following relationships apply to diagnostic X-rays in soft tissue:
    • 1 rad = 0.01 gray (Gy) = 0.01 sievert (Sv) = 1 rem (roentgen-equivalent man)
    • 1000 millirad (mrad)= 10 milliGy (mGy) = 10 milliSv (mSv)= 1000 millirem (mrem)
  • In the United States, the average person is exposed to an effective radiation dose equivalent of approximately 3.1 mSv (310 mrem) whole-body exposure per year from natural sources.
  • The US Nuclear Regulatory Commission (10 CFR 20) recommends that occupational radiation exposure of pregnant women not exceed 5 mSv (500 mrem) to the embryo/fetus during the entire pregnancy.
  • You would be exposed to about 0.035 mSv (3.5 mrem) of cosmic radiation if you were to fly within the United States from the east coast to the west coast. This amount of radiation is less than the amount of radiation we receive from one chest x-ray.
  • There is no evidence of an increased risk of fetal anomalies, intellectual disability, growth restriction, or pregnancy loss from ionizing radiation at doses less than 0.05 G = 50mGy = 50mSv = 5000mrad
  • The margin of safety is augmented by the fact that most human exposures from diagnostic imaging will be fractionated over a period of time; this type of exposure is less harmful than acute exposure

Fetal Dose of Radiation

A few practical pearls:
  • Diagnostic x-rays of the head, neck, chest, and limbs produce almost no scatter to the embryo; any radiation received would not result in a measurably increased risk.
  • BUT, the patient should wear a lead apron to minimize fetal exposure from radiation scatter whenever non-abdominopelvic sites are being imaged.
    • A posterior-anterior (PA) exposure lowers the radiation dose by 0.02 to 0.04 mGy (2 to 4 mrad) compared with the traditional anterior-posterior (AP) exposure because the uterus is located in an anterior pelvic position
  • Fetal radiation exposure during CT scans not involving the abdomen or pelvis is minimal. As an example, the radiation exposure from maternal head CT is approximately 2 mGy (200 mrad) for the mother and less than 0.10 mGY (10 mrad) for the fetus if the abdomen is shielded.
  • Iodinated contrast materials cross the placenta and can produce transient effects on the developing fetal thyroid gland, although clinical sequelae from brief exposures have not been reported. Iodinated contrast materials may be used in pregnancy, when indicated.
  • No biologic effects have been documented from diagnostic ultrasound in the pregnant patient, despite intensive use over several decades.
  • However, Doppler ultrasound does have potential to cause problems, and there are many society guidelines around this
  • There are no reported harmful effects from MRI of the pregnant woman or fetus
  • However, safety studies have been performed predominantly at or below 1.5 Tesla magnetic field strengths. There may be an increased risk of tissue heating at higher field strengths.