All posts by gsmith003

ZSFG AM Report Pearls 6/19/2017: SHOCK – Differentiating Etiology and Treatment of Cardiogenic Shock

Thanks to Chloe Ciccariello for presenting a case of afib with RVR found to have cardiogenic shock and new onset heart failure.

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Top Pearls:

  • When working up new Afib, work up should include considering your “T’s and E’s.” T = Thyroid studies, Troponin. E = EKG and ECHO.
  • ScVO2 (central venous oxygen saturation) is an oxygen SATURATION (not a PaO2) and can be used to differentiate cardiogenic shock from distributive shock. It is measured from a blood draw from a central catheter (often in the SVC), and it is a surrogate for SVO2 (mixed venous oxygen saturation).
  • Norepinephrine can be used as a vasopressor in cardiogenic shock for rapid, initial circulatory support especially if shock is not completely differentiated (See reference below).

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“SHOCK”

Diagnosis:

  • Hypotension (although can be mild) = typically SBP <90mmHg, MAP <70mmHg with tachycardia
  • Tissue Hypoperfusion (think 3 organ systems)
    • Skin – cold, clammy, cyanotic (low-flow state, i.e. cardiogenic) or warm, diaphoretic (vasodilation, i.e. sepsis)
    • Kidneys – low urine output, i.e. less than 0.5cc/kg/hr or elevated Cr
    • Brain – altered mental status
  • Elevated lactate – a sign of abnormal cellular oxygen metabolism

Differential:

Type of Shock Preload Afterload (SVR) Cardiac Output
Cardiogenic Low High Low
Distributive Low Low High (but can get low)
Hypovolemic Low High Low
Obstructive High or Low Low Low

Tips on Differentiating:

  • Warm extremities (septic, distributive) vs. cold extremities (cardiogenic, obstructive, hypovolemic)
  • ScVO2 (central venous oxygen saturation) = Low (low cardiac output), High (high cardiac output)
  • Volume Exam – (edema, elevated JVP to point to elevated R-sided cardiac pressures)
  • Limited U/S Exam (Volume – IVC, JVP, cardiac function)

 

Brief Discussion of Pressors in Cardiogenic Shock:

  • A question was raised about whether Norephinephrine can be used in cardiogenic shock. A 2010 trial compared norepi to dopamine, but it did not have a comparison group to inodilators (dobutamine and milrinone) in the study which are also used in cardiogenic shock.
  • Some authors would advocate that an inopressor (norepi, epi, dopamine (high dose)) would be indicated for circulatory support when a patient’s MAPs are very low and you are worried about the vasodilatory effect of inodilators.
  • In a trial of 1679 patients with circulatory shock from VARYING etiologies, who were randomly assigned to initial therapy with either dopamine or norepinephrine, there was a trend toward a higher rater of death at 28 days with dopamine and there were significantly more arrhythmias, predominantly atrial fibrillation. No difference in the treatment effect based on shock type, including the 280 patients with cardiogenic shock.

 

References:

  • De Backer et al. (2010). Comparison of dopamine and norepinephrine in the treatment of shock. NEJM 363(9): 779.
  • Vincent JL and De Backer D. (2013). Circulatory Shock. NEJM 369: 1725-1734.

Evernote link: https://www.evernote.com/shard/s509/sh/c8fc9051-e2ef-4df4-b2f9-871259ae56bd/476852550f394db4e8afe9afb628a0da

ZSFG AM Report Pearls 6/16/17: Diarrhea, Weight Loss, and Use of Fecal Calprotectin, Fecal WBCs, and Fecal Fat

Thank you to Scott Goldberg for presenting the case of a man with anemia, diarrhea, and significant weight loss who was ultimately found to have a colonic stricture and fistula unveiling the diagnosis of Crohn’s disease. The case brought up a lot of questions about some of the diagnostic test we send and how to use and interpret them.

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Top Pearls:

  1. The American Gastroenterological Association suggests that chronic diarrhea should be defined as three or more loose or watery stools daily lasting for four or more weeks
  2. A malabsorption diarrhea can occur when someone has not been eating for a prolonged amount of time. This “refeeding diarrhea” results from decreased villous to crypt ratio in the bowel wall and reduced ability to absorb nutrients.
  3. Strictures in the colon impair that tissues ability to perform the task of fluid reabsorption and can result in watery diarrhea

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Fecal Calprotectin:

  • What is it?
  • Fecal calprotectin is a zinc and calcium binding protein derived from neutrophils and monocytes
  • Why use it?
  • It is a marker of neutrophil activity. Levels are increased in intestinal inflammation and can help distinguish inflammatory from non-inflammatory causes of chronic diarrhea.
  •  -93% Sensitive, 96% Specific for IBD in adults with chronic diarrhea or suspected IBD
  • How to use it?
  •  For now, consider as an adjunctive test, not a final say in deciding diagnosis. In “low prevalence” settings (i.e. primary care office for abdominal pain, consider as data to help rule out IBD). In “high prevalence” settings (i.e. GI doctors’ office), may be data to help rule in and consider additional testing)

  Fecal WBC/Leukocytes:

  • What is it?
  • A gram stain of a stool sample that looks for the presence of leukocytes in stool
  • Why use it?
  • Well, consider not using it. A meta-analysis suggests that it has a peak sensitivity of 70% and a specificity of 50% (although this study was performed in children).
  • How to use it?
  •  Don’t use this in the hospital. If you think someone has infectious diarrhea, you should complete an infectious diarrhea work-up. Of note, it is not a test that should be sent for hospital-acquired diarrhea (the lab does not offer it at Moffitt if patient has been admitted >72 hours).

 Fecal Fat (Quantitative):

  • What is it?
  • Fecal fat is fat in the stool. Health individuals typical excrete less than 6grams of fat even when fat consumption is increased to 100-125 g of fat/day. There can be increases in fat excretion when people take laxatives or are having a very large amount of stool (1000g/day). In order to be accurate, the patient must eat 60-100gms of fat for 3 days prior to collection and during the collection period. Stool is typically collected over 72 hours
  • Why use it?
  •  To determine if the patient is having diarrhea due to malabsorption.
  • How to use it?
  • A quantitative fecal fat >6g/day is abnormal and >20g/day is consistent with steatorrhea. If you can keep track of the dietary intake of fat, you can also calculate a fractional fat absorption (fat intake – fat output / fat intake). A value of >94% is normal.

 Sources:

Van Rheenen PF, et al. (2010). Faecal calprotectin for screening of patients with suspected inflammatory bowel disease: diagnostic meta-analysis. BMJ 341, c3369.

Huicho et al (1993). Occult blood and fecal leukocytes as screening tests in childhood infectious diarrhea: an old problem revisitied. Pediatr Infect Dis J. 12(6): 474.

Evernote link:  https://www.evernote.com/shard/s509/sh/5ffc8aae-a19d-49b8-a806-a59ae105657c/c41bf3cc4680aeacb5af3c095c5f08e5

ZSFG AM Report 6/13/2017: Unresolving Fever and Work-Up for Active Tuberculosis

Thank you to Tim and Sarah for presenting a case of a patient with sepsis physiology with unresolving fevers, significantly elevate alk phos, despite broad-spectrum antibiotics who was ultimately thought to have military TB.

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Top Pearls:

  1. In a patient with abnormal findings on chest X-ray, not responding to antibiotic therapy, reassess and think about wrong bug, wrong drug, or poor source control
  2. The ability of Gene X-pert and all testing for active tuberculosis is dependent upon a good sputum sample.
  3. When there is a high index of suspicion, ordering a 2nd Gene X-pert and a 2nd AFB smear and culture is indicated.

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Additional Tips for Testing for Active M. Tuberculosis (and Concern for Miliary TB):

-Remember that PPD and quantiferon-gold have no role in assessing for active TB (these assess for latent tuberculosis)

-If these tests are performed and positive, it can support the diagnosis of tuberulcosis but positive tests cannot distinguish between active and prior infection or the degree of spread. Negative tests DO NOT exclude the diagnosis of tuberculosis.

 

-Acid-fast smear and culture:

  • -If multiple sites are available for sample (i.e. sputum, pleural fluid, ascites), the more locations, the better as this can support dx of miliary TB
  • -IDSA Guidelines recommend sputum volumes for AFB smear and culture of at least 3mL although 5-10mL is the optimal volume.

 

-Gene Xpert assay can detect M. tuberculosis within 2 hours with a sensitivity much higher than that of smear microscopy, especially in patients with HIV (increased rate of case detection by 45% compared to smear microscopy).

  • -In a study of 1730 patients, Gene X-pert identified 98.2% of patients who were AFB smear positive and 72% of patients who were  AFB smear negative
  • -In patients who were AFB smear negative, culture positive tuberculosis, the addition of a 2nd Gene X-pert increased the sensitivity by 12.6%

 

**Note: If diagnosis is miliary TB, sputum samples may be negative as the spread of organism is hematogenous. Diagnosis may require bronchoscopy with biopsy.

 

-AFB Blood Culture:

  • Should be obtained in patient when hematogenous spread is suspected
  • Note that positive AFB cultures are rarely positive (but may be seen in immunocompromised patients)

 

-Histopathology:

  • -If you can biopsy an area that you think has TB, you may see granulomas, organisms on acid fast staining.
  • -Remember that you can also send AFB cultures from these tissues

As a reminder of the ZSFG TB Testing Guidelines:

TB Work-Up Flowsheet

References:

Boerhme et al. (2010). Rapid molecular detection of tuberculosis and rifampin resistance. NEJM 363:1005-1015.

Zulma et al. (2013). Tuberculosis. NEJM 368:745-755.

Lewinsohn (2016). Official American Thoracic Society/Infectious Diseases Society of America/Centers for Disease Control and Prevention Clinical Practice Guidelines: Diagnosis of Tuberculosis in Adults and Children. Clinical Infectious Diseases. 64:e1-33

 

Evernote Link: https://www.evernote.com/shard/s509/sh/4f565a9c-a512-4704-be44-b769807803aa/f0c99b5766d625868415f52936c679b7

ZSFG Intern Report Pearls 6.8.17: Upper Extremity Swelling Secondary to Osteomyelitis

Thanks to Mike Incze for presenting an amazing case of a really gnarly right upper extremity that was ultimately found to be a case of osteomyelitis with a key learning point of going for bone biopsy prior to antibiotics if patient is clinically stable.

 

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Top Learning Pearls:

  1. When osteomyelitis is suspected, bone biopsy should be obtained (and it yield a positive finding in 87% of cases).
  2. Cessation of antibiotics 48-72 hours prior to bone biopsy can help increase microbiological yield, although some authors argue that bone biopsy can still be positive since osteomyelitis often occurs in areas of poor vascularization.
  3. Complex regional pain syndrome can be considered when other etiologies have been ruled out and can include symptoms of pain, sensory changes (although typically more pain instead of less pain), motor loss, as well as edema

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Differential Of Large, Swollen Upper Extremity:

High Acuity (“Can’t Miss”)

  • Necrotizing fasciitis
  • Compartment Syndrome
  • Tenosynovitis (especially of hand)
  • Osteomyelitis
  • Other skin & soft tissue infection

 

Moderate Acuity:

  • DVT of upper extremity (spontaneous rare)
  • Septic thrombophlebitis
  • Acute gout
  • Lymph obstruction
  • Atypical infections (TB, Nocardia)
  • Charcot arthropathy
  • Fracture
  • Bursitis
  • Malgnancy
  • SAPHO (Synoviitis, Acne, Pustulosis, Hyperostitis, Osteitis)

 

Lower Acuity (Dx of Exclusion):

  • Complex Regional Pain Syndrome

 

Work-Up of Osteomyeltis:

Exam:

-“Probe to Bone” as a screening – (recommended to do w/ metal object, if hit hard, gritty substance, that’s bone) – Sensitivity 0.87, Specificity 0.83.

 

Labs:

-CBC, ESR, CRP, blood cultures (only positive in about ½ of cases of acute osteo)

-Bone Biopsy is needed to tailor treatment

 

Imaging:

–Start with X-ray of the area, advanced imaging is patient, location, and situation dependent

 

For more information on A Systematic Approach to The Swollen Extremity: Click here

 

 

 

 

 

ZSFG AM Report Pearls 6.6.17 – Disseminated Zoster in Immunocompromised Patient

Thank you to Kenny (rockstar presenter!) for presenting a case of disseminated herpes zoster in a patient with HIV.

Top 3 Learning Points:

  1. Patient with HIV, despite having a normal CD4 are still at increased risk of developing VZV reactivation and disseminated zoster.
  2. When admitting a patient with VZV, think about can’t miss complications (disseminated zoster, CNS involvement, eye involvement, bacterial superinfection)
  3. When zoster is disseminated or the patient is immunocompromised, the patient needs airborne precautions.

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Triage:
Inpatient treatment if:
     -Immunocompromised
     -Disseminated Zoster
     -Any concern for CNS or eye involvement
     -Systemically-ill appearing
 
Diagnosis:
-Look for classic rash, that can be enough for dx
-VZV cultures not necessary if classic appearance
-HSV should be considered if peri-oral or genital lesions present
Complications to Consider:
-Postherpetic Neuralgia (7.9%)
-Superficial skin infection (2.3%)
-Ocular complications (including Acute Retinal Necrosis and Herpes Zoster Ophthalmicus) (1.6%)
-Motor neuropathy (0.9%)
-Meningitis (0.5%)
-Ramsay Hunt Syndrome (a.k.a. Herpes Zoster oticus) (0.2%)
Work-Up:
History/Exam:
-ROS: Visual changes, HA, fevers, weakness, vertigo, change in mental status
-Skin Exam (localized vs. disseminated, superinfection)
-Eye/Face (if involved, call Ophtho for eval)
-Nose (Ramsay Hunt Syndrome)
-Ear – can get vesicles limited to inner ear canal
-Pulm – can have a VZV pneumonia
-Neuro (Neuro changes, meningeal findings, encephalitis) -> Consider LP (should not delay treatment)
Labs:
-Chem panel (renal dosing may be needed for acyclovir)
-LFTs (VZV can cause a hepatitis)
-Consider CXR if pulmonary symptoms
Management:
Infection Control:
     -If disseminated or immunocompromised, needs airborne precautions
     -If single dematomal and immunocompetent, standard precautions (no special)
Treatment:
-IV Acyclovir
-Consider glucocorticoids in complicated herpes zoster (guidelines are variable in strength of recommendations on this and depends on the location of zoster outbreak
For CDC Guidelines on Preventing Transmission of VZV in hospitals:
https://www.cdc.gov/shingles/hcp/hc-settings.html
Evernote Link:

ZSFG AM Report – 6.2.17 – HIV-Associated GI Pathology

Thank you Kenny for presenting a case of a patient with AIDS, abdominal pain, diarrhea, and fevers found to have a partial SBO and inflammation in the terminal ileum.

Top Pearls:

  1. Partial or complete small bowel obstruction in a patient without prior surgery is very unusual and should raise suspicion for tumors, complicated hernias, Crohn’s disease or other inflammatory processes, gallstones, volvulus, or intussusception.
  2. CT Abdomen/Pelvis is better than KUB for identifying the specific site and severity of obstruction (partial vs. complete), as well as potentially determining the etiology.
  3. Infections in HIV can localize to different parts of the bowel with small bowel etiologies including: HIV enteropathy, MAC, protozoan (Giardia and the spordia), and helminths (strongy)

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More Information on HIV-Associated GI Pathology by Location in GI Track:
HIV-Associated GI Pathology (By Location):
Esophageal:
                -Candidiasis
                -CMV, HSV
                -Kaposi’s Sarcoma
                -Idiopathic ulceration
Gastric:
                -CMV
                -MAC
                -Neoplasia (Kaposi’s sarcoma, lymphoma)
Small Bowel:
                -HIV enteropathy
                -MAC
                -Protozoa (Giardia, Isospora, Cryptosporidia, Microsporidia)
                -Helminths (Stronglyoides)
Colorectal:
                -Viral (CMV, HSV)
                -Bacterial (Clostridia, Salmonella, Shigella, Campylobacter)
                -Fungal (Cryptococcus, histoplasmosis)
                -Neoplastic (KS, lymphoma)

 

For more info on HIV-associated diarrhea, see this Evernote from Rachel Greenblatt:

http://www.evernote.com/l/AoMGT-TiXM9Kvr7m83VuFlGi-G5w58cJwto/

References:

Bhaijee F, Subramony C, Tang SJ, Pepper DJ. Human immunodeficiency virus-associated gastrointestinal disease: common endoscopic biopsy diagnoses. Patholog Res Int 2011;2011:247923.

Evernote Link:

http://www.evernote.com/l/Af1CP_jgWCRGc70jFbvQgEgr1GfcfPdZJ7I/