Moffitt Renal Report Pearls 6.16.17

Thank you to Kenny for his sense of humor AND for presenting an elderly patient with h/o BPH, recent acute prostatitis, now presenting with altered mental status and acute renal failure w/ hyponatremia 2/2 multiple mechanisms including obstruction with concurrent use of NSAIDs and an ACEi. We discussed the management of post-obstructive diuresis, hyponatremia, and volume overload.


Key Pearls:

  1. The old rule of thumb that you get an elevation in creatinine of 1 for each day of renal injury turns out NOT to be totally accurate. [20mg/kg/day with volume distribution of 0.6 allows for increases in Cr by as much as 3mg/dL per day!!]
  2. Approach to AKI anatomically: Pre, Intrinsic and Post-renal (more below)
  3. Postobstructive diuresis is primarily a problem with CHRONIC, not ACUTE, urinary retention with management details outlined below.


More Review on AKI

– Definition: < 48 hours (abrupt) time course with 1 or more of the following:

  1. Increase in serum Cr > 0.3 mg/dL
  2. Greater than 50% increase in serum creatinine from baseline
  3. Reduction in urine output of < 0.5 mL/kg/hr for > 6 hours

– Oliguria is defined as UOP < 400 mL/day, while anuria is < 100 mL/day

Approach to AKI based on anatomy

  • Pre-renal – 70% of community acquired and 40% of hospital acquired AKI
    • Hypovolemia: vomiting, diarrhea, diuretics, hemorrhage, burns
    • Decreased effective circulation volume: Cardiorenal, hepatorenal
    • Change in renal vascular tone: ACEi, NSAIDs
  • Intrinsic Renal – urinalysis is the key here!
    1. Glomerular – RBCs; Anti0GBM, Pauci-immune, Immune complex
    2. ATN – muddy brown casts; prolonged pre-renal -> ischemic, toxic, septic shock (most common)
    3. AIN – WBCs; drug-induced, Infectious (fevers, rash and eosinophilia ~ 15% of pt)
    4. Vascular – micro: HUS/TTP or macro: renal artery stenosis, thrombosis
  • Post-renal – important to exclude early
    1. Obstruction from BPH, acute prostatitis, constipation, pelvic masses, neuogenic bladder


 Post-obstructive diuresis

  • A postobstructive diuresis is primarily a problem with CHRONIC, not ACUTE, urinary retention and usually represents an appropriate attempt to excrete excess fluid retained during the period of obstruction


  • Management of post-renal obstruction:
    1. Relieve the obstruction
    2. Anticipate a post-obstructive diuresis if chronic (more below)
    3. Frequent monitoring of I/Os and electrolytes (q6-q8)
    4. If going to give fluid, caution with chloride-containing fluids: Loss of hypotonic urine, may need replacement fluid, usually in a 2:1 ratio (replace approximately half the volume the patient is putting out).
    5. Fluid replacement is usually with one-half isotonic solution
    6. Remember that “The kidney is a better judge of the volume status than the doctor!” per Dr. Chi Hsu – In most patients, things will correct themselves.

Altered Mental Status (AMS)

Remember the MISTO mnemonic for AMS:

    1. Metabolic (electrolytes, esp Na and Ca; endo, esp thyroid and glucose; liver; kidney)
    2. Infectious
    3. Structural (stroke, mass, bleed)
    4. Toxin
    5. Oxygen/Other
    6. As Jen O mentioned in report “AMS” can be a very nonspecific description – it’s helpful to break this down into more specific characteristics, such as decreased level of consciousness, agitation, confusion, disorientation, etc. This helps one to narrow your differential – also remember MISTO!!

Evernote Blog:

VA ICU report 6.16.17: Hypernatremia

Case summary

47M with mutism p/w AMS, profound weight loss and found to have marked hypernatremia

Take aways

  1. Approach to hypernatremia
    1. Consider free water loss (renal, GI, insensible loss)
    2. Reduced access to free water (dementia)
    3. Hypertonic intake (3% NS, ocean water)
  2. Diabetes insipidus implies impaired urinary water reabsorption and therefore urine osms are inappropriately lower than serum osms.
  3. Treatment
    1. Determine acute versus chronic
    2. Calculate free water detect
      1. If acute correct over 24 hours
      2. If chronic correct 10mEq/day
    3. Reassess frequently


Approach to hypernatremia




The principles of treatment in hypernatremia are similar to those in hyponatremia and therefore it also important to determine:

  • Acute (< 24 hours) versus chronic (> 24 hours)
    • Acute: correct over 24 hours
    • Chronic: correct by 10mEq/24 hours
      • Why? With aggressive repletion of free water, there is a risk of cerebral edema. This risk is less than that of aggressive correction of hyponatremia (–> osmotic demyelination syndrome) but is more likely in patients with higher initial Na
  • Symptomatic versus asymptomatic

Details of correction of chronic hypernatremia 

  • Step 1: use the (1) patients’ weight (2) current sodium and (3) goal sodium (usually 10mEq less than current sodium) to calculate the free water deficit for the day.
  • Step 2: divide the free water deficit/24 hours and infuse D5 H20 at that rate
  • Frequently recheck your Na and adjust your rate by starting back at step 1

*Consider making the patient NPO to ensure accuracy of free H20 intake (especially initially).

*In patients with DI, their free water clearance via the kidneys may be dynamic. Therefore, monitoring the urine osm (along with renal or endocrine) is important.

Concomitant hypovolemia

  • For patients with concomitant hypovolemia obtain second PIV (if possible) and bolus PRN (e.g. soft blood pressures)
    • Separating the treatment of hypovolemia from addressing your free water deficit will help  maintain better control of your sodium correction.


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.


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


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.


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:

Moffitt Pearls 6.14.17 – GI Report

Pearls 6.14.17 – GI – Morning Report

Thank you to Salman for presenting an amazing case of a young woman with history of EtoH hepatitis p/w with fatigue, lightheadedness found to be severely anemic with evidence of active hemolysis and new cirrhosis. Work-up is ongoing.


  1. Acute alcoholic hepatitis is a chronic disease (despite the name!). Presentation is based on predominantly cumulative burden – a single binge in a patient with otherwise minimal alcohol intake is unlikely to cause severe alcoholic hepatitis.
  2. In a young patient (< 35 yo) with new diagnosis of liver injury consider genetic causes including Wilson’s, hemochromatosis and alpha-1 antitrypsin disease in addition to autoimmune, vascular and infectious hepatitis.
  3. The smear and reticulocyte count are the key initial lab studies to frame your differential for hemolytic anemia.


For those who want more information:

Alcoholic Hepatitis

The clinical syndrome of acute alcoholic hepatitis includes the following compilation of laboratory and clinical features:

  • Moderately elevated transaminases in a 2:1 ratio of AST/ALT
    • Typically less than 300, rarely greater than 500
  • Elevated bilirubin and Jaundice
    • Jaundice generally develops within 3 months prior to presentation
  • Fever & Neutrophilic Leukocytosis
    • Both should only be ascribed to alcoholic hepatitis after ruling out infection!
  • Right upper quadrant pain – can often palpate tender hepatomegaly
  • Clinical history of chronic drinking with or without recent bing
    • It’s not uncommon that patients have actually decreased their drinking in the weeks-months preceding acute alc hep due to the onset of symptoms with alcohol intake.

See this RCT from NEJM regarding pentoxifylline vs. prednisolone for the treatment of alcoholic hepatitis. Bottom line:  Acute alcoholic hepatitis is a profoundly morbid disease with very high mortality (30-40% in 6 months).  Prednisolone was associated with a reduction in 28-day mortality, but did not reach significance and there were no improvements in 90-day or 1 year mortality.


Approach to abnormal liver function tests (table from



Approach to Hemolytic Anemia:



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.


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.


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)



  • -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


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:

VA Morning Report: Solid liver lesion without cirrhosis

Case summary: Rockstar MS3 Axel Adams did a fantastic job presenting the case of a 70M with PMH schizophrenia and HCV without cirrhosis, who presented with LE edema and was found to have an IVC thrombus and multifocal hepatic mass.

Top pearls:
1. Recall that 80-90% of hepatocellular carcinomas are associated with cirrhosis. HCC can develop without cirrhosis in patients with HBV, NASH, alpha-1-antitrypsin, and transformation from hepatic adenoma.
2. Work-up of a solid liver lesion without HBV, cirrhosis or extrahepatic malignancy should include checking tumor markers, getting CT or MRI, and considering biopsy versus resection if the preceding tests are non-diagnostic.
3. The three cancers that classically can be diagnosed without a biopsy are: hepatocellular carcinoma, renal cell carcinoma, and testicular cancer.

Solid liver lesion WITHOUT HBV, cirrhosis or extrahepatic malignancy
Thanks to Chief of Medicine/Gastroenterologist Ken McQuaid for joining us today and giving us this great framework
Conditions leading to HCC without cirrhosis: NASH, alpha 1 antitrypsin, conversion from adenoma
– Lesions <1cm: get MRI with contrast, resect if confirmed HCC, or follow serial imaging if not.
– Lesions >1cm:
1. Check AFP and obtain triple-phase CT or MRI with contrast.
2. If imaging non-diagnostic for HCC, check CA 19-9 for cholangiocarcinoma (can be falsely elevated in biliary obstruction).
3. If work-up remains non-diagnostic, consider biopsy versus resection.
Differential diagnosis:
– hepatic hemangioma
– focal nodular hyperplasia
– hepatic adenoma
– idiopathic noncirrhotic portal hypertension
– regenerative nodules
– HCC (including fibrolamellar variant)
– cholangiocarcinoma
– non-Hodgkins lymphoma
– mucinous cystic neoplasms
– mesenchymal tumors (rare soft tissue/vascular sarcomas)
– hepatoblastoma
– metastases

Cancers where tissue is not the issue

1. Renal cell carcinoma- tissue diagnosis obtained via nephrectomy or partial nephrectomy
2. Testicular cancer- tissue diagnosis obtained via orchiectomy
3. Hepatocellular carcinoma- diagnosed radiographically on triple-phase CT or MRI with contrast
Mittal S, El-Serag HB. Epidemiology of hepatocellular carcinoma: consider the population. J Clin Gastroenterol. 2013;47(Suppl):S2–S6.
El-Serag HB. Hepatocellular carcinoma. N Engl J Med. 2011;365:1118-1127.

Gupta S, Bent S, Kohlwes J. Test characteristics of alpha-fetoprotein for detecting hepatocellular carcinoma in patients with hepatitis C. A systematic review and critical analysis. Ann Intern Med. 2003 Jul 1; 139(1):46-50.

Moffitt Cardiology Pearls 6.13.17

Thank you, Salman, for presenting a case of a middle-aged man with HIV presenting with repeated “ICD zaps,” fevers, back pain, and night sweats over the last several months. This patient was ultimately found to have a dual-chamber pacemaker with right ventricular under-sensing and spine imaging with evidence of septic emboli and discitis! His unifying diagnosis was enterococcus device infection complicated by endocarditis and discitis.

Key Pearls:

  1. Chest imaging can provide important information about the type of cardiac conduction device and can be used to assess lead placement for pacemakers and ICDs.
  2. MRIs and Pacemakers – almost all newer pacemakers are compatible with MRIs (see below for more details).
  3. You can breakdown the likely bacterial organisms to cause infection of cardiac conduction devices into early and late device infections, similar to how we classify other prosthetic hardware infections.



What can a chest radiograph tell you about a cardiac conduction device?

  1. ICD vs. Pacemaker – can differentiate based on size of generator, presence or absence of a “coil” – the thicker wire that is present in ICDs
  2. Lead placement – can assess for presence of leads in the right atrium, right ventricle, and coronary sinusCheck out this radiology pictorial review of pacemakers and ICDs:

Approach to Pacemaker Malfunction:

  • Under-sensing – inability for PM to detect native beats, often resulting in inappropriate pacing.
    • Lead failure: fracture, misplacement/migration, infection
    • Program failure: not sensitive enough
    • Change in patient’s intrinsic amplitude (infiltrative cardiomyopathy, scar)
  • Over-sensing – PM detecting electricity other than native heart beats, resulting in a failure to pace when it should.
    • Lead misplacement/migration, inappropriate programming (too sensitive)
    • Interference from alternative electronic device
  • Loss of Capture – inability for PM to capture the heart and cause contraction when it delivers a paced beat.
    • Lead failure: fracture, misplacement, infection
    • Metabolic derangements: electrolytes, acidosis

My patient has a pacemaker. Can she get an MRI?

  • Most modern pacemakers are “MRI compatible” and should be safe (though not all radiology departments are comfortable). Interestingly, even older devices are likely safer than previously thought. In this 2017 NEJM study of 1500 patients with non-MRI-conditional pacemakers or ICDs, there were no deaths, lead failures, losses of capture, or ventricular arrhythmias during non-thoracic MRI!
  • Institutions have varying levels of comfort with pacemakers. If the imaging is of high clinical importance, consider involving your EP colleagues to assess safety and facilitate the imaging.

Approach Cardiac Conduction Device Infections (from NEJM link below)