How sensitive are muddy brown casts for ATN?

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Muddy brown casts are diagnostic for ATN, or acute tubular necrosis, which is an intrinsic form of AKI. But if you don’t see muddy brown casts, can ATN be ruled out? The literature on this is surprisingly light. There is one study of 267 patients with AKI who were classified as low or high pretest probability for ATN and had urine samples analyzed. The study concludes: “In patients with a low pretest probability of ATN (initial diagnosis of prerenal AKI), lack of casts or RTEC on urinary sediment examination had a sensitivity of 0.73 and specificity of 0.75 for a final diagnosis of prerenal AKI. The negative predictive value of lack of casts or RTEC in patients with low pretest probability of disease was 91%.” One important point to take away is that your pretest probability matters a lot for how confident you should be about making a diagnosis.

This review, by the same group, has a nice discussion section about making the diagnosis of ATN through a combination of methods, including microscopy, and use of FeNa and FeUrea.


What’s the difference between dobutamine and dopamine?

These two medications SOUND similar, but are in different categories.

  Dobutamine Dopamine
Class Inotrope Vasopressor
Receptors affected B1 agonist A1 agonist (dose dependent)
Effect Increased cardiac contractility Vasoconstriction, increased systemic vascular resistance
Common uses “Tailored therapy” for heart failure, ?septic shock Septic shock (>8), cardiogenic shock (4-7), promoting urine flow (0.5-3)
Side effects Tachycardia, may even cause hypotension (mild vasodilation), do not use in patients with HOCM Tachycardia/VT, tachyphylaxis, ischemic limb necrosis (do not give through a peripheral IV)



Whole blood potassium versus serum potassium: which is better?


Here’s something you may see sometimes: a patient presents with a (non-hemolyzed ) potassium of 7.0. Scary! But you check a potassium on VBG, and it returns 5.5. Which is the right value? What’s going on here?

Serum potassium, generally speaking, is more accurate. Serum samples contains potassium released by platelets (which are separated out in the phlebotomy tube) so is usually 0.1-0.7 mmol/L higher than plasma samples. Whole blood potassium is usually accurate enough, especially when you need a potassium level quickly in a critical care/emergency setting.

Serum potassium Whole blood (plasma) potassium
Type of tube Serum-separating tube “tiger top,” “gold top,” “marble top” Heparin whole blood tube “green top” for a VBG or ABG kit
Timeliness Rapid turnaround time
Accuracy More accurate Usually accurate, but may underestimate hyperkalemia
Affected by hemolysis? Yes No

In the example above, there is a significant difference between the serum and whole blood potassium, suggesting that there may be a degree of pseudohyperkalemia.

Troubleshooting pseudohyperkalemia:

  • Did the patient clench their fist or have a traumatic blood draw?
  • Was the patient in acute respiratory alkalosis when the blood was drawn?
  • Does the patient have thrombocytosis? (Platelets can release potassium, causing false elevation)
  • Is the specimen hemolyzed–has it been sitting in the lab for a long time before being processed?

Is everyone with HIV immunosuppressed?

This question came up when one of my co-residents stated during our discussion of a case that the patient, who had HIV, should not be considered immunosuppressed because his CD4 count was in the 300s.

Patients who are HIV-positive with a CD4 count <200-250 or who have had an AIDS-defining illness are immunocompromised. Patients with a CD4 count above this level may not necessarily count as immunocompromised.

As a reminder, CD4 counts dictate what patients should be prophylaxed against:

  • CD4 <250: IgG and IgM serologic screening for coccidiomycosis in endemic regions, administer fluconazole if positive.
  • CD4 <200: administer Bactrim/dapsone/atovaquone for PJP prophylaxis
  • CD4 <100: administer Bactrim or alternative for toxoplasmosis prevention. Patients are at risk for cryptococcus.
  • CD4 <50: patients are at risk for MAC, and if not on antiretrovirals, should be prophylaxed with azithromycin (if on ART, do not need prophylaxis)

A list of AIDS-defining illnesses from the CDC (see website for more details on the asterisks/caveats):

  • Bacterial infections, multiple or recurrent*
  • Candidiasis of bronchi, trachea, or lungs
  • Candidiasis of esophagus
  • Cervical cancer, invasive§
  • Coccidioidomycosis, disseminated or extrapulmonary
  • Cryptococcosis, extrapulmonary
  • Cryptosporidiosis, chronic intestinal (>1 month’s duration)
  • Cytomegalovirus disease (other than liver, spleen, or nodes), onset at age >1 month
  • Cytomegalovirus retinitis (with loss of vision)
  • Encephalopathy, HIV related
  • Herpes simplex: chronic ulcers (>1 month’s duration) or bronchitis, pneumonitis, or esophagitis (onset at age >1 month)
  • Histoplasmosis, disseminated or extrapulmonary
  • Isosporiasis, chronic intestinal (>1 month’s duration)
  • Kaposi sarcoma
  • Lymphoid interstitial pneumonia or pulmonary lymphoid hyperplasia complex*
  • Lymphoma, Burkitt (or equivalent term)
  • Lymphoma, immunoblastic (or equivalent term)
  • Lymphoma, primary, of brain
  • Mycobacterium avium complex or Mycobacterium kansasii, disseminated or extrapulmonary
  • Mycobacterium tuberculosis of any site, pulmonary,†§ disseminated, or extrapulmonary
  • Mycobacterium, other species or unidentified species, disseminated or extrapulmonary
  • Pneumocystis jirovecii pneumonia
  • Pneumonia, recurrent†§
  • Progressive multifocal leukoencephalopathy
  • Salmonella septicemia, recurrent
  • Toxoplasmosis of brain, onset at age >1 month
  • Wasting syndrome attributed to HIV




Testing for adrenal insufficiency: random cortisol level versus cort stim test

Let’s say a patient presents to the medical floor with hypotension and hyperkalemia, and generalized fatigue and weakness. Adrenal insufficiency might be on your differential. What’s the most accurate way to test for it? Can you get away with using doing a random cortisol level?

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A random serum cortisol level must always be in the context of what time of day it was taken. There are different laboratory cutoffs depending on what time of day the sample was taken. Typically, a morning cortisol level is most helpful. An AM cortisol level >15 mcg/dL is very reassuring that someone doesn’t have adrenal insufficiency. But any level <15 does not exclude adrenal insufficiency! As this case report shows.

A cort stim test (also called ACTH/cosyntropin stim test) involves measuring an AM serum cortisol, injecting 250 mcg of ACTH or cosyntropin, waiting 30 minutes, and then measuring serum cortisol again. An “adequate response” ruling out adrenal insufficiency is  ≥18 to 20 mcg/dL before or after ACTH injection. If there is an inadequate response, you may consider directly measuring ACTH levels or doing other tests to further evaluate for primary vs. secondary adrenal insufficiency.

Note 1: patients with higher levels of cortisol-binding globulin (like cirrhotics or those with nephrotic syndrome) may have lower levels of cortisol, and may be incorrectly diagnosed with adrenal insufficiency using normal cut-off ranges.

Note 2: this doesn’t apply to patients who are really, really sick in the ICU. As this review discusses, critically ill patients are probably relatively adrenally insufficient because they need tons of cortisol to maintain perfusion and create an inflammatory response.

One point that this review makes is:

Our belief is that adrenal insufficiency appears to be unlikely when a random cortisol measurement is greater than 34 μg per deciliter. Conversely, adrenal insufficiency is likely if the serum cortisol level is below 15 μg per deciliter during acute severe illness. For persons with cortisol levels between these two values, a poor response on a corticotropin test would indicate the possibility of adrenal insufficiency and a need for supplemental corticosteroids.

Does my patient have a UTI? (urinary tract infection)

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All too frequently, patients are started on antibiotics for a UTI because of a “positive UA” alone. This should not be! Sometimes, especially if a patient is unstable or really sick, it may be wise to empirically treat for a UTI, but in an otherwise stable patient, please think carefully about whether they truly have a UTI.

Technically, a UTI is defined in part by a positive urine culture that has >10,000 organisms, of no more than two species. (“Mixed genital flora” does not count!) However, often we let this slide if a patient has a “positive UA” and one of the following criteria:

  1. fever >38.0 C
  2. suprapubic tenderness or CVA tenderness
  3. urgency
  4. dysuria
  5. frequency

If a patient has a Foley in place, they will not be able to reliably tell you about urgency, dysuria, or frequency because the Foley catheter itself can cause these symptoms.

Does my patient have hepatorenal syndrome?

This is intended to provide a quick list for diagnosis of HRS, since HRS is a diagnosis of exclusion and should only be made once other conditions are “ruled out.” HRS is a clinical diagnosis, and there is no one perfectly sensitive or specific test. But if your patient meets these criteria, you should be worried.

  1. Ascites is present
  2. There is an AKI (creatinine >1.5)
  3. Rule out infection: there is no UTI or pyelonephritis
  4. Rule out prerenal injury: there is no improvement in serum Cr after resuscitation with 2 days of 1 mg/kg albumin, 100 g max
  5. Rule out intrinsic disease: there is no hematuria (>50 RBCs) or proteinuria (>0.5 g) to suggest renal disease
  6. Rule out meds: no nephrotoxic meds recently given
  7. Rule out hypotension/ATN: no signs of ATN in the urine, no shock or profound hypotension

In the past, there were minor criteria including oliguria (<0.5 L urine output/day), low urine sodium (<20), and low serum sodium. These were found to have poor specificity and were dropped in 2007.

There are two types of HRS: Type 1 is rapid (develops in <2 weeks) and severe, with a 10% survival rate over 3 months. Type 2 is more gradual and on a spectrum with diuretic-resistant ascites.

You should also ask yourself: what triggered this episode of HRS? Common precipitants include infection (check a chest x-ray for pneumonia, urine studies for UTI, blood cultures, and rule out SBP), prerenal causes (not giving enough albumin after large-volume paracentesis, diuretics), post-TIPS, and nephrotoxic drugs.