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.
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
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?
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.
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.
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:
fever >38.0 C
suprapubic tenderness or CVA tenderness
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.
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.
Ascites is present
There is an AKI (creatinine >1.5)
Rule out infection: there is no UTI or pyelonephritis
Rule out prerenal injury: there is no improvement in serum Cr after resuscitation with 2 days of 1 mg/kg albumin, 100 g max
Rule out intrinsic disease: there is no hematuria (>50 RBCs) or proteinuria (>0.5 g) to suggest renal disease
Rule out meds: no nephrotoxic meds recently given
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.
Very few men are brave enough to ask me, a woman, about “man troubles,” but when they do, I want to give them good counsel.* So, this post is really more like “here’s what I read on the Internet, hopefully it’s a helpful summary”:
Testosterone deficiency. Andropause. Male menopause. Low T. These are the terms your patient may have read about, and they want to know if you think they have it, and furthermore, if you think they need testosterone replacement therapy.
Is testosterone deficiency a real thing?
Short answer: yes, but you have to be strict in how you diagnose it. This is bolded in Up To Date, and whenever something is bolded in Up To Date, it’s important. This Science-Based Medicine article makes a convincing argument that testosterone deficiency has been oversold by the pharmaceutical industry in order to peddle patches, injections, etc. for profit.
What is the range of normal for testosterone in males?
How is testosterone deficiency diagnosed?
Testosterone deficiency cannot be diagnosed in a single visit. Let me repeat that: it will take at least 2-3 visits/lab draws to make a diagnosis. That’s because testosterone levels fluctuate, and that is a normal thing!
Diagnosis requires repeatedly low morning-level testosterone levels PLUS factors like low libido, loss of morning erections, gynecomastia, loss of body hair, loss of bone density, or small testes.
Vague symptoms, like fatigue, depression, anemia, and loss of muscle strength are NOT enough on their own and should receive a broader workup.
What about in older men? I heard it’s different.
Kind of? There is no one clear answer. It seems reasonable to treat older men for truly low testosterone levels, like <200 ng/dL who are having symptoms. Data shows that it does improve mood, energy, and sexual function. But there are no big studies of long-term side effects, so if one day it’s found that testosterone secretly causes cancer or dementia, you’ll be glad you were conservative.
Who can NOT receive testosterone?
Patient with severe prostatic hypertrophy, PSA >4.0, history of prostate cancer, erythryocytosis, uncontrolled heart failure. Some people say sleep apnea–this is not totally clear, but may be more of a co-variate. Obesity can lower testosterone levels, and is also associated with sleep apnea.
Before starting anyone on testosterone, make sure to do a prostate exam and PSA level. If the PSA is markedly elevated, you might need to make sure he doesn’t have prostate cancer first…
What are the different kinds of testosterone replacement?
Transdermal: most people consider this the easiest method of administration, but it can be more expensive
Injections: can be given every 1-3 weeks depending, but the farther apart the injections are the more labile someone’s symptoms might be
Pills are an option, but have been linked with higher rates of hepatic disease
Subcutaneous implantable pellets (seriously, when there is money to be made, the possibilities are infinite)
What are the side effects of testosterone replacement?
Acne: the patch in particular can cause a nasty localized rash, although I think this is more like a contact dermatitis
Polycythemia: rare, but shows up on board questions
Infertility: this is not immediately apparent to people, and you should ask your patient if they are planning on conceiving prior to prescribing testosterone. Interestingly, testosterone has been explored as a contraceptive agent.
Labs should be monitored regularly: CBC, LFTs, lipid panel. Testosterone levels can be checked every few months for efficacy, too.
How is testosterone for transgender patients prescribed? Are there any caveats to be aware of?
Testosterone is prescribed in any of the forms described above at similar doses. Many providers will cite “other endocrine dysfunction” instead of “gender identity disorder” or “gender dysphoria” as this is less stigmatizing.
The patient expects to experience deepening of the voice, male pattern hair growth, clitoromegaly, and atrophic vaginitis, among other things. However, breast tissue atrophies less than most people expect. Typical side effects also apply.
* This information is relevant to adults, not to children or adolescents.
You may see Candida growing because of a chronic in-dwelling urinary catheter, instrumentation/urologic procedures, contamination, or because of a true UTI or even bloodstream infection.
If the patient has a catheter, remove it and see if the Candida persists. If it cannot be removed, replace it with a new one.
Asymptomatic candiduria should only be treated in high-risk populations: neutropenic patients and those undergoing surgery or urinary tract procedures. Also, if the patient has dysuria, then it should be treated. Most strains are susceptible to fluconazole so this is a first-line agent.