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.
Immunosuppressants aim to prevent this from happening:
But too much immunosuppression can cause this:
That’s why people can’t just be on ONE immunosuppressant after transplant: the doses required would be too toxic, so the effect is spread out over 2-3 medications.
Considering that the historical option was total body irradiation, we’ve come a long way. Azathioprine was the first chemical immunosuppressant, but cyclosporine, which came onto the scene in the 1970s, revolutionized kidney transplant survival rates.
***One of my chiefs last year made an amazing figure on maintenance transplant immunosuppression. It is worth this whole post and I highly encourage you to take a look!***
For us peons, what are the commonly used immunosuppressants?
Mechanism of Action
Calcineurin inhibitor (CNI)
Cr, drug trough
Neurotoxicity, nephrotoxicity, diabetes, alopecia *many drug interactions
Pneumonitis, arthralgias, edema, hypertension, bone marrow suppression, hyperlipidemia
0.75-1 mg twice daily
arthralgias, edema, hypertension, bone marrow suppression, hyperlipidemia
The dozens of things steroids do
Varies widely, minimum 7.5 mg every other day or 5 mg daily
Osteopenia, diabetes, headache, Cushing’s, weight, cataracts, psychosis (and many others)
## Mycophenolate can be either mycophenolate mofetil vs. sodium. The difference is that the sodium formulation (Myfortic) is an enteric capsule that may prevent some GI effects like diarrhea(?) but the jury is still out.
What are the major side effects of immunosuppression?
What is the underlying biology? ***This is a gross oversimplification.
Normally, T cells go scouting and if they encounter an antigen-presenting cell with foreign material on it, a chain reaction of events is started: calcineurin is activated, leading to a surge of IL-2 and its receptor, IL-2R, which upregulates the mTOR pathway, which leads to DNA nucleotide synthesis so that the T cell can multiply and generate an immune response.
Notice that the bolded words are the targets of the 6 immunosuppresants in the chart above.
Transplant pharmacology is REALLY COMPLICATED and you can do an entire fellowship training program for this. This is an excellent, but 100-page document from a Canadian transplant website. Here are two organ-specific guides/reviews regarding immunosuppression:
There used to be 3 separate bottles hooked up to the chest tube itself: Bottle #1 is where the patient’s empyema fluid or blood leaked into. Bottle #2 is the waterseal: air is forced to travel through water and can only move in one direction (it cannot move back into the patient). Bottle #3 sets suction power based on how much water is in the bottle–more water=less suction, less water=more suction, and you need to make sure the suction power is just right. You can see how the drainage system has evolved over time on the right.
Should patients be “placed to waterseal” or “placed to -20 suction?”
“Place to waterseal”= don’t be too crazy with drainage, which is appropriate for most pleural effusions or a mild pneumothorax. If the lung is not fully expanded, you can “turn up the suction.”If you apply suction too aggressively, you put the patient at risk for re-expansion pulmonary edema.
How do I know if there is an “air leak” and what the eff does it mean?
An air leak is present if there is bubbling in the waterseal chamber when the suction is clamped/on waterseal–this indicates there is positive pressure coming from the pleural space=air getting into the pleural space. Intermittent bubbling with expiration (when pleural pressure is highest in the non-ventilated patient) may be normal, but a continuous air leak is pathological.
ruptured bleb (severe emphysema)
simple traumatic pneumothorax (from placing the chest tube)
a leak in the actual tubing system
mechanical ventilation (may see decreased tidal volumes, failure of PEEP increase)
bronchopleural fistula (usually more severe or continuous)
lung entrapment vs. trapped lung
NB: if your patient has a persistent air leak, think twice about pulling their chest tube because if you do, you may cause a recurrent pneumothorax.
What is “tidaling?”
You may see movement in the waterseal chamber with respiratory variation. It’s the water being sucked back towards the lung with inspiration due to negative inspiratory pressure. (In mechanically ventilated patients, it’s the opposite.)
How do I know when the tube can be taken out?
In a 2013 study out of Michigan State, the team found it is reasonable to remove chest tubes when drainage <200 ml/day, on waterseal, with no air leak. In stable patients on the floor, theoretically you don’t need a chest x-ray after removal, but given our litigious society, everyone gets one. In mechanically ventilated patients, you should get a chest x-ray 1-3 hours after removal.
What do I do if the tube falls out?
Use common sense: cover the area and prepare to re-insert a chest tube. Maintain sterility. The patient is at risk of a tension pneumothorax, so someone should stay with them for close monitoring. More troubleshooting at this nursing website.