“Why does potassium have to be repleted to 4?”

There is general agreement–but not an official statement that I could find–that in all comers, K <3.0 should be repleted. In patients with a history of past cardiac surgery, heart disease, and definitely in the post-MI population, K<3.5 should be repleted for a goal of 4.0. When there is acute concern for torsades or other arrhythmia, there is again general agreement but no official consensus that the goal is raised to >4.5.

Remember action potentials? The ins and the outs with K, Na, and Ca with the alphabet soup of channels? (Brief review in the first section of this editorial.) In the short-term, having a low serum K affects repolarization and has a chain effect on the action potential, causing increased automaticity, excitability, and QT prolongation, potentially triggering fatal arrhythmia. In the long-term, hypokalemia is associated with cardiovascular mortality in patients with underlying heart disease, arrhythmias like RBBB, and heart failure.

NB: Kind of supporting this are findings that higher doses of thiazide diuretic are linked to sudden cardiac death. Some argue that the mortality benefit of ACE inhibitors and beta-blockers in heart failure comes in part from an ability to better stabilize potassium levels. (Beta-blockers keep potassium extracellular through beta-2 receptors.)

Many studies linking hypokalemia to arrhythmia were relatively smaller studies (it seems like anything fewer than n=5,000 is not impressive in general cardiology) done in the 1980s, with mixed patient populations of mostly acute MI, hypertension (looking specifically at thiazide diuretics), or heart failure. These studies implied that the higher the potassium (K>4.5) the better:


A more recent population-based cohort study of post-MI patients in JAMA (n>38,000), on the other hand, showed the following:

Because the lowest rate of mortality was found in the group with K 3.5-4.5, a goal of 4.0 is generally set for post-MI patients, which was extrapolated to any patient with heart disease. A similar distribution was found in patients who also had renal disease, and this study based on data from MERLIN-TIMI 36. This is a good reminder that hyperkalemia is linked to increased cardiovascular mortality, too.

When is colonoscopy indicated for colonic ischemia (ischemic colitis)?

The underlying pathophysiology of colonic ischemia (frequently called “ischemic colitis”) is much like that of ischemia anywhere else in the body: ischemia of the heart (MI), ischemia of the kidney, ischemia of the brain (stroke), etc. The reason it should be called “colonic ischemia” is because not every case of ischemia results in colitis, but the type of injury is the same.

The incidence of colonic ischemia cannot be accurately stated, because so many cases are relatively “meh” or benign. Someone gets some cramping, maybe they pass a little blood in their stool, things get better after a day or two on their own. That makes strongly evidence-based guidelines hard to come by. This is my caveat for the answers below. My source for this post is the 2015 ACG clinical guideline.

But you’re probably wondering, “Do I need to consult GI for every single case of suspected colonic ischemia? Do I need to ask if colonoscopy is indicated for every single patient?”

Appropriate consultation is an art, of course. GI consultation should not be automatic, but for ischemia, which can be vague and multifactorial, never shy away from consulting GI just because “it’ll get better on its own.” A consultant can help identify contributing factors, like meds that should be discontinued, workup for rheumatologic or hematologic disease, suggest other input from cardiology, etc. Think about the following factors:

  • How confident are you about the diagnosis? Some cases are slam dunks: cramping abdominal pain, some red stools, double halo sign on CT in a patient with a history of vascular disease. But a lot of these findings are non-specific. The differential includes diverticulitis, IBD, infectious colitis, and even malignancy. If you want to rule out another cause and prove it’s ischemic injury, ask GI about more imaging vs. colonoscopy.
  • How severe is the case? Mild cases will likely resolve on their own after a couple of days. Moderately severe cases (see algorithm below) seem most likely to benefit from the additional diagnostic of colonoscopy. Colonoscopy can show the extent of ischemic damage; in particular colonoscopy can visualize right-sided ischemia and pancolitis, which are associated with worse outcomes. As discussed below, anyone with severe findings/peritonitis should NOT have colonoscopy.
  • Is this the first time it happened, or is there a pattern of recurrence? If it’s a mild, first-time case, it’s probably not a big deal. Multiple episodes deserve a more detailed workup with endoscopic evaluation and histopathology to prove ischemic injury.
  • Are there implications for the future? Because of the differential diagnosis above, consider your patient’s other symptoms, medical conditions, and overall state of health. Would it matter for this particular case whether other types of colitis or masses were excluded?
From Brant, Feuerstadt, ACG guideline

NB: no prep is indicated for colonoscopy being done for colonic ischemia.

When should colonoscopy NOT be performed? The yield decreases substantially >48 hours after symptoms begin (to about 30%) so colonoscopy won’t be as helpful then. Colonoscopy is not recommended in severe cases, peritoneal signs, or diverticulitis because of theoretical risks of insufflation worsening pressure-related injury or causing perforation.

As a corollary–the ACG guidelines from 2015 also state that there is no evidence to support specific rules on when antibiotics are indicated and how long to give them for. Antibiotics not only prevent bacteremia/sepsis, they probably also help reduce the body’s inflammatory response to bowel injury…but there’s not a whole lot of human studies to show how helpful or unhelpful they are. Therefore, the guideline authors recommend antibiotics that cover bowel flora (like a third-gen cephalosporin + metronidazole) in “moderate” and definitely “severe” cases of colonic ischemia. They suggest 72 hours, but I think if someone is rapidly clinically improving, it’s reasonable to stop antibiotics after 1-2 days.

What is pulmonary toilet?

AKA “pulmonary hygiene.” Pulmonary toilet is advocated by many people, and does sound like a good idea in theory. However, the literature on whether pulmonary toilet actually improves outcomes for various patient populations is very mixed. In general, the patients who seem to benefit most are the cystic fibrosis and critically ill/intubated populations.

The purpose is to THIN and LOOSEN secretions. Having an awake, alert patient who can cough on their own is the best kind of pulmonary toilet.

What are the specific components of pulmonary toilet?

  • Bronchodilator (albuterol)
  • Mucolytic (such as NAC or Mucomyst): NAC in particular has become less popular because of lack of demonstrated utility (a good example is    this meta-analysis on cystic fibrosis). I still see it used in the ICU, though.
  • Hypertonic (7%) saline: may cause bronchospasm, coughing
  • Chest PT
    • Vibrating chest vest
    • Percussion (clapping patient on the chest)
    • Postural drainage
  • PEP device and flutter valve (such as Accapella)  
    •       NB: the Accapella =/= incentive spirometer
  • Suctioning
  • Bronchoscopy: using a bronchoscope to “wash out” secretions for atelectasis. This is only helpful in patients who are critically ill/intubated who cannot do any other kind of secretion clearance on their own. My personal observation is that when BAL is used for pulmonary toilet, it turns into a problematic cycle of provoking even more secretions and the need for repeated bronchs. A bronch is also not a completely benign procedure and may be associated with barotrauma, temporarily worsened oxygenation, etc.

When is pulmonary toilet useful? This clinical review is pretty negative. It states that chlorhexidine oral rinses are the only intervention that reduces rates of nosocomial pneumonia, and that other common practices like mucolytics and chest PT are not associated with improved outcomes and may in fact cause harm like bronchospasm and mechanical trauma, respectively. (A lot of evidence comes from pre-2000’s papers/guidelines, though). Let’s look at some common situations:

  • COPD: This meta-analysis reports that daily oral NAC was associated with fewer COPD exacerbations in patients who had a spirometric diagnosis of COPD, but also in patients who did not have a spirometric diagnosis of COPD. However, this joint paper from ACP-ACCP states that multiple trials have not found benefit for mucolytics or chest PT in COPD exacerbations.
  • Cystic fibrosis: Yes to chest PT. There is also good evidence that dornase alfa (DNase) and hypertonic saline have small effects.
  • Atelectasis: for acute atelectasis, if patients cannot cough on their own, chest PT is helpful. (The same review talks about how “bronch for airway clearance” is only indicated in selected cases of atelectasis that are multilobar or severe.)
  • Post-surgical patients :There is very limited objective evidence that pulmonary toilet decreases pulmonary complications (pneumonia, atelectasis, edema, etc.) in the postoperative period. This Cochrane review shows that in patients who underwent  upper abdominal surgery, incentive spirometry didn’t make a difference. Maybe this will make us feel better about all those unused incentive spirometers sitting by patients’ bedsides.        

Giving normal saline for SIADH

First question: will giving normal saline even help? Normal saline has an osmolality of 308 mEq (Na+Cl). In hypovolemic and some cases of euvolemic hyponatremia, it can help raise Na appropriately. If the urine osmolality is too high, giving normal saline will actually worsen hyponatremia because it will be like giving a more dilute fluid. 

Example: You have a man with suspected SIADH (he’s a smoker and has a new diagnosis of lung cancer). His Na is 120. His serum osm is 265 and his urine osm is 320. Your total free water loss is -37.5 mL, which is to say, if you give him 1 L NS, you will make zero difference. 

Let’s say the same man has a urine osm of 100. Your total free water loss is +2.08 L. If you give him 1 L NS, you will dramatically increase his Na. 

Let’s say the same man has a urine osm of 600. Now your total free water loss is -486 mL, which means if you give him 1 L NS, you will actually cause him to gain free water and worsen his Na. 

*It’s technically serum “osmolality” 
**D5 1/2NS osmolarity is often listed around 405, but it’s really less than that because dextrose moves more freely across cell membranes, and what I care about is the Na component

This chart is also very helpful for understanding how fluids are selected in common scenarios. 

Second question: How much normal saline should I give? The equation below is extrapolated from a calculation for how much hypertonic saline to give (see this post)

How much hypertonic saline should I give?

You have a patient with hyponatremia and you’ve determined that salt tabs and normal saline just won’t do, they need some 3% hypertonic saline. Great! You go to write the order…how many cc’s should they get? At what rate? Is there a better way of calculating it rather than just saying, give 50 cc x1 and hope for the best? 

As it turns out, giving 50 cc boluses and checking Na every 2 hours is an accepted form of empiric treatment. But if that makes you uneasy, there is a more mathematical solution. (Reference

You are solving for “predicted Na.” 513 refers to the amount of Na in 1 L 3% NS. Total body water is kg x0.5 for women, kg x0.6 for men

Example: a 60 kg woman with an Na of 108. Your goal is to increase her Na by 4 mmol over the next 4 hours. 

So far, your answer should be: the predicted change in Na will be 13.06 for every 1 L 3% NS. Therefore, to increase Na from 108 to 112 over four hours: 

=0.294 L or 294 mL. However, because you want to run this over 4 hours, 294/4=73.5 mL/hour. And that’s your hypertonic saline infusion rate!

Remember your Na correction goals:

  • 2-4 mEq in the first 2-4 hours (if you go over that, consider giving some free water back)
  • <8-10 mEq over 24 hours
  • You can stop being aggressive about correction around the time Na >125 mmol/L

Who needs to be on stress dose steroids and how do you taper them?

This post is about perioperative stress dose steroids, for adult patients, only. 

Who is at risk for perioperative adrenal insufficiency? The goal of stress dose steroids is to prevent hypotension and adrenal crisis/shock. The Society of Hospital Medicine (in one of their great learning modules), states: 

  • Low risk: <5 mg prednisone daily or ❤ weeks of prednisone over the past year
  • Moderate risk: >5 mg prednisone for >3 weeks in the past year
  • High risk: >20 mg prednisone daily for >3 weeks in the past year
  • Obviously, someone with primary adrenal insufficiency is the highest risk. 

What kind of steroid should be used? IV hydrocortisone is the most physiologic (+mineralocorticoid effect) and should be used until the patient can be transitioned back to prednisone/oral steroids. This letter makes an argument for dexamethasone that is interesting–I myself have never seen dexamethasone used for this indication, though. 

Does the kind of surgery affect whether someone should get stress dose steroids? Yes. 

  • Low stress: local anesthesia, ophthalmologic procedures, some small joint or hernia surgeries <1 hour
  • Moderate stress: general anesthesia, open procedures (hysterectomy, hemicolectomy)
  • High stress: lengthy, complex surgeries (CABG, pancreatectomy)
  • Patients at moderate-high risk undergoing moderate-high stress surgeries should be given stress dose steroids in the perioperative period. (Take this with a grain of salt–the objective evidence is very limited and there are good arguments for being even more conservative and only giving steroids to patients at high risk.)
    • Should you test for HPA axis suppression prior to surgery? If the patient is at moderate risk and undergoing moderate or high stress surgery, and you have the time to wait on results, then sure, you can. What test should you use? You can probably get away with an AM cortisol, although the cort stim test is more accurate

How the heck do I taper stress dose steroids? Stress dose steroid tapers, like ALL steroid tapers, are made up. We as a medical community prescribe tapers based on what “sounds reasonable.” What is usually reasonable is something along the lines of: 

  • Moderate stress surgery: 50 mg IV hydrocortisone x1 –> 25 mg Q8H x24-48 hours –> 10 mg prednisone x3-4 days –> usual dose
  • High stress surgery: 100 mg IV hydrocortisone x1 –> 50 mg Q8H x24-48 hours  –> 20 mg prednisone x3-4 days –> 10 mg prednisone x3-4 days –> usual dose 

Some people would advocate going straight from IV hydrocortisone back to the home dose, which is fine if the patient looks clinically well. Patients at higher risk of complications from steroids (hyperglycemia, fluid retention, agitation) should be tapered more quickly and patients at higher risk of adrenal insufficiency should be tapered more slowly.