Why do so many MICU patients get lipid panels and lipase?

You may see lipid panels and lipase ordered on MICU patients who have conditions ranging from septic shock to neurologic devestation. This is because of the potential for propofol reaction syndrome (PRIS):

-pancreatitis

-hypertriglyceridemia

-“collapse” syndrome where the BP and HR fall suddenly

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Can you use beta-blockers in patients with COPD?

Lots of people have both heart failure and COPD or asthma. Should you be concerned that the beta-blocker they’re on will make them more likely to have a COPD flare?

The short answer is: no. A review by Abouaini et al in 2007 reports that beta-blocker use is well-tolerated in COPD patients and does not worsen respiratory symptoms or worsen FEV1. The fears that beta-blockers may aggravate bronchospasm is based on case reports/anecdotes. That being said, it’s safer to start a patient with COPD on a cardioselective beta-blocker like metoprolol. Carvedilol (non-selective) is also okay if the patient has severe heart failure, though.

NB: Try to look for evidence that your patient has COPD, such as PFTs or characteristic findings on x-ray or exam. Too often, older adults get diagnosed with COPD when they have dyspnea and wheezing “just because.”

Mushroom poisoning

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I am a fan of searching for botanical cures for cancer and the movement to eat local, and eat weeds. But if you choose to forage for plant food, remember that safety trumps enthusiasm. The example I want to discuss is mushroom-hunting, which for some, is a happy pastime and a way to stick it to commercially farmed mushrooms, and for others, turns into a trip to the emergency department and for author and gentleman Nicholas Evans, a kidney transplant.

Make sure that you talk to local experts and read a guide on how to pick mushrooms (such as this Guardian article) so that you can identify the specific mushrooms that grow in your area. David Fischer’s online guide to poisonous American mushroomsis a good place to start. If you have any doubts about the mushroom, take it home or show it to someone who will be able to positively identify it. It is estimated that mushroom toxins can be deadly in up to 50% of children and 20% of adults who are poisoned.

Mushroom hunting is more popular in Europe, so there are more reports of severe/fatal poisonings from Russia, Poland, France, the UK, etc. From my side of the Atlantic, here is a paper from Mexico City that describes two cases of liver toxicity that occurred after ingestion of Amanita mushrooms: one case recovered normal function, while the other one died in multi-organ failure within a week. Amanita mushrooms are especially dangerous because they contain several different toxins, including amatoxins, which cannot be destroyed by cooking or digestive enzymes. A single mature Amanita phalloideae mushroom contains a lethal dose of amatoxins.

The course of Amanita poisoning is divided into four stages. Stage 1 is an asymptomatic period of 6 to 12 hours. Stage 2 is an “upset stomach” period that can involve cramping stomach pain, nausea, vomitting, and watery diarrhea. Stage 3 is the turning point: after 24 to 48 hours of seeming improvement, the toxic effects on liver, kidney, and gut cells causes progressive deterioration of liver and kidney function that may appear as increased prothrombin time, decreased albumin, elevated LFTs, and dark, scant urine production. From here, stage 4 is the march towards liver and kidney failure, which can result in hepatic encephalopathy, bleeding problems, and pH and electrolyte derangements. Liver and kidney transplants, or else dialysis, must be considered by stage 3.

There is no specific antidote for mushroom poisoning, so a treatment plan might involve:

  • resuscitation fluids if the person is dehydrated or hypovolemic
  • in the early hours, sodium bicarbonate or nasogastric lavage followed by activated charcoal to try to flush out the toxins
  • Silymarin (derived from milk thistle), as well as other drugs, like ceftazidime, cimetidine, or N-acetylcysteine (which is used for Tylenol overdoses) have been used empirically but there’s no statistical evidence supporting their use
  • MARS therapy, a form of albumin dialysis used in liver transplantation protocols, although this is an expensive and invasive treatment.

Is it okay to give a patient morphine, codeine, etc if they have an “opioid allergy?”

I direct your attention to this great overview in US Pharmacist, Opioids: Allergy vs Pseudoallergy.

A frequent problem on the wards is a patient who comes in with severe pain, who you’d like to give narcotics to, but they claim they have an allergy to morphine. They state that their allergy is “hives,” or “rash,” or “vomiting.” Can you still give them morphine? Can you give any opioid at all?

Based on my reading of the article, the only TRUE opioid allergies are:

  • hives
  • maculopapular rash
  • erythema multiforme
  • pustular rash
  • severe hypotension
  • bronchospasm
  • angioedema

Patient with a true allergy can be given the opioid at a lower dose with administration of an antihistamine, as long as you think the patient can tolerate the adverse effect.

Reactions like nausea, vomiting, itching, agitation and delirium are pseudoallergies. It should be noted that nausea is common, and usually resolves in 5-10 days. (It may also be a side effect of the pain itself.)

However, calling a reaction a pseudoallergy doesn’t mean your problem is solved. You can still give an antihistamine, but likely, the patient will refuse to take a medication they think they have an allergy to. If they have an allergy to a natural opioid like codeine or morphine, you can try a synthetic opioid like meperidine or fentanyl, although these are not preferred in general on the medicine floors. Tramadol is contraindicated.

Interesting note: heroin users say they can tell the difference between fentanyl (no itch) and heroin (sometimes get an itch or mild rash). Important to note that heroin is increasingly cut with fentanyl which gives a “better high” but also is associated with more deaths.

Is 325 mg aspirin an acceptable form of anticoagulation for atrial fibrillation?

Basically: NO.

Sometimes patients are put on aspirin monotherapy, but studies show that it’s not as effective as coumadin or the NOACs. Aspirin by itself reduces the risk of stroke by 20%, but it’s not a significant difference from placebo. The Stroke Prevention in Atrial Fibrillation II provides evidence for this.

As a tangent, the ACTIVE trials looked at aspirin monotherapy vs dual antiplatelet therapy and whether that was comparable to warfarin. Basically, NOACs > warfarin > dual antiplatelet > aspirin. However, there were more major bleeding events with dual antiplatelet therapy.

Treating fungemia

The first step, even before starting treatment, is to identify who would be at risk for fungemia. Risk factors include neutropenia, being in the ICU, on TPN, on broad spectrum antibiotics, long-time central-line. Fungus in the sputum or urine may be a red herring, but fungus in the blood is NEVER normal.

Treating fungus depends on what kind it is. The major strains include:

  • Candida albicans
  • C. glabrata
  • C. krusei (which is virtually fluconazole-resistant)

If a patient without risk factors at an institution where <15% are fluconazole resistant, it’s safe to treat with fluconazole. However, if not, then micafungin or even the terrible amphotericin B may be used.

P.S.- patients with fungemia should get a formal ophthalmology consult!

Peaks and troughs and vanc dosing

When do you get a vanc trough? What about a peak? What does it mean, anyway?

Vancomycin is a renally cleared drug used to treat serious infections. A vanc TROUGH is obtained when you expect the patient to be treated for a serious/life-threatening infection, to be treated with other nephrotoxic medications at the same time, or to be treated for >4 days. A trough should be obtained within 30 mins before the 4th dose.

A vanc PEAK is obtained less frequently, when high penetration of a hard-to-reach space is required (osteomyelitis or endocarditis). It should be obtained an hour after vanc finishes infusing.

A RANDOM vanc level should only be obtained in patients on dialysis or with severe renal disease.