Why is dialysis free?

Today, I’ll be touching on kidney failure and the reimbursement structure in the United States. As we all know, there’s been decades of debate regarding universal healthcare in the US. However, dialysis is different – lucky for you, your kidneys are completely covered under Medicare.

What part of kidney disease is covered under Medicare?

In 1972, President Nixon and Congress signed a bill ensuring free dialysis and renal transplants for US citizens. On average, Medicare covers 80% of dialysis costs. Medicare covers most of the costs for kidney transplants, and Medicare B covers 80% of immunosuppressant medication costs.

Quick stats:

  • Roughly 750,000 people in the US have kidney failure

  • ~550K patients get dialysis each year, and the numbers each year keep rising.

  • ~200K patients have kidney transplants in the US.

  • Over 100,000 patients are on the kidney transplant list. ~20-22K patients get kidney transplants each year.

What’s the cost to Medicare?

On average, each dialysis patient costs Medicare about $90,000/year. This totals $28 billion/ year, and composes roughly 7% of Medicare spending. 

The racial disparities:

African Americans represent 35% of dialysis patients, despite making up only 13% of the US population. Hispanics/Latinos, Native Americans, and Pacific Islanders are also much more likely to have kidney disease.

Types of dialysis:

There are two types of dialysis: hemodialysis and peritoneal dialysis. About 90% of US patients get hemodialysis in the US.

~12% of ESRD patients receive HD at home in the US, while the remainder receive it at dialysis centers. Not all countries work like this. Some countries favor peritoneal dialysis at home. For reference, over 80% of ESRD patients get peritoneal dialysis at home in Hong Kong.

The controversies:

I’m not going into the controversies too much about in-center dialysis. You can quickly Google it, or ask John Oliver about it. Just a few things to note: the US has some of the highest mortality rates for ESRD patients in the world, despite the highest spending. Shocking, I know. There are some theories about this: 

  • Per federal guidelines, a doctor does not need to present at the HD center. 

  • Only one nurse must be present at the facility. Many for-profit dialysis centers have minimal staffing.

  • Quick patient turnover leading to poor sanitation practices and higher infection rates.

Morbidity & mortality:

Not surprisingly, kidney failure portends a bad prognosis. There’s a 20% mortality rate within 1 year of starting HD, with a large fraction falling into the initial 90 day period. The 5 year survival rate is about 50%. 

On the other hand, kidney transplant receivers have a survival rate > 80% over 5 years.

The 2 most common causes of death for dialysis patients are:

#1 Cardiovascular disease and sudden cardiac death

#2 bacteremia (26x higher risk than the general population)

  • ¾ are from gram+ bacteria. Most commonly from Staph Aureus, MRSA, Staph epidermidis. 

  • Also gram- ¼ of the time: E Coli, Klebsiella.

Tell me more about home hemodialysis?

There are three types of *home* hemodialysis (not peritoneal dialysis.) It takes a bit of legwork for a patient to arrange this, but it is possible.

  1. Conventional home HD: Q2D, 3-4 hours long; just like the center

  2. Short daily home HD: 5-7 times per week, lasting about 2-3 hours

  3. Nocturnal home HD: QD or Q2D, lasting roughly 6-8 hours

****If there is ANYTHING to take away from this post, please remember this:****

Some patients are never informed about kidney transplants. I recommend quickly having a conversation with your dialysis patients to ensure they are educated about it. As you can see from above, there’s a huge survival benefit. Patients have to contact a transplant center to get added to the waitlist: https://optn.transplant.hrsa.gov/about/search-membership/ 

References:

https://www.washingtonpost.com/news/powerpost/paloma/the-health-202/2019/07/11/the-health-202-the-government-funds-kidney-dialysis-for-all-who-need-it-but-the-program-needs-fixing/5d25f517a7a0a47d87c570ac/ 

https://www.kidney.org/atoz/content/homehemo 

https://pharm.ucsf.edu/kidney/need/statistics#:~:text=Hemodialysis%20care%20costs%20the%20Medicare,patient%20care%20is%20%243.4%20billion

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5099594/


Salicylate Poisoning

Welcome to today's POTD: Aspirin overdose, and by extension, salicylate poisoning!

Background: Salicylates are found in a lot of over the counter drugs and "natural" remedies. Most commonly in the form of Aspirin (acetylsalicylic acid, or ASA), it also exists in Pepto-Bismol, Maalox, Alka-seltzer, and the classic stem question, Oil of Wintergreen. Aspirin is rapidly converted to salicylic acid in the body. Fun fact: Aspirin used to exist as Aspergum, with each stick dosed at 227mg of aspirin. You even had your choice between orange and cherry flavors. Discontinued in 2006.

Normally, at therapeutic levels, aspirin is ingested and absorbed in the stomach. It makes its way to the blood stream, and almost all of it is bound to protein. It is first metabolized by the liver, and these metabolites are then excreted by the kidneys into the urine.

This method of metabolism is quickly overwhelmed in overdose. More free salicylate exists unbound by protein, and the liver's ability to detox becomes saturated. Elimination then proceeds via renal elimination, which is much slower.

Pathophysiology and Symptoms:

The effects salicylates have on specific organs and generalized metabolism are what produce its toxicity.

Acid Base Abnormality

-Salicylates directly stimulates the medullary respiratory center, causing hyperventilation. This hyperventilation blows off CO2 and leads to a respiratory alkalosis. This is usually the first acid-base disturbance.

-This is followed by an anion gap metabolic acidosis. Salicylates uncouple oxidative phosphorylation in the mitochondria, leading to a reliance on anaerobic metabolism and a resultant increase in lactic acid. Build up of organic acids lead to a metabolic acidosis. This is on top of the original respiratory alkalosis, leading to a mixed acid-base picture.

Uncoupling oxidative phosphorylation produces heat; patients are usually hyperthermic.


Tinnitus: Salicylate is ototoxic, and can cause temporary hearing loss and reversible tinnitus. Symptoms usually subside 1-3 days following cessation of salicylate cessation.


Vomiting:

Aspirin and salicylates are gastric irritants, and in overdose, leads to direct stimulation of the chemoreceptor trigger zone in the medulla that causes vomiting. Large amounts of emesis may also create a metabolic alkalosis.


AMS and seizures: Salicylates can cross the blood brain barrier, and can build up in the CNS. This can cause AMS in three different ways: through direct toxicity to CNS through acidemia, neuroglycopenia (through increased demand in CNS), and cerebral edema.


Pulmonary edema and acute lung injury: Salicylate toxicity leads to increased pulmonary vascular permeability.


Arrhythmia: Acidosis and electrolyte disturbances lead to cardiac arrhythmia through altering membrane permeability of cardiac myocytes. 

Bleeding: Acidosis lead to thrombocytopenia and platelet dysfunction.

Word to the wise: Aspirin as a means to suicide is often accompanied by a coingestion of one or more medications. Have a low threshold to check levels/treat for other common overdoses.


Workup:

ASA, Acetaminophen, and levels of any other suspected measureable coingestant

BGM, CBC, BMP, repeated blood gas, mag, phos, UA, utox, coags, LFTs

CT head, EKG, CXR, KUB

Treatment:

These patient are potentially SICK. As always, start with you ABCs.

Airway and Breathing: These patients are tachypneic and may go on to develop respiratory distress when they can no longer compensate for their metabolic acidosis. However, for similar reasons to your DKA patients, avoid intubating if possible. It will be difficult to match the patient's respiratory drive, and the short period of apnea occurring when intubating may spell disaster for your patient.

Circulation: These patients are usually volume down from insensible losses and from vomiting. Help them out with some IVF. Be wary if there are signs of cerebral edema pulmonary edema.

Consider activated charcoal and whole bowel irrigation for decontamination.

Administer glucose. There is a real risk of neuroglycopenia, even if plasma levels are normal.

Alkalinize that urine: Providing sodium bicarb helps alkalinize the urine, facilitating renal clearance and also helps with decrease in CNS/plasma levels of salicylic acid. Alkalinization (increasing pH) increases conversion of salicylic acid to its base form.

Dosing is 1-2meq per kg bolus followed by infusion of 100 to 150meq in 1L sterile water with 5% dextrose.


Correct electrolyte abnormalities.

DIALYSIS: Indications are as follows:

AMS or cerebral edema, pulmonary edema, AKI/chronic kidney disease as this will impair salicylate clearance, salicylate level >90, pH <7, or if patient continues to get worse despite care.

Keep your nephro, tox, and ICU friends handy.

Special notes:

AVOID ACETAZOLAMIDE: though it may make sense to try to alkalinize urine via acetazolaminde, it does it at the cost of reducing bicarb reabsorption.

Chronic Salicylate poisoning: Occurs in patients who routinely take salicylates, and sometimes to the point of excess. More common in young children and elderly patients. Symptoms may be all of the above, but the levels of salicylate may be normal or only mildly elevated. Have a lower threshold for dialysis.

Sources:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341117/

https://wikem.org/wiki/Salicylate_toxicity

https://www.uptodate.com/contents/salicylate-aspirin-poisoning-in-adults

https://www.ncbi.nlm.nih.gov/books/NBK499879/

 · 

Stop Giving Amps of Bicarb!

Chapter 1: What dafuq is in an amp of bicarb?

Take a look!

  • 50mL

  • 8.4% NaHCO3 -> 50mEq

  • The osmolarity of this solution is 2,000mOsm/L - twice that of 3% saline. < (click for emcrit)

Screen Shot 2020-11-05 at 7.56.02 PM.png

Chapter 2: Sodium bicarbonate doesn't just magically raise pH...

Remember this thing?

CO2 + H20 <=> H2CO3 <=> HCO3 + H

It's complicated. Bicarb binds to acid. Then it turns to CO2 and water, so you can breathe it out.

Basically if you're giving bicarb, you can only raise your pH as long as you can breathe off your CO2, increasing your RATE or VOLUME.

**This is particularly a problem in patients who are not in control of their breathing (vented), aren't breathing (arrest), or who have maximized the efficiency of their breathing (Kussmal breathing in DKA).**

That's right - you need to increase your minute ventilation to have a change in pH.

Here's Weingart's take.

Chapter 3: Sodium bicarb amps can cause harm!

FIRST:

One amp of bicarb is like giving 100cc of 3% hypertonic saline!! But as Josh Farkas points out, we typically have no hesitation giving "a couple of amps of bicarb."
This is a huge osmotic load which can lead to huge fluid shifts - prepare for that amp to increase intravascular fluid by 1/4 liter with every push. (Is this what you want to give to your renal failure pt? Your heart failure pt?)

SECOND:

You are worsening acidosis.
What? Huh? But I thought...
No. Stop. Shush. You're worsening acidosis.

Remember, you're increasing CO2 - whether you can breathe it off or not, this CO2 rises in but blood BUT ALSO rises in the tissues and may worsen acidosis in these tissues. < (click for litfl.com article)

THIRD:

Be ready to cause hypernatremia - expect a rise of 1mEq Na per amp of bicarb.

FOURTH:

Extravasation can cause tissue necrosis.

FIFTH:

CSF acidosis, hypocalcemia. Increased lactate. (Some may argue that's not a bad thing.)

If you do manage to fix the acidosis, you can overshoot and create an alkalosis and even screw up the oxygen dissociation curve (in a bad way).

Chapter 4: It just doesn't f&$%ing work
Cardiac arrest: it doesn't do anything. No increased survival. and AHA says it should not be given routinely.

Lactic acidosis: There's a whole section on UpToDate - there's minimal research for pH < 7.1 so you can consider it at that point... but otherwise, nah.

DKA: Take it from a nephrologist: In ketoacidosis, it is almost never necessary to give bicarbonate even though the patient is bicarbonate deficient unless renal function is permanently impaired. Therapy with fluids and electrolytes restores extracellular volume and renal blood flow, thus enhancing the renal excretion of acid and regenerating bicarbonate.

Hyperkalemia: Amps of bicarb, even in hyperK emergencies, have not been shown to lower potassium. Click that UpToDate link or listen to Scott Weingart talk about it on EMRAP.
Patients with hyperK should be started on isotonic bicarbonate drips for 4-6hours, a treatment that works better in acidotic patients.

CHAPTER 5: Soooo who gets bicarb?
AMPS:

  • Bicarb ampules in sodium channel blockade (like TCAs) are, as Dr. Bogoch said yesterday, the cornerstone of therapy

  • Bicarb ampules may be appropriate to alkalinize urine in certain toxicities

  • Seizing hyponatremic patients

DRIPS:

  • Appropriate in hyperK patients who can handle fluid

  • Appropriate in patients with AKI and pH < 7.2 (BICAR-ICU Trial)

  • May be appropriate for pH < 7.0 or 7.1, depending on who you talk to...

**If the pH is < 7.1 and you wanna give an amp of bicarb, there isn't enough data to say you're wrong. If it's a last-ditch effort, you might as well.

https://www.uptodate.com/contents/bicarbonate-therapy-in-lactic-acidosis?search=sodium%20bicarbonate&source=search_result&selectedTitle=3~148&usage_type=default&display_rank=2

Other references embedded in text.