Category: Intensive Care Unit

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Intensive Care Unit Medical Economics

An Epidemic Of Endocarditis

Last week, I was called about triaging a patient to the intensive care unit. A 38-year-old woman had come to a rural Ohio hospital emergency department with sepsis and chest x-ray changes that looked like septic emboli. She uses intravenous heroin.

The opioid epidemic in the U.S. has primarily received a lot of press because of the exponential rise in overdose-related deaths and the recent use of intranasal naloxone to revive patients with opioid overdose. But America’s heroin and fentanyl epidemic has had another result that no one talks about… the recent epidemic of endocarditis.

15 years ago, the primary risks for infective endocarditis were mitral valve prolapse and rheumatic heart valvular disease. We taught our medical students to look for Roth spots in the retina and splinter hemorrhages under the fingernails. Why? Because most endocarditis was the result of infection of the mitral and aortic valves on the left side of the heart, resulting in showering of the body with little bits of infected material that flowed through the arterial blood and embolized the retina or small blood vessels under the nails. But things have changed and now we see much more tricuspid valve endocarditis from IV drug use. Rather than embolizing the peripheral arterial system, the infected bits break off of the tricuspid valve and embolize the lung.

This summer, the Center for Disease Control reported on how the increase in IV drug use has resulted an increase in endocarditis in North Carolina. From 2010 to 2015, endocarditis resulting from IV drug use increased 12-fold. The total cost of hospitalization increased 18-fold, from $1.1 million/year in 2010 to $22.2 million per year in 2015. The median hospital charge per patient was $54,281. Most of these patients were young (under age 40), non-Hispanic white, and from rural areas. They were also usually low-income, with 19% uninsured and 22% on Medicaid. That means that for 42% of these patients, the costs are ultimately covered by society and not by private insurance or by the individual patient.

From personal experience, I can tell you that the same thing is happening in Ohio. And if the experience in North Carolina is representative of what is happening in the rest of the country, then by extrapolating by the population of North Carolina compared to the U.S., then our country spent $707 million treating 8,724 patients with endocarditis from IV drug use in 2015. And at that pace, we will be well over $1 billion this year. Even more, because 36% of patients with endocarditis from IV drug use also have hepatitis C, to treat the hepatitis C in these patients alone adds another $300 million per year.

Treatment of IV drug users with endocarditis is complicated. If you treat them medically, with antibiotics, then you are often faced with a prolonged course of intravenous antibiotics. The means placing a PICC line and either keeping them in the hospital for prolonged periods of time (at a huge cost) or discharging them with a ready-access for them to inject themselves with more drugs. Although oral antibiotics have been used in selective patients with tricuspid valve endocarditis, even this can be challenging since IV drug users are often not very good about taking their medications reliably or showing up for their clinic appointments.

Surgery is even more problematic. Patients with endocarditis from IV drug use have a very high rate of IV drug use recidivism and if you treat the endocarditis with an artificial heart valve, there is a much higher risk of another bout of endocarditis involving the artificial valve. Also, if an artificial valve is placed that requires chronic anticoagulation, there is the risk of the valve thrombosing if the patient is not compliant with anticoagulants. These patients do not fare well long-term: studies show that about one-half of patients with endocarditis from IV drug use treated with surgery are dead within 2 years. Many surgeons will not operate on IV drug users with endocarditis unless they are in a drug rehab program.

From the hospital’s standpoint, these patients are like hot potatoes, no one wants to be stuck with them because they will likely be in the hospital for at least 6 weeks getting IV antibiotics and the hospital will take a financial loss on each patient. Because management of the patients almost always requires cardiothoracic surgery consultation (even though we know up front that the surgeons will likely decline doing surgery), the patients get transferred up the hospital chain to large hospitals that have heart surgeons with experience operating on infected heart valves. Therefore, the cost of these patients is borne mainly by tertiary care hospitals, most commonly our nation’s academic medical centers.

The total costs of IV drug use-associated endocarditis are enormous. If the patients are treated only to die from continued drug use (as is the case with half of those getting heart surgery), they they never get a chance to become employed and to be tax-paying contributors to society. If they are treated but become disabled, then they incur decades of Social Security disability costs and Medicare costs. These are all over and above the $54,000 cost incurred by the initial hospitalization. The ultimate solution is to get Americans to quit using intravenous drugs. But that is not going to happen anytime soon.

August 31, 2017

Categories
Intensive Care Unit

Living Longer Or Dying Longer

Much of my clinical practice is in the intensive care unit. Currently, health care costs Americans 17.5% of the gross domestic product and ICU costs account for about 4% of health care. Therefore, I practice in a service area that accounts for nearly 1% of the gross domestic product of the United States. Therefore, it is incumbent on me to be a good steward of ICU resources.

It is pretty common for a patient to be admitted to the ICU and to be placed on life support: a mechanical ventilator, dialysis, vasopressor medications, etc. If the patient did not leave clear written advance directives, then it is up to the family to decide about the use of life support equipment. All to often, the family members’ instructions to me are “We want everything done, doc”. Having everything done means one thing when you are talking about a 30-year-old with severe asthma, but having everything done means a totally different thing when you are talking about a patient in a permanent coma from a large stroke or widely metastatic terminal cancer or severe multiple organ systems failure for which there is no reasonable chance of surviving. From the family members’ perspective, having everything done equates to being an advocate for the patient and is a measure of their love for the patient.

The way I approach this is to tell the family that we now have tremendous life support tools that we can use on patients but these life support measures were created to bridge patients through reversible illnesses so that the patient can return to a reasonably normal life. The problem with these life support measures is that sometimes, all they do is prolong the process of dying. We therefore have to decide for each patient when the life support is going to make them live longer or just make them die longer. I tell them that it is my job as the physician to tell the family when I think the patient has reached a point that the life support is merely prolonging their death. When put this way, most family members will opt to not escalate life support if all that life support will do is to prolong death. It gives the family another way of showing how much they care about their loved one by avoiding unnecessary suffering and pain.

I’m in a unique position. When I was a college student, before I became a doctor, my father was in the ICU at the Ohio State University medical center. He had advanced leukemia that was no longer responding to chemotherapy and was on a mechanical ventilator with sepsis and respiratory failure. The decision that my family and I was presented with was whether or not to start him on dialysis. I said no and 37 years later, I still think that was the right decision. All it would have done was make dying longer.

May 14, 2017

Categories
Emergency Department Intensive Care Unit

What Do You Do If You Can’t Intubate The Patient?

At our larger, tertiary care, University Hospital, we have a “difficult airway team” with an experienced anesthesiologist with a surgeon for back-up available in the hospital 24-hours a day. At University Hospital East, we don’t have a difficult airway team in the hospital at night and the anesthesiologist and surgeon have to be called in from home when a difficult-to-intubate patient develops respiratory failure. In the operating room, the percentage of patients with a difficult airway is 1-4% but in the ICU or ER, it is as high as 20%. So what can the hospitalist or emergency room doctor do to ventilate the patient for the 20 minutes it takes before help arrives? 15 years ago… not much. But now, we have a lot of devices that we can use when an endotracheal tube cannot be placed. Here are some of the more common ones:

  1. The video laryngoscope. One of the first of these to come to market was the Glidescope®. Similar devices include the McGrath, the King Vision®, the IntuBrite®, the APA™, the C-MAC®, and the Marshall Video Laryngoscope®. These laryngoscopes have largely replaced the rigid steel Macintosh and Miller laryngoscopes in many hospitals. They are easier to use and improve intubation success for less-experienced physicians. Many EMS units now carry them in their emergency squads. In our hospital, we have Glidscopes available in our ICU, OR, and ER. We still use standard laryngoscopes in our intubation kits that are in our crash carts but the respiratory therapists can get a Glidescope to the bedside on very short notice. They have been shown to double the likelihood of a successful intubation on the first pass of the endotracheal tube and can reduce the time of intubation to one-third the time it takes with a standard laryngoscope. Watch a video of how to use the Glidescope here.
  2. The bougie. Think of this as a guide wire for an endotracheal tube. Many times, when looking at an airway with a laryngoscope, you can see part of the vocal cords but not enough to confidently pass an endotracheal tube. Or, you may be able to get a good look at the vocal cords but as soon as you introduce the endotracheal tube, you obliterate your view. The bougie can solve this problem by being being small and semi-rigid. Also, it is colored blue so it is easy to see the tip of it, even if the is a lot of blood, fluid, or floppy laryngeal tissues covering up the vocal cords. Once you pass the bougie into the trachea, you then simply slide an endotracheal tube over the bougie and into the airway. If you can’t slide an endotracheal tube over the bougie, you can put an adaptor on the end of it and at least blow oxygen through it. Watch a video of how to use a bougie to facilitate intubation here.
  3. The laryngeal mask airway (LMA). These are very simple to insert and in fact, anesthesiologists will often use them during short duration surgeries to ventilate patients in the operating room. They require little skill to place and can ventilate patients sufficiently until you can get someone with advanced airway skills into the hospital to place an endotracheal tube. The LMA consists of an elliptical inflatable cuff that is inserted into the mouth (after lubricating it) and over the top of the tongue, along the hard palate until you meet resistance. You then inflate the cuff. In the middle of the cuff, is an opening that leads to the ventilation tube. When the cuff is inflated, it occludes the esophagus so that air coming out of the port can only go one way – down through the vocal cords into the trachea. They do need to be secured, particularly when transporting a patient, because if they migrate out of the mouth, air may not go into the trachea properly. Watch a video of insertion of an LMA here.
  4. The Combitube. This is somewhat similar to the King airway (see below). It is a fool-proof tube that you place into the mouth so that it can either go into the esophagus or the trachea – it will usually go into the esophagus. Either way, you can ventilate the patient. Inside the Combitube, there are two tubes – one with an opening at the distal tip of the tube and one with an opening on the side of the tube about a third of the way back from the distal tip. There are two balloons on the Combitube – one at the tip and one about half way back from the tip. So, if the tube goes into the esophagus, then you blow both the proximal and the distal balloon up and ventilate through holes on the side of the Combitube. The distal balloon prevents air from going into the stomach and the proximal balloon prevents air from going back out of the mouth. If the Combitube ends up going into the trachea, then you can ventilate the patient through the distal tip of the tube. If you are not sure where the tube is, you can use an end-tidal CO2 detector connected to each of the two ports of the Combitube to determine if you are in the esophagus or the trachea. Watch a video of how to place a Combitube here.
  5. The King airway. This looks a lot like a Combitube but it is designed to only go into the esophagus. Although there is a hole at the distal tip, it is only there in order to pass an NG/OG tube through it into the stomach and not designed to ventilate through it. Ventilation is through the side ports. Like the Combitube, the ventilation holes in the King airway are on the side of the tube, in between the two balloons. In a study of 27 emergency medical responders comparing the King airway to the Combitube, the King airway insertion time was 24 seconds and the Combitube insertion time was 38 seconds; the King airway was perceived by the responders to be easier to place and was preferred over the Combitube by 26/27 of the participants. Watch a video of how to place a King airway here.
  6. The nasal intubation. OK, so this is not exactly a new device. This is an old-school approach that I was taught to use for difficult airways back in the early 80’s, before LMAs, King airways, and Glidescopes were invented. You simply liberally lubricate a small (#7 or #6) endotracheal tube and insert it into the nares like you would a nasogastric tube. A little neosynephrine in the nose will open things up and make passage of the tube easier. Once the endotracheal tube makes the curve in the back of the pharynx, you listen over the end of the tube (or, better yet, place an end-tidal CO2 monitor on the end of the tube). If you position the patient’s head in the “sniffing position” (as opposed to bending the neck forward like you would when inserting a nasogastric tube) then you will have more success getting the tube to go into the trachea instead of the esophagus. Insert following the breath sounds (or end-tidal CO2 waveform) until you are in the trachea. This is a particularly useful approach when you can’t open the patient’s mouth fully to insert an endotracheal tube orally and can also be useful in the patient with angioedema. Watch a video of how to place a nasotracheal tube here.

The whole idea of using any of these techniques is to be able to ventilate the patient as quickly as possible. So when should they be used in the hospital? First, if the physician is not trained or proficient in performing endotracheal intubation with a standard laryngoscope – there is just too much that can go wrong such as placing the endotracheal tube in the esophagus or causing airway trauma that can create difficulty even for the skilled operator who performs an attempt later. Second, if the physician cannot get the patient intubated quickly using a standard laryngoscope – my rule is that if it takes 3 tries, you need to go to another option. If all else fails, then the cricothyroidotomy is the procedure of last resort. The last time I did one of these was on a dog during an Advanced Trauma Life Support course in 1983 and I hope that I never have to do one again.

If you are on call by yourself in the hospital at night, make sure you know what is available because when you are responding to a cardiorespiratory arrest and you encounter a difficult airway, you’re not going to have time to go to a computer and search the internet for advice.

February 28, 2017

Categories
Intensive Care Unit

2,3-DPG Is A Wonderful Thing

Yesterday, I responded to a code blue in one of the procedural areas of our hospital. The patient had severe hypoxemia due to flash pulmonary edema from combined systolic + diastolic heart failure and then had an IV dye load that tipped him over into pulmonary edema. He had a previous tracheostomy and still had a residual stoma that had not entirely closed. We put an endotracheal tube into the stoma until we could obtain a large enough tracheostomy tube to fit his tracheal diameter. Despite mechanical ventilation with 100% oxygen and a very high level of PEEP (positive end-expiratory pressure), his oxygen saturation stayed in the 70’s and 80’s for at least a half hour.

If that had happened to me, I would likely have severe anoxic brain injury. Yesterday, we had 4 patients in our ICU with severe anoxic brain damage that had been admitted after suffering cardiorespiratory arrests. But the patient who coded yesterday is waking up just fine this morning. So why do some patients get anoxic brain injury from prolonged hypoxemia and others seem to get by without any brain damage? I think it comes down to the wonders of 2,3-DPG.

2,3-diphosphoglycerate (2,3-DPG) is a chemical normally present in relatively small amounts in red blood cells. Its job is to change how oxygen binds to hemoglobin in order to make oxygen fall off of hemoglobin more easily so that when a red blood cell passes through vital organs (like the brain), more oxygen can be released by that red blood cell. Normally, a red blood cell will release about 25% of its oxygen as it passes through tissues; it then goes to the lungs and re-loads with oxygen. 2,3-DPG makes the red blood cell release more oxygen. This is particularly important in people who are traveling to high altitude (e.g., mountain climbers) and people who chronically are hypoxemic (e.g., patients with untreated sleep apnea). A normal person will have an oxygen saturation of nearly 100% as blood leaves the lungs; the red blood cells will release about 25% of its oxygen in the tissues so that the oxygen saturation is about 75% when that venous blood returns to the lungs. If you are at high altitude, your arterial blood’s oxygen saturation may only be 80% and if the red blood cells can only release oxygen down to a saturation of 75% as they pass through the tissues, then there isn’t much oxygen being released and the tissues can be starved for oxygen. 2,3-DPG allows the red blood cells to release oxygen down to a saturation that is much lower than 75%, say 60%, so that enough oxygen is being off-loaded into the tissues to keep them functioning normally. From a physiologic standpoint, we call this a “right shift of the oxyhemoglobin dissociation curve”.

One of my heroes is Lonnie Thompson. He is an OSU Professor of Earth Sciences. He is arguably one of the most renowned faculty members at the Ohio State University and his research involving high-altitude glacial ice core samples has led him to spend more time at extreme altitude than any other human in history. 2,3-DPG is one of the main reasons he can do it.

My patient yesterday most likely had non-human high levels of 2,3-DPG that allowed him to come through a period of prolonged hypoxemia unscathed. And that got me wondering. What if I could bottle 2,3-DPG and put it in a syringe? Who would I give it to? Here is who I would give an amp of 2,3-DPG if I could:

  1. Everyone in a cardiopulmonary arrest. I would change the ACLS algorithms to push 2,3-DPG even before giving epinephrine every time cardiopulmonary resuscitation was required.
  2. Patients with unstable angina. If a coronary artery was partially blocked, wouldn’t it be great if you could off-load every last oxygen molecule from the red blood cells that did get through to the myocardium?
  3. Jehovah’s Witnesses undergoing surgery. It is every surgeon nightmare who operates on a Jehovah’s Witness – that there will be unforeseen bleeding in a patient that you can’t give blood transfusions to. An infusion of 2,3-DPG would allow you to get more out of what little blood the patient has left.
  4. Patients in shock. Ultimately, shock is an imbalance between oxygen consumption and oxygen delivery. Currently, when a patient is in shock, we try to improve oxygen delivery by giving vasopressor medications to increase the blood pressure. I think we’d be far more successful if we could increase tissue oxygen delivery if we gave an IV infusion of 2,3-DPG.
  5. Mountain climbers. If everyone who climbs mountains had Lonnie Thompson-levels of 2,3-DPG, we wouldn’t have to worry about altitude sickness anymore.

It is going to take someone a lot smarter than me to figure out how to make 2,3-DPG into a marketable pharmaceutical. But for now, I’m just really glad that the patient yesterday had a lot more of it than a normal person.

February 24, 2017

Categories
Intensive Care Unit

BRAVE New World In the ICU

Glucometers are one of the most common medical devices in use today. They cost about $20 or $30 to buy at the drugstore and every nursing station and doctor’s office has one. Most of the time, they work great and are very accurate to measure the blood glucose level by pricking the skin to obtain a drop of capillary blood to put into the glucometer.

In 2001, a study published in New England Journal of Medicine showed that tight glucose control in critically ill patients resulted in improved ICU outcomes. In this study, blood was drawn every 1-4 hours and glucose levels were checked on a laboratory chemistry analyzer. In response, ICUs across the country started practicing “tight glucose control” in critically ill patients and this often meant an insulin drip with glucose checks every hour.

But over the next 10 years, outcomes in most ICUs did not improve with tight glucose control and a lot of patients actually did worse. As a consequence, critical care physicians backed off on the tight glucose control strategy. One of the reasons patients did worse may be that in the original study, blood was drawn up in regular blood tubes and sent to the hospital lab but in normal clinical practice, most of the time, the blood to be tested is not in tubes sent to the hospital lab but instead is from a drop of capillary blood tested with a point-of-care glucometer after pricking the skin on a finger.

It turns out that in our sickest patients, glucometers using capillary blood often don’t work. Because of this, the FDA has not approved glucometers for use in critically ill patients with capillary stick specimens and in 2013, the FDA advised against using glucometers in these patients. The problem is that patients with edema, low blood pressure, and poor capillary filling can have inaccurate results from that drop of capillary blood and it may not truly reflect the real blood glucose level. These patients must have regular arterial or venous blood specimens drawn rather than a skin prick capillary blood specimen.

This means that blood must be obtained from a intravenous line, arterial line, or venipuncture. This is a problem for patients who are on insulin drips because they need glucose measurements as frequently as every hour. Since the FDA does not approve glucometers to be used on capillary blood specimens in critically ill patients, their use in these patients is considered “off label” which poses medical-legal risk for using them. The FDA and CMS did not define what “critically ill” means and left this up to individual hospitals to define; at our medical center, we developed the BRAVE criteria to identify those critically ill patients in whom the capillary blood specimens are inaccurate and should not be used:

Blood Pressure: systolic blood pressure < 80 mm Hg or mean arterial pressure < 55 mm Hg.

Reduced capillary refill rate at collection site: capillary refill > 3 seconds

Acidosis from diabetic ketoacidosis or non-ketotic hyperosmolar acidosis

Vasopressors: norepinephrine, phenylephrine, vasopressin, or dopamine (> 5 mcg/kg/min)

Edema: pitting edema at the capillary stick site

For these patients, you need to get regular blood, commonly from a central venous line or an arterial line. In the past, nurses would need to draw a 5-10 ml blood discard to clear the central line or arterial line of saline or other fluids and this would result in a lot of discarded blood (you could waste an entire unit of blood in 3-4 days in patients needing hourly glucose checks). We now use the VAMP system manufactured by Edwards Lifesciences that allows the “discard” blood to be re-infused into the patient.

For documentation purposes in our electronic medical record, our nurses now have to select whether BRAVE criteria are met when documenting glucometer use and then they have to documents what type of blood specimen they are using. If there is a mismatch in the two selections, then the result is flagged by our point-of-care software. Weekly, our point-of-care staff notify the nurses and nurse managers that have mismatches to provide regular feedback to the nurses. We now have data showing a nice weekly improvement in the number of events since inception of the BRAVE program.

nova-stripIf blood was sent to the lab for a regular glucose check, this would require a full blood tube (another 5 ml). In 2014, the FDA approved one brand of glucometer, the Nova StatStrip Glucose Hospital Meter System, to be used on venous or arterial blood in critically ill patients. This is now the glucometer that we use in our ICU. It permits nurses to just draw up less than 1 ml of blood to put in the point-of-care glucometer (rather than filling up a blood tube to go to the lab) and this has greatly cut down on wasted blood.

In medicine, as with many other disciplines, bad data is often worse than no data. By using BRAVE, we can improve the data on glucose measurement in critically ill patients. Going forward, this may allow us to re-think the advisability of tight glucose control in the ICU for critically ill patients by ensuring that we are accurately measuring glucose levels.

December 1, 2016