Categories
Intensive Care Unit

Your ICU Needs More Toothbrushes

Hospital-acquired pneumonia is disturbingly common, affecting about 1% of hospitalized patients. Hospitals have adopted all sorts of strategies to reduce these infections but we have overlooked what is arguably one of the simplest – brushing patients’ teeth.

A new study published this week in the journal JAMA Internal Medicine examined the effects of brushing patients’ teeth on the outcomes of hospital-acquired pneumonia, hospital and intensive care unit mortality, duration of mechanical ventilation, ICU and hospital lengths of stay, and use of antibiotics. This was a meta-analysis that included 15 published clinical trials in 8 different countries. There were 10,742 patients (2,033 ICU patients and 8,097 non-ICU patients); however, after adjustment for cluster analysis (by one study that randomized hospital wards, as opposed to individual patients, to intervention versus control), the total number of patients included in the meta-analysis was reduced to 2,786.

Outcomes

Pneumonia. Overall there was a significant reduction in hospital-acquired pneumonia in all patients randomized to toothbrushing with a risk ratio of 0.67. A similar benefit was noted in reducing pneumonia in ICU patients (risk ratio = 0.64) and patients on mechanical ventilators (risk ratio = 0.68). To put these statistics into perspective, brushing 12 patients’ teeth prevented 1 ventilator-associated pneumonia. There was no benefit to brushing teeth more frequently than twice a day. 

Mortality. There was also a statistically significant reduction in ICU mortality in patients assigned to teeth brushing, with a risk ratio of 0.81. 

Lengths of stay. There was a significant reduction in average duration of mechanical ventilation in patients randomized to toothbrushing (1.47 fewer days on the ventilator). There was also a significant reduction in average ICU length of stay (1.36 fewer days in the ICU).

Other outcomes. There was no significant reduction in total hospital length of stay but only 2 of the 15 studies reported this outcome. There was also no significant reduction in antibiotic use but only 3 of the studies reported this outcome. 

Implications

It has long been believed that oral hygiene is important in ICU patients. To date, most studies have focused on the use of chlorhexidine mouthwashes and older guidelines recommended the routine use of chlorhexidine mouthwashes in order to reduce ventilator-associated pneumonias. However, more recent studies and meta-analyses have not demonstrated a significant benefit of chlorhexidine and newer guidelines have not made recommendations regarding the use of chlorhexidine. In addition, concerns have been raised about the potential harm from drug allergy, chlorhexidine aspiration, and development of resistant bacteria.

Dentists mostly focus on the importance of toothbrushing after eating in order to reduce dental caries. But most patients in the ICU (and all intubated patients) are NPO and thus not eating. The reason to brush teeth in ICU patients is not to prevent cavities but to prevent pneumonias. Because teeth carry a large burden of oral bacteria, toothbrushing can be seen as analogous to hand washing to prevent infections.

Any study of toothbrushing is by necessity non-blinded since it is obvious to the ICU staff whether or not they are brushing their patients’ teeth for them. Therefore, this new data is not as strong as data from randomized, double-blinded, placebo-controlled clinical trials, for example in clinical trials of new experimental medications. Also, it is unclear if there is an advantage to having dental assistants versus nurses do the toothbrushing or an advantage of using a regular toothbrush versus an electric toothbrush. Similarly, it is unclear what kind of toothpaste (if any) is best. In all likelihood, any method of reducing the amount of gunk on patients’ teeth will be effective.

Toothbrushing is simple. And in the ICU, we should do it more often.

December 20, 2023

Categories
Intensive Care Unit

Vacutainer® Size For Blood Testing In The ICU: Smaller Is Better

Blood tests are the cornerstone of laboratory monitoring for patients in the intensive care unit but can result in significant blood loss. Modern laboratory analyzers require smaller volumes of blood than previous analyzers but most ICUs still use large volume blood tubes. A new study shows that ICUs can safely switch to smaller volume tubes that can reduce blood loss.

In the past, most collection tubes used for blood testing were made of glass with rubber stoppers and interior vacuum to facilitate blood filling. Currently, most hospitals primarily use plastic collection tubes that are safer than glass tubes. In the United States, the Becton Dickinson Corporation’s Vacutainer® is the dominate blood specimen tube used in most hospitals. Blood collection tubes are taken to the hospital’s clinical lab where tests are run on laboratory analyzers. The original analyzers required several milliliters of blood to perform testing, however the current generation of analyzers generally require only 0.5 ml of blood (or less) for testing. But blood specimen tube size has changed little over the past 40 years. As a consequence, most blood sent to the lab for testing is unused. Blood tubes come in a variety of sizes and each hospital determines the size of each type of tube to stock. The typical standard-sized Vacutainer® tubes used in most U.S. adult hospitals are as follows:

When drawn directly from a peripheral vein, no blood needs to be discarded for most laboratory tests. However, when drawn from a central venous catheter or a tunneled catheter, the initial aliquot of blood removed should be discarded since it can be diluted by electrolyte-containing IV fluids or catheter flushes used to maintain catheter patency. The recommended discard volume varies between hospitals but is typically 5 or 6 ml.

Let’s take a typical example of a patient with a central venous catheter admitted to the ICU with sepsis requiring regular blood draws consisting of a chemistry panel, CBC, and lactate every 6 hours plus a PTT/INR every 12 hours and a vancomycin level daily.

  • Discard x 4 = 20 ml
  • Chemistry x 4 = 28 ml
  • Lactate x 4 = 16 ml
  • Hematology x 4 = 12 ml
  • Coagulation x 2 = 9 ml
  • Drug level x 1 = 7 ml
  • TOTAL DAILY VOLUME = 92 ml

The average 70 kg healthy adult has 5.3 liters of blood (5,300 ml). Therefore, blood loss for laboratory test specimens in this patient would be 1.7% of the blood volume per day. For a 5-day ICU stay, this would add up to 8.7% of the blood volume or 460 ml. This is also the volume of 1 donated unit of blood. Many critically ill patients are already anemic at the time of ICU admission and thus start off their ICU stay with a much lower amount of red blood cells than a normal healthy person, thus compounding the effect of blood removal for lab testing. This is a significant amount of blood and can affect oxygen carrying capacity of the blood to target tissues. It can also mean the difference between whether or not a patient needs a blood transfusion. The unfortunate irony is that most of this blood gets wasted.

In the past, the threshold hemoglobin level in the ICU to order a blood transfusion was 10.0 g/dL. More recently, that threshold has dropped to a hemoglobin level of 7.0 g/dL for most ICU patients based on clinical studies indicating that ICU patient outcomes are better when using the lower hemoglobin value. The effect of blood loss for laboratory testing will be greater for patients who are already anemic in whom lab testing-related blood loss is more likely to push the hemoglobin below the 7.0 g/dL level and thus require transfusion.

Reducing blood collection tube size

A study in this week’s JAMA examined whether ICU patient outcomes can be improved by changing to smaller Vacutainer® tube sizes. This was a large study involving 21,201 patients in 25 ICUs in Canada. Patients had specimens drawn into standard-size blood collection tubes (4 -6 ml) or small tubes (1.8 – 3.5 ml). Red blood cell transfusion was less common in patients assigned to the small volume tubes (10 units of RBCs fewer per 100 patients). The drop in hemoglobin level was also lower in small volume tube patients. The frequency of specimens with insufficient quantity of blood for analysis was not higher using low volume tubes (in fact, it was statistically significantly lower when using the smaller-size tubes).

The implication of this study is that ICUs can safely shift to use of small volume blood collection tubes without risk of an insufficient quantity of blood to perform laboratory tests. By changing to small volume tubes, ICU patients have a smaller ICU-related drop in hemoglobin and require fewer units of transfused blood during their ICU stay. This should come as no surprise to pediatricians who have successfully used smaller volume blood tubes for many years to perform the exact same blood tests ordered in adult ICUs.

Reducing blood discard volume

A 2021 study in the Journal of Laboratory Physicians examined whether a 3 ml blood discard volume was as good as a 5 ml blood discard volume in patients with central venous catheters. There was no significant difference in chemistry lab test results between specimens obtained after the two discard volumes. The implication is that ICUs can shift to using smaller discard volumes, thus further reducing ICU-related blood loss.

A typical triple lumen central venous catheter has 3 lumens that are each either 18 gauge (1 mm) or 16 gauge 1.3 mm) in diameter. The catheter length is selected based on which central vein is chosen for insertion and is either 15 cm or 20 cm. The volume of each lumen can range from 0.12 ml to 0.27 ml, depending on lumen gauge and catheter length. PICC line lumens are typically 18 gauge and are 50 – 60 cm in length. This equate to a lumen volume of 0.47 ml. Thus, even using a 3 ml blood discard volume allows for several times the volume of fluid contained in the catheter to be removed before obtaining venous blood through a triple lumen central venous catheter or a PICC line.

Implications for ICU policies

When it comes to blood draws for lab testing in the intensive care unit, less is more. We can reduce ICU-related blood loss and reduce blood transfusions in ICU patients with several policy changes.

  • Reduce standard central venous catheter blood discard volume to 3 ml.
  • Change to small volume Vacutainer® tube sizes. The vast majority of laboratory tests can be performed using 1.8 to 3.5 ml tubes.
  • Consolidate blood draw time intervals. Avoid ordering some blood tests at 6 hour intervals and others at 8 hour intervals – this results in six or seven blood draws per day, wasting excessive blood for discards and occupying valuable nursing time.
  • De-escalate lab testing as soon as clinically indicated. The need for lab tests and test frequency should be reassessed on a daily basis and incorporated into multidisciplinary rounds checklists.

Simply reducing the blood discard volume to 3 ml and changing to smaller volume blood collection tubes should reduce ICU-related blood loss from lab testing by 50%. These policy changes should not be made unilaterally by any one hospital leader. Ideally, these should arise from a consensus of the laboratory medical director, the ICU medical director, the ICU nurse manager, and the director of hospital supply. The reasons for the change should also be communicated to all of the nurses and physicians who practice in the ICUs in order to ensure a consistent message to the hospital staff. Smaller volume blood collection tubes can also be well received by patients and families who in the past have frequently raised concern about the volume of blood regularly removed from ICU patients for lab test purposes.

Overcoming inertia

There is always resistance to change in our intensive care units. We get comfortable with certain practices because that is the way that we have always done things and because we fear that any change could have deleterious effects on patient outcomes. Change in the ICU should be steered and not forced. New findings in the medical literature now make reducing blood loss for lab testing a change that will be much easier to steer.

November 24, 2023

 

Categories
Emergency Department Intensive Care Unit

It’s Time To Trade In Your Direct Laryngoscope

Emergency endotracheal intubation is commonly performed in patients with cardiac arrest, loss of consciousness, or severe respiratory failure. A study published this month in the New England Journal of Medicine found that emergency intubation using video laryngoscopes is more successful than intubation using direct laryngoscopes. In the hospital, emergency intubations typically occur in the emergency department, intensive care unit, or in a regular hospital bed and these patients are by definition physiologically unstable. In contrast, elective intubations are performed in the operating room under controlled conditions in surgical patients who are usually physiologically stable. Over the decades, I have performed or supervised hundreds of emergency intubations and there are always two goals: (1) do it fast and (2) do it right the first time. During the emergency intubation procedure, the patient is unable to breath effectively and if too much time is taken or too many attempts are required, the patient can become dangerously hypoxemic.

Direct laryngoscopy

For years, the only way to intubate a patient was by using a direct laryngoscope. There are two main types, the Macintosh laryngoscope and the Miller laryngoscope. Both have a handle that contains batteries and a blade that is inserted into the mouth to pull the tongue out of the way in order to get a view of the vocal cords. In the blade of the direct laryngoscope, there is a small light bulb to help improve the ability to see the vocal cords. Once the laryngoscope is inserted into the mouth, a plastic endotracheal tube is guided through the vocal cords and into the trachea.

The Macintosh laryngoscope has a curved blade and comes in a variety of sizes. My go-to laryngoscope blade for most of my career was a #3 Macintosh. For large patients, I would sometimes use a #4 Macintosh. The Miller blade is straight. I personally found it harder to use for most patients but it was sometimes helpful for obese patients and in situations when I just could not get a good view of the vocal cords with a Macintosh blade. The Miller blade also comes in a variety of sizes. In the past, direct laryngoscopes were reusable after sterilization but most hospitals now use disposable, non-reusable laryngoscopes.

Intubation using a direct laryngoscope requires the operator to be directly behind and above the patient’s face, within a few inches of the mouth. You have to wear a face mask and plastic face shield – it is pretty common to get spattered with sputum, blood, saliva, or vomit. Because you are so close to the patient’s airway, there is also a risk of becoming infected with a contagious microorganism. This was a big danger during the COVID pandemic and we largely abandoned direct laryngoscopy when intubating COVID patients because of this risk.

Video laryngoscopy

About 15 years ago, a new type of laryngoscope emerged on the market that uses a tiny camera at the end of the laryngoscope blade, adjacent to the light bulb. The view from the end of the blade can then be displayed on either a small video monitor attached to the laryngoscope handle or a larger video monitor connected to the laryngoscope by wires. The downside of video laryngoscopes is that they are far more expensive to purchase and maintain than direct laryngoscopes.

 

The video laryngoscope blades are all curved and have a greater degree of curve than the Macintosh blade. Because of this, they require a special curved rigid metal stylet to be inserted into the endotracheal tube. Once the tip of the endotracheal tube is positioned just above the vocal cords, the endotracheal tube is advanced while simultaneously pulling back on the stylet so that the endotracheal tube can assume a straight path in the trachea, below the vocal cords. This usually requires an assistant to control the stylet or an extremely dexterous operator who can control both the stylet and the endotracheal tube with one hand.

There are three main advantages to the video laryngoscope. First, you can get a better view of the vocal cords than with the direct laryngoscope. This is especially true in patients with “anterior” larynxes that are hard to see with direct visualization through the mouth and in patients with large tongues that obstruct direct visualization. The Mallampati score is often used to classify the airways – those with Mallampati class III or IV airways are better seen with the video laryngoscope. Second, the video laryngoscopes allow the operator’s face to be a couple of feet away from the patient’s nose and mouth, rather than a few inches as with direct laryngoscopes. This can reduce the chances of acquiring a communicable disease. For this reason, video laryngoscopy became our preferred approach to intubating patients with COVID infections. Third, it is easier to teach trainees how to perform endotracheal intubation since the attending physician can point out the anatomy and see if the trainee is inserting the endotracheal tube correctly. In contrast, during direct laryngoscopy, only the person actually performing the intubation can see the vocal cords and watch the tube insertion so it is not possible for the attending physician to know if the trainee is performing the intubation correctly.

Which method of laryngoscopy is better?

Anecdotally, our pulmonary/critical care fellows tell me that they get proficient with endotracheal intubation faster using video laryngoscopy than using direct laryngoscopy. They cite the better view of the vocal cords plus the improved feedback from the supervising attending physician. From my own personal experience, I found that video laryngoscopy was particularly useful in those patients who I could not get a good view of the vocal cords during an initial intubation attempt with a direct laryngoscope. But anecdotes are not as persuasive as randomized, controlled, multi-center trials. So, what does the medical literature show?

A 2021 study in JAMA found that worldwide, 81% of emergency intubations are performed using direct laryngoscopy. There have been a number of studies comparing direct and video laryngoscopy for endotracheal intubation. Some have shown that both techniques are equally successful, others have shown that video laryngoscopy is superior, and others have shown that direct laryngoscopy is superior. But until recently, there have been no large, randomized, multi-center trials comparing the two techniques for emergency intubation. In a 2020 review of tracheal intubation in critically ill patients published in the American Review of Respiratory and Critical Care Medicine, the recommendations stated that video laryngoscopy should be available in every ICU and ER and that the first attempt at emergency intubation should be made using video laryngoscopy. The recent study in the New England Journal of Medicine now provides the most convincing evidence to date that video laryngoscopy is superior to direct laryngoscopy during emergency endotracheal intubations.

What the study found. In this study, 1,417 patients undergoing emergency endotracheal intubation at 11 U.S. hospitals in 2022 were randomized to the use of video laryngoscopy or direct laryngoscopy for the first attempt at intubation. 70% of patients were in emergency departments and 30% were in ICUs. Because all of the hospitals were teaching hospitals, the vast majority of intubations were performed by trainees: 72% were by residents and 24% were by fellows. Notably, these are less experienced physicians who have performed fewer intubations than more senior attending physicians. The findings were statistically significant: 85% of patients were successfully intubated on the first attempt using video laryngoscopy but only 71% of patients were successfully intubated on the first attempt using direct laryngoscopy. It also took the operators less time to perform intubation using video laryngoscopy (38 seconds) than using direct laryngoscopy (46 seconds).

What the study did not find. Because the overwhelming majority of intubations (96%) were performed by trainees, it is uncertain whether video laryngoscopy is also superior to direct laryngoscopy when experienced attending physicians are performing emergency intubation. Anecdotally, I believe that video laryngoscopy is superior, at least from my own personal experience using both types of laryngoscopes. The study only examined emergency intubations and not elective intubations (such as occur regularly in the operating room). Therefore, the results do not necessarily mean that we should abandon direct laryngoscopy for elective surgeries. Finally, there were no differences in procedural complications using the two types of laryngoscopes.

So, what should hospitals do?

For the hospital medical director or the medical director of an emergency department or intensive care unit, there are several practical implications from the most recent study:

  1. Training programs should incorporate video laryngoscopy. All health care providers who perform emergency endotracheal intubation should be taught to use video laryngoscopy during their formal training programs. In the United States, emergency intubations can be performed by a variety of providers including residents, fellows, attending physicians, respiratory therapists, EMTs, CRNAs, nurse practitioners, and physician assistants. Each hospital is different, depending on the staff availability, state laws, and hospital regulations. Moreover, emergency intubations in the ICU and during cardiopulmonary arrests often occur at night or weekends when experienced attending intensivists and anesthesiologists are not immediately available.
  2. Make training available to existing staff. Newly trained ER residents and critical care fellows will already be experienced using video laryngoscopy devices and should not be required to undergo additional training as attending physicians. However, it is necessary to have a process in place to train more senior physicians and other health care providers in the use of the equipment. Because internal medicine residents are no longer required to be trained in intubation, at our hospital, we developed a “Difficult Airway Course” for our hospitalists who covered the ICU at night and who responded to cardiopulmonary arrests in the hospital. This included demonstration of the video laryngoscope equipment and opportunity to use the video laryngoscope to intubate manikins. It took less than an hour and was included as part of orientation for new hospitalists. To make training even more palatable, offer CME credit.
  3. Video laryngoscopes should be available wherever emergency intubations are performed. At a minimum, this should include emergency departments and intensive care units. However, cardiopulmonary arrests can occur anywhere in the hospital so there should be protocols in place in order to deploy video laryngoscopes rapidly to any location in the hospital.
  4. Choose a brand (and stick with it). To date, there are no studies comparing one type or brand of video laryngoscopes to another. The decision about which video laryngoscopes the hospital should purchase should be made based on preference consensus of physicians who perform emergency intubation and on cost. In my own experience using multiple types of video laryngoscopes, I recommend choosing one type and then using that one type throughout the hospital, rather than having different types or brands in different hospital locations. Although they are all relatively similar, even a few extra seconds required to figure out how to use an unfamiliar brand of a video laryngoscope during cardiopulmonary resuscitation can result in patient harm.
  5. Buy enough devices. Medical equipment periodically breaks and has to be sent out for repair or replaced. It is important to always have back-ups in event of breakage. In addition, patients do not schedule their need for emergency intubation and there can be several emergency intubations during any given ER or ICU shift. Have enough video laryngoscopes to accommodate multiple intubations occurring simultaneously and if your video laryngoscope requires cleaning and sterilization, be sure you have enough video laryngoscopes on hand to last until equipment can be cleaned.
  6. Don’t completely abandon direct laryngoscopy. Because direct laryngoscopes are inexpensive and small, hospitals can afford to keep them in every crash cart and airway kit. It is prudent to always have a direct laryngoscope on hand in case the video laryngoscope quits working in the middle of an intubation. Furthermore, the availability of multiple sizes and shapes of the direct laryngoscope blades allows a more tailored selection of equipment for patients with larger or more unusually shaped mouths. When it comes to emergency airway management, it is always important to have a back-up plan and direct laryngoscopy is the key component of the back-up plan for video laryngoscopy. The implication is that we must therefore continue to teach our trainees how to use direct laryngoscopes and not completely abandon them from ER residencies and critical care fellowships.
  7. Recommend but do not require the use of video laryngoscopy. When ultrasound to guide central venous catheter placement first came out in the late 1990’s, many of us thought that ultrasound would soon come to used for all central line procedures. Indeed, almost all residents and fellows adopted ultrasound. But many attending physicians who were very experienced and adept at performing central lines found ultrasound slowed them down and did not improve their already very high success rates. A physician who is highly skilled using direct laryngoscopy may have better outcomes continuing to use the equipment he/she is comfortable and experienced with, rather than being forced to change to new equipment. Many physicians are resistant to change but most physicians find that once they actually use video laryngoscopy, they do not want to go back to direct laryngoscopy.
  8. Avoid special credentialing. Another lesson from vascular ultrasound for central line placement was credentialing. When hospitals first acquired these ultrasound devices, there was concern that the operation of the ultrasound equipment and the interpretation of the ultrasound images required specialized skills. Consequently, hospitals required physicians to have special credentials in order to use ultrasound to facilitate central venous catheter placement. Credentialing required several hours of training and required proctored performance of several ultrasound procedures before the physician was permitted to use vascular ultrasound. This posed a barrier to its implementation because many attending physicians found it easier to continue to do non-ultrasound guided procedures rather than take the time and effort to get credentialed for the use of ultrasound. In hindsight, this was a mistake and should be avoided with video laryngoscopy.

Final thoughts

The two goals of emergency endotracheal intubation are to: (1) get it done fast and (2) get it done right the first time. Video laryngoscopy offers an improvement in both of these goals compared to direct laryngoscopy. It is time to equip our emergency departments, intensive care units, and crash carts with these devices. And it is time to encourage our health care providers to adopt their use.

June 21, 2023

Categories
Emergency Department Intensive Care Unit

A Better Way to Defibrillate Patients In Cardiac Arrest?

I have taken the American Heart Association’s Advanced Cardiac Life Support (ACLS) certification/recertification course every 2 years since 1983. That’s 20 times since medical school. The resuscitation algorithms have changed dramatically over the past 39 years and based on a new study, it may be time to change them once again.

Summary Points:

  • Currently, defibrillation is performed using 2 electrode pads located in the upper right chest and lateral left chest.
  • Vector-change defibrillation is performed using 2 electrode pads located in the left anterior chest and left posterior chest. In a recent study, vector-change defibrillation was superior to standard defibrillation in patients in refractory ventricular fibrillation.
  • Double-sequential external defibrillation is performed using 2 defibrillators, each attached to 2 electrode pads located on different parts of the chest. Double-sequential external defibrillation was superior to either standard defibrillation or vector-change defibrillation in patients with refractory ventricular fibrillation

 

In 1984, every patient in ventricular ventricular fibrillation got lidocaine and sodium bicarbonate as first line medications. The second line antiarrhythmics were quinidine, procainamide, and bretylium. Amiodarone was not yet in use. The current ACLS algorithm for ventricular fibrillation is much simpler. In addition to CPR, patients receive electrical defibrillation every 2 minutes, epinephrine every 3-5 minutes, and amiodarone if sinus rhythm is not restored within the first 6 minutes.

For decades, defibrillation has consisted of placing 2 electrode pads on the patient’s chest – one just below the right clavicle and the other just below and lateral to the left nipple. Then, a single shock of 300 or 360 joules is delivered followed by resumption of chest compressions. A new Canadian study published in the New England Journal of Medicine suggests that there may be a better way to do electrical defibrillation. In the study, 405 patients with out-of-hospital cardiac arrest with refractory ventricular fibrillation were randomly assigned to receive one of three different defibrillation techniques. All patients had an initial three defibrillation attempts using standard defibrillation technique with each attempt occurring 2 minutes after the previous attempt. Patients remaining in ventricular fibrillation were considered to have refractory ventricular fibrillation and were eligible for inclusion in the study. The three salvage defibrillation techniques consisted of (1) standard defibrillation, (2) vector-change defibrillation, or (3) double-sequential external defibrillation.

  1. For standard defibrillation, the electrode pads are located in the traditional locations: one pad below the right clavicle and the other pad on the lateral part of the left chest, just below the left nipple. After the initial 3 defibrillation attempts, all additional attempts occurred with with the pads located in their original position.
  2. For vector-change defibrillation, the pads were re-located with one pad on the anterior chest just below the left nipple and the other pad on the posterior chest, just below the scapula and just left of the spine.
  3. For double-sequential external defibrillation, the two standard pads are left in place and two additional pads are placed with one pad on the anterior chest between the sternum and the left nipple and the other pad on the posterior chest, just below the scapula and left of the spine. With this technique, 2 shocks are delivered within 1 second of each other with the first shock via the anterior/lateral pads (in red on the adjacent figure) and the second shock via the anterior posterior pads (in blue on the adjacent figure).

The primary outcome of the study was survival to hospital discharge and the findings were statistically significant. For patients receiving salvage defibrillation via the standard technique, only 13.3% survived to hospital discharge. For those receiving salvage defibrillations via the vector-change technique, 21.7% survived to hospital discharge. And for those receiving salvage defibrillations via the double-sequential external defibrillation technique, 30.4% survived to hospital discharge. The double-sequential external defibrillation was also superior to the other techniques in terminating defibrillation, achieving return-of-spontaneous-circulation, and modified Rankin scale score (a measure of neurologic disability).

As with all clinical trials, there are limitations to the study. It included only out-of-hospital cardiac arrest patients so it is not clear whether similar results would be achieved in patients arresting in the hospital. It was not a blinded study so it is possible that the EMS personnel could have had unconscious bias in their resuscitation efforts. The number of patients was relatively small so it is possible that larger studies may not achieve the same results. The post-arrest care received in the hospitals was not protocoled so there may be differences in targeted-temperature management, cardiac catheterization management, sedation, mechanical ventilation, etc. Because all patients had 3 initial attempts at standard defibrillation before randomization, it is unclear whether either vector-change defibrillation or double-sequential external defibrillation is superior to standard defibrillation as an initial defibrillation technique. Lastly, it is unclear whether the results can be extrapolated to other tachyarrhythmias such as ventricular tachycardia, atrial fibrillation, or supraventricular tachycardia.

Implication for hospital care

So, what does this mean for physicians responding to cardiac arrests in the emergency department, intensive care unit, and hospital nursing units? It is unlikely that the American Heart Association will change the ACLS algorithm for ventricular fibrillation management in the immediate future. However, the study does at least indicate that when patients do not respond to initial defibrillation efforts, we have two other options that we can try.

Vector-change defibrillation is the easiest technique to implement since it simply requires moving the existing defibrillator pads to different locations. Double-sequential external defibrillation may be more challenging for hospitals to implement since it requires the use of a second defibrillator. In addition, although vector-change defibrillation can be performed using an automated external defibrillator (AED), double-sequential external defibrillation cannot be performed using an AED.

When a patient is in refractory cardiac arrest and is not responding to usual advanced cardiac life support measures, physicians may find themselves in a position of having nothing to lose by trying alternative defibrillation techniques. In this situation, vector-change defibrillation or double-sequential external defibrillation may be worth a try.

November 28, 2022

Categories
Intensive Care Unit Procedure Areas

Credentialling For Common Bedside Procedures

In the past, nearly all internal medicine residents were required to perform common bedside procedures during residency. However, currently, bedside procedure competency is no longer required during residency and the result is that hospitals are often challenged to have credentialed hospitalists available to perform them. These procedures include central venous catheter placement, arterial line placement, thoracentesis, paracentesis, lumbar puncture, endotracheal intubation, arthrocentesis, and bone marrow aspiration/biopsy. In order to ensure that the hospital has coverage for these different procedures requires innovative provider coverage models and careful wording of credentialing requirement documents.

Summary Points:

  • Fewer internal medicine residents learn to perform common bedside procedures during residency than in the past.
  • Hospitalists are less likely to be able to perform these procedures than in the past.
  • Hospitals require innovative tactics to ensure that credentialed healthcare providers are available 24-hours a day to competently perform common bedside procedures.

 

Residency & fellowship training program requirements

There are two organizations that dictate residency and fellowship training requirements, the Accreditation Council for Graduate Medical Education (ACGME) and the specialty board. In the case of internal medicine, the specialty board is the American Board of Internal Medicine (ABIM). The ACGME determines what the training programs have to teach and the ABIM determines what competencies trainees must have in order to become board certified. For internal medicine residents, the ACGME program requirements document states: “Residents are expected to demonstrate the ability to manage patients by demonstrating competence in the performance of procedures as appropriate to their career paths“. The ACGME document further states: “Experience must include opportunities to demonstrate competence in the performance of procedures listed by the ABIM as requiring only knowledge and interpretation“. In other words, the ACGME defers to the ABIM to dictate what procedures are required. The ABIM procedure for certification document states: “Not all residents need to perform all procedures. Program directors must attest to general competence in procedures at end of training. Residents must have the opportunity to develop competence in procedures which will further their development as fellows in their chosen subspecialty or as independent practitioners in their intended fields if entering practice after residency“. In other words, the ABIM leaves it up to the resident to decide what procedures he/she wants to do and leaves it up to the residency program director to determine if the resident is competent to perform the procedure.

The ABIM also dictates competency requirements for subspecialties. As relevant to bedside procedures, the ABIM requires the following:

Notably absent are the procedures of lumbar puncture and paracentesis that are not required by any ABIM subspecialty for board certification.

The ACGME has different requirements for what procedures subspecialty fellows need to be competent to perform during their fellowship training. In many cases, the ACGME subspecialty requirements differ from the ABIM subspecialty board requirements. Notably, paracentesis is required for gastroenterology, pulmonary, and critical care fellowship training. Also, lumbar puncture is required for pulmonary and critical care training. The ACGME has the following requirements for subspecialty fellows:

Although most hospitalists do internal medicine residencies, some hospitalists do family medicine residencies. Neither the ACGME nor the American Board of Family Medicine have specific procedure requirements.

In some hospitals, emergency medicine physicians perform many bedside procedures for hospital inpatients when there is no other provider available to perform those procedures. The ACGME training requirements for emergency medicine includes competency (with required numbers of procedures) in endotracheal intubation (35), central lines (20), lumbar puncture (15), sedation (15), and chest tubes (10).

The bottom line from the ACGME and ABIM is that hospitalists come out of residency training with variable procedural skills. Increasingly, many of them are not proficient to perform any bedside procedures. Over time, it can even become difficult for those residents who do want to be trained in bedside procedures to get that experience. Residents can only perform a procedure under the supervision of an attending physician who is credentialed for that procedure. As fewer of their internal medicine attendings perform these procedures, it can become difficult for the residents to get experience doing procedures during their training. This can result in a patchwork of consultation for procedures: anesthesia for endotracheal intubation, pulmonary for thoracentesis, rheumatology for arthrocentesis, interventional radiology for lumbar puncture & paracentesis, and surgery for central lines. In the middle of the night, it often falls to the emergency medicine physician on-duty to perform any bedside procedure.

Hospital credentialing

The ACGME and ABIM only determine what procedures are necessary to be taught during training or to become board-certified. Decisions about whether or not a physician is permitted to perform a procedure lies with the hospital’s credentials committee to set criteria for hospital privileges. There are two types of privileges: core privileges and optional privileges.

Core privileges are those that any physician credentialed in a given specialty can perform, without additional requirements. It can be easy to select a procedure to include in core privileges when either the ACGME dictates that competency in that procedure is required to complete residency/fellowship training or the ABIM dictates that competency is required to become board certified in that specialty. For example, the ACGME requires cardiology fellows read at least 3,500 EKGs during fellowship training and the ABIM requires pulmonologists be proficient in conscious sedation to become board certified. But credentials committees can also add additional procedures into core privileges that are not required by either the ABIM or the ACGME. These are typically procedures that are commonly performed by residents or fellows in their training even though they may not be specifically required by the ACGME or ABIM. In this case, the procedures are usually listed in the hospital privilege application with the option for the applicant to either request or opt out of each individual procedure privilege. It is then up to the department chair to attest whether or not the applicant is competent to perform that particular procedure. Including lumbar puncture in core privileges for hospitalists is an example.

Optional privileges are those for procedures that some physicians in a given specialty perform but others do not. These are generally not procedures that either the ACGME or ABIM specifies in their requirements and are procedures that require a relatively high level of skill or high level of risk. Often, the credentials committee will require documentation of successful completion of a certain number of these procedures under supervision. Including endotracheal intubation as an optional privilege for a hospitalist is an example.

When a physician get his/her initial appointment to a hospital’s medical staff, it is usually for a short probationary period – typically 6-months. At the end of the probationary period, if the new physician has not had any major quality issues, that physician then moves from a probationary appointment to a regular, full medical staff appointment. The probationary period is an opportune time for physicians who lack adequate training in a procedure to learn how to do that procedure and generate sufficient procedure numbers to qualify for hospital privileges for that procedure when they move from a probationary appointment to a regular appointment to the medical staff.

Hospital privileges usually last for 2 years at which time the physician must apply for re-credentialing. For core privileges, this usually just requires the physician to request those privileges without additional documentation (other than approval by the department chairman). Optional privileges will usually require documentation of on-going competency, such as a patient procedure log documenting the number of that particular procedure the physician has performed in the past 2 years. It is important that the credentials committee is careful and realistic in choosing which procedures require a specific number every 2 years to retain privileges for that procedure. For example, if the hospital has 18 hospitalists and there are a total of only 25 lumbar punctures performed in the hospital every 2 years, then if the credentials committee requires every hospitalist to perform 10 lumbar punctures every 2 years to retain lumbar puncture privileges, none of the hospitalists will realistically be able to do enough lumbar punctures to meet the privilege requirement. That hospital will soon find itself with no hospitalists credentialed to perform lumbar puncture.

Some practical solutions

It is the credentials committee’s obligation to ensure that anyone performing a procedure in the hospital is competent to do that procedure. It is the medical director’s obligation to ensure that when a patient needs a particular procedure, there is a person with hospital privileges available to do it. In order to meet both of these obligations, there are some specific tactics that the hospital can take.

  1. Include procedures that are already in ACGME or ABIM requirements in core privileges. In this case, there is no need to “recreate the wheel” by requiring procedure logs and it only results in applicants keeping unnecessary duplicate records. For example, since the ABIM requires that cardiology fellowship directors attest that a cardiology fellowship graduate is competent to perform cardioversion and since the ACGME requires cardiology fellows to document doing at least 10 cardioversions to graduate from fellowship, there is no need for a new cardiologist to have to provide procedure logs in order to become privileged to perform cardioversion as a member of the medical staff.
  2. Strategically include other low-risk procedures in core privileges. Since most hospitalists are general internists and neither the ACGME nor the ABIM have requirements for any procedures, this will apply to just about any procedure included in hospitalist core privileges. These should include those procedures that are commonly performed during residency and are relatively low risk. Examples are skin punch biopsies, arthrocentesis, and lumbar puncture. Giving the applicant the ability to opt-in or opt-out for individual procedures on the hospital privilege applications allows those hospitalists who have not been trained in these procedures to opt-out. The responsibility of confirming that the hospitalist is competent to perform these procedures thus lies with the division director or department chair who has to sign-off on the application before it goes to the credentials committee. This overcomes the problem of performing a specific number of a rarely performed procedure every two years, especially for procedures that pose relatively low risk of complications, such as a skin biopsy or lumbar puncture.
  3. Include optional privileges for any conceivable bedside procedure that a hospitalist might perform. This is particularly useful for procedures such as central venous catheters and endotracheal intubation. Some internal medicine residents perform many of these during residencies and become quite proficient with them. If a medical staff applicant can produce a procedure log documenting 20 successful proctored endotracheal intubations during internal medicine residency (which is the same number of intubations required by the ACGME for emergency medicine), then that internal medicine hospitalist should be eligible for intubation privileges.
  4. Develop training opportunities for optional procedures. If the hospitalists are the only physicians in the hospital at night, then hospitalists need to be credentialed to perform endotracheal intubation and central venous catheterization. If they were not adequately trained to do these procedures during residency, then the hospital needs to provide that training. At our hospital, we had new hospitalists without prior intubation training spend a couple of mornings in the operating room with our anesthesiologists to get a minimum number of proctored intubations. We additionally required then to perform a specific number of emergency intubations in the ICU and during code blues that were observed by one of the senior hospitalists. We also required them to attend an airway course in our simulation lab in order to get additional experience using different laryngoscopes, bougies, and end-tidal CO2 monitors.
  5. Don’t forget about ultrasound. Bedside ultrasound is routinely used during thoracentesis, paracentesis, arterial lines, and central venous catheters – it makes performing these procedures safer and reduces complications. In fact, many residents and fellows have never performed these procedures without using bedside ultrasound. Residents and fellows typically go through a formal ultrasound training course in a simulation lab. Completion of such a course is often required for bedside ultrasound privileges. We found that many of our older physicians learned how to use bedside ultrasound during their regular clinical practice and never attended an ultrasound course. When documentation of attending a course was required for hospital privileges, these physicians had to stop using ultrasound. The hospital has to be careful with ultrasound privileges – by being too strict, it can force physicians to do procedures such as central line placement without ultrasound guidance with the unintended result that patients are being made less safe. The reality is that today’s bedside ultrasounds are simple to use – it took me longer to learn how to use my fish finder sonar than the hospital ultrasound device. As ultrasound becomes increasingly ubiquitous during residency training, separate credentialing to use ultrasound for venous access guidance makes about as much sense as requiring separate credentialing to use a stethoscope.
  6. Utilize simulation labs. Particularly when credentialing or re-credentialing a physician for an infrequently performed procedure, a simulation lab can be invaluable. Performing a procedure is a skill and like every skill, the more you practice, the better you get. A simulation lab can allow a physician to do many practice procedures and can provide an opportunity for a more skilled proceduralist to give technique pointers and feedback. Although intubating a manikin is a lot different than intubating a live patient during CPR, practice in a simulation lab can at least allow a reduction in the number of live patient procedures required for re-credentialing every 2 years.
  7. Allow non-physician staff to work at the top of their license. Once again, endotracheal intubation is a great example. Respiratory therapists are trained in performing intubation during respiratory therapy school and most states allow respiratory therapists to perform intubations. When our hospital replaced our previous hospitalist group with a new hospitalist group, the new group did not perform intubations (and did not want to). We permitted our respiratory therapists to be credentialed to perform intubations at night (when hospitalists were the only physicians physically in the hospital). We used the same process of anesthesia proctored intubations in the OR, attendance at a simulation lab airway lab, and a specific number of emergency intubations observed by a previously credentialed provider.
  8. Utilize advance practice providers. Nurse practitioners and physician assistants do not have any specific procedure experience required during initial training. There are some advance practice provider fellowships (for example, our medical center has a 1-year critical care nurse practitioner fellowship) and these fellowships often include procedural training. Our critical care NPs and PAs can be credentialed to perform intubation, central venous line placement, and arterial line placement in the ICU.
  9. Consider procedure teams. These are particularly useful in large hospitals that have a reliably large number of regularly performed bedside procedures. These are sometimes lead by a physician credentialed in common procedures but are often staffed by advanced practice providers (NPs and PAs). Elective and semi-elective procedures that lend themselves for NP/PA procedure teams include central lines, lumbar puncture, thoracentesis, paracentesis, and bone marrow biopsy.
  10. Do not over-rely on surgeons and anesthesiologists. Some hospitals are large enough to have a designated in-house anesthesiologist (or CRNA) available to perform emergency intubations outside of the operating room. But small and medium-sized hospitals usually have all of their anesthesiologists assigned to operating rooms during the day and may not have an in-house anesthesiologist at night. Anesthesiologists and surgeons need to be in the operating room and usually cannot just pause a surgical procedure to run out to the ICU to place a central line or intubate a patient. Reserve using anesthesiologists for intubating only difficult airways and using surgeons for only difficult venous access situations.
  11. Have a back-up plan. Emergency medicine physicians are credentialed for most bedside procedures. However, ER doctors really need to remain physically in the ER whenever possible. They can be an important back-up at night in situations when the provider covering the ICU or covering code blue calls is unable to successfully intubate a patient or place a central venous catheter. Anesthesiologists often can play this same back-up role for intubations and surgeons can often play the same back-up role for central lines. But they should generally only be called as a last resort when the first line provider is unsuccessful.
  12. Promote a hospital culture of mutual assistance. As a pulmonary/critical care physician, I had hospital privileges for all common bedside procedures as well as deep sedation. As the hospital medical director, I was usually present in the hospital when not seeing outpatients in the clinic building. I frequently had the cardiologists (who were credentialed for moderate sedation but not deep sedation) schedule cardioversions between my hospital meetings and would pop in to push intravenous propofol and fentanyl for deep sedation. I also frequently performed lumbar punctures and endotracheal intubations when there was not a credentialed provider present. Not every medical director is credentialed for bedside procedures or has the time during the day to perform bedside procedures. But there is frequently other experienced physicians present in the hospital at any given time who can assist a hospitalist or other physician who is not experienced in performing a given procedure. The medical director can promote a culture of mutual assistance

It’s a new era

In bygone times, teaching hospitals were run by internal medicine and surgical residents. They were in the hospital 24-hours a day and did any and all bedside procedures by the time they were senior residents. The training process consisted of “see one, do one, teach one”. And the volume of procedures was so great that there were plenty of them for all residents to become proficient.

But things have changed. Antiseptic catheter coatings eliminated the need to place fresh central lines and arterial lines every 3 days. Ultrasonography reduced the need for pulmonary artery balloon catheters. PICC lines eliminated the need for many central lines. Better imaging reduced the need for lumbar punctures, thoracenteses, and paracenteses. In addition, quality initiatives increased the training requirements to demonstrate procedure competency. The ACGME and the ABIM reduced and in come cases eliminated the requirements for procedure proficiency for residency/fellowship completion or board certification.

As a consequence, internal medicine trainees now perform fewer procedures during residency/fellowship and hospitalists are frequently not prepared to perform those procedures when they join the medical staff. Hospitals must develop innovative new strategies so that all patients and get the procedures they need anytime of the day and night. The best solution for one hospital may not be the best solution for another hospital. But it is clear that hospitals can no long rely on the training and credentialing processes that were used 20 years ago.

September 26, 2022

Categories
Intensive Care Unit

Vitamin C Doesn’t Cure Sepsis

In 2017, an article in the journal Chest reported a 5-fold reduction in the mortality of septic shock by a simple treatment with steroids, vitamin C, and thiamine. A study published last month refuted those results and showed that vitamin C has no benefit in sepsis. It is time for physicians to accept that vitamin C is not the cure for sepsis.

When the 2017 article was published, many critical care physicians wanted to believe it. Sepsis is an enormous public health problem affecting 1.7 million Americans every year and resulting in death in 250,000 of these. Worldwide, sepsis affects 50 million people and causes one-fifth of all deaths. For decades, the treatment of sepsis has focused on antibiotics and restoration of blood pressure. However, much of the damage from sepsis is not from the bacteria and other pathogens that initially cause sepsis, but instead is from the body’s immunologic reaction to those pathogens. For that reason, by the time antibiotics and intravenous fluids are started on a patient with sepsis, the cascade of inflammatory mediators and other substances produced by the body’s immune system has already started. In severe sepsis, this cascade of mediators turns into an avalanche of mediators resulting in refractory hypotension, organ failure, and death, despite antibiotics. Medical science has been searching for the magic bullet that would cure sepsis for years and thus the appeal of vitamin C.

Why vitamin C?

Vitamins are chemicals that our bodies need to function properly. We are unable to produce sufficient quantities of these ourselves so they must come from our diets. When we don’t have enough of one of these vitamins, a vitamin deficiency disorder develops. Some vitamins are fat-soluble and can be stored in our body’s fat tissues for slow release over a long period of time. Other vitamins are water-soluble and cannot be easily stored in the body. Vitamin C is one of those water-soluble vitamins our bodies cannot produce and without dietary vitamin C, scurvy can develop. Scurvy was once a common condition in people who lacked fruits and vegetables in their diets, most famously in 16th century sailors. Scurvy can result in gingivitis, bruising, shock, and death. I remember diagnosing scurvy a few years ago in a patient with alcoholism who was admitted to our ICU with his teeth falling out, dermatitis, and bruising. He had undetectable plasma vitamin C levels and improved with intravenous vitamin C.

Vitamin supplements are $30 billion a year business the United States. The theory is that if too little of them makes you sick and the recommended daily dose prevents you from getting a deficiency disease, then maybe a lot more might prevent you from getting even more diseases. One of the most famous advocates of vitamin C supplementation was Linus Pauling. He is one of only 4 people to win 2 Nobel Prizes: in his case, the 1954 Nobel Price in Chemistry and the 1962 Nobel Peace Prize. In the 1970’s, he became enamored with vitamin C and claimed that it could treat cancer, brain-injured children, and the common cold. Although subsequent clinical trials showed no benefit compared to placebo and re-examination of Pauling’s research in vitamin C was shown to be flawed, he continued to promote vitamin C as a cure for the common cold and as a treatment for cancer. Because of his stature as a scientist, he influenced many people to take large doses of vitamin C to treat or prevent various diseases. The result was a legacy of a belief that vitamin C was a miracle cure in search for a disease to treat.

The arguments for vitamin C’s benefits had some basis in science. Sepsis is accompanied by oxidative stress and the resultant oxidants cause damage to various tissues. In the lab, antioxidants can reduce the amount of injury to cells by oxidants. Vitamin C is a naturally-occurring antioxidant and so it seemed logical that vitamin C could reduce oxidant injury from sepsis.

When physicians at Eastern Virginia Medical School were faced with three patients with sepsis and in whom death appeared inevitable, they gave the patients intravenous vitamin C as a last-ditch effort. The patients recovered, leading the physicians to believe that vitamin C could be the cure for sepsis that medical science had been looking for. So, they treated 47 septic patients with a combination of intravenous vitamin C, hydrocortisone, and thiamine and compared those patients to 47 other patients who that had sepsis in the past, before they had the idea of IV vitamin C. The results were astounding with a mortality rate of 40.5% in the untreated patients and 8.5% in the vitamin C treated patients. Their findings were published in the June 2017 edition of the journal Chest.

Vitamin C enters the mainstream

Physicians throughout the United States saw the publication and jumped on the vitamin C bandwagon. The lay press was all over it. NPR reported: “Doctor turns up possible treatment for deadly sepsis”. NBC reported: “Virginia doctor’s possible cure could save millions from deadly sepsis”. A Smithsonian Magazine headline was: “Could vitamin C be the cure for deadly infections?”. In our hospital, some of the critical care physicians were convinced and started using the cocktail of vitamin C, hydrocortisone, and thiamine in patients with sepsis but other critical care physicians remained skeptical. Soon, family members of patients in our ICU were asking that their loved ones be treated with vitamin C and became angry if they were not treated with it.

I was in a unique position, I was both a critical care physician and the medical director of the hospital. Should I mandate the use of vitamin C in sepsis? Should I forbid the use of vitamin C in sepsis? Physicians are notoriously independent and critical care physicians even more so. We are often in the position of providing the treatment of last resort to dying patients. We have to make treatment decisions quickly, often without time to get consultation from other specialists or get second opinions. And since so many of our patients die, there is often a sense of “what could trying something new hurt?” It is rarely a good idea for a medical director to make a unilateral decision for the entire hospital about a controversial treatment in these situations.

Practice guidelines are a help, whether from national medical societies or from internal hospital experts. As the medical director, I could use these guidelines to base decisions about what treatments the hospital should adopt. But it takes months or years to bring together a guideline committee and have that committee deliver a final guideline document. In the short term, we could have convened a workgroup of physicians at the hospital to develop recommendations and we used these workgroups quite regularly during the first year of the COVID-19 pandemic. Instead, we influenced physician behavior by example.

One of the benefits and curses of being a senior physician is that everyone thinks you have a lot more wisdom than you actually do have. For the past 30 years, I had seen promising treatments for sepsis come and go. When I was young, I was often an early-adopter of proposed new treatments in the ICU but by 2017, I had become considerably more cautious and skeptical of treatments that seemed on the surface to be too good to be true. And so I and other senior critical care physicians did not order the vitamin C cocktail on patients during our shifts in our ICU. Soon, the other physicians started saying “Well, if the old guys aren’t prescribing it, maybe I shouldn’t either.” After an initial flurry of vitamin C orders, the doctors in our ICU stopped prescribing it.

The final nail in the vitamin C coffin

The strongest medical evidence comes from clinical trials that (1) are randomized, (2) are double-blinded, (3) involve multiple hospitals, and (4) are placebo-controlled. The 2017 vitamin C study was open-label, had no placebo group, was only performed at one hospital, and was not randomized. In other words, it used a very weak study design. But it was convincing enough to prompt the creation of other, more rigorous clinical trials. In 2019, a multicenter, randomized, double-blind, placebo-controlled study published in JAMA found no improvement in outcomes of patients with sepsis who were treated with vitamin C. In 2020, a second multicenter, randomized, double-blind, placebo-controlled study published in JAMA also found that the vitamin C cocktail did not improve any of the outcomes in sepsis. Earlier this year, two meta-analyses were published that contested the value of vitamin C in sepsis.

The most recent study in the New England Journal of Medicine showed that not only did patients with sepsis treated with vitamin C fail to improve, the vitamin C patients actually had a higher death rate than those treated with placebo. This was a massive study involving 872 patients from 35 hospitals in 3 countries. The study was randomized, double-blinded, and placebo-controlled. 31.6% of patients receiving placebo died whereas 35.4% of those receiving vitamin C died.

It would appear that this study will be the final word on vitamin C and sepsis – it doesn’t make patients better and may actually make them worse.

Lessons learned (again)

Medicine has seen remarkable breakthrough treatments over the past 50 years. And we as physicians are constantly looking for the next remarkable treatment to improve the lives of patients who have the diseases that we treat. History has shown us over and over again that the future always brings more effective treatments for almost every health condition. It is that inherent optimism for the future of medicine and our drive to find something to make our own patients better that causes us to latch our hopes onto promising preliminary studies.

In my own outpatient interstitial lung disease practice, I have treated idiopathic pulmonary fibrosis patients with medications from promising preliminary studies, only to have the medications be proven ineffective in randomized, placebo-controlled, double-blinded, multi-center trials. In the 1980’s, it was Cytoxan, In the 1990’s, it was prednisone and Imuran, In the 2000’s, it was gamma interferon and later, N-acetyl cysteine. Each drug offered hope to patients with a terminal disease… and each one was later found to not work.

Studies that suggest that a treatment is effective get a lot more attention and press coverage than studies that show a treatment doesn’t work. All too often, these negative studies are the more rigorously designed randomized, placebo-controlled, double-blinded, multi-center trials that should be the final word. Last month’s study in the New England Journal of Medicine may not get as much coverage in the lay news but it underscores the importance that as physicians, it is essential that we base our own medical practice on well-designed studies published in peer-review journals.

July 15, 2022

Categories
Emergency Department Intensive Care Unit Medical Education

Clinical Interpretation Of Arterial Blood Gases

In the previous post, the physiology of the acid-base system was discussed. This post will focus on the practical interpretation of arterial blood gases for clinical diagnosis. The arterial blood gas (ABG) is usually the quickest lab test to obtain in a critically ill patient. In the emergency department, in the ICU, in the operating room, and during cardiopulmonary resuscitation, the ABG often leads to a correct diagnosis and directs initial treatment. There are four steps in interpreting the acid-base components of an ABG:

  1. Determine if the primary process is an acidosis or alkalosis
  2. Determine if the primary process is respiratory or metabolic
  3. Determine if the primary process is appropriately compensated
  4. Check the anion gap

This post will focus on the acid-base components of the ABG and will not discuss oxygenation.

Steps 1 &2: Determine the main acid-base disorder

Although normal values for pH, PCO2, and HCO3 are in reality a range, it is much easier to assume a single normal numeric values for each when interpreting an acid-base disturbance. Therefore, assume normal values of:

  • pH = 7.40
  • PCO2 = 40
  • HCO3 = 24

If the ABG shows a pH < 7.40,  then there is an acidosis; if the PCO2 is elevated, then it is a respiratory acidosis and if the HCO3 is reduced, then it is a metabolic acidosis.

On the other hand, if the ABG shows a pH > 7.40, then there is an alkalosis; if the PCO2 is reduced, then it is a respiratory alkalosis and if the HCO3 is elevated, then it is a metabolic alkalosis. Therefore, each of the four primary acid-base disturbances can be defined as follows:

Respiratory Acidoses:

Respiratory acidoses can be divided into those that are acute (duration of minutes to hours) and those that are chronic (duration of days, weeks, or years). The patient’s clinical history will dictate whether the condition is acute or chronic. For example, a newly unconscious patient with a fentanyl ingestion 45 minutes ago will typically have an acute respiratory acidosis whereas a smoker with long-standing, stable COPD will typically have a chronic respiratory acidosis. There are six main causes of respiratory acidosis:

Respiratory Alkalosis:

Respiratory alkaloses can also be divided into those that are acute and those that are chronic. Once again, the patient’s clinical history will dictate whether the condition is acute or chronic. There are eight main causes of a respiratory alkalosis:

Metabolic Acidoses:

There are two subcategories of metabolic acidosis: (1) increased anion gap metabolic acidosis and (2) normal anion gap metabolic acidosis. The anion gap can be calculated using the equation:

Anion Gap = Na – (Cl + HCO3)

The anion gap is normally composed of miscellaneous anionic molecules in the blood such as albumin and phosphate. When the anion gap is increased, then there are abnormal anions in the blood that will result in a lowering of the HCO3 level. The anion gap is often reported from the lab when ordering an electrolyte panel but for general ABG calculation purposes, a normal value of up to 12 mEq/L can be assumed (normal range = 6-12 mEq). However, when the pH is very high (> 7.50), the anion gap will increase to 15-16 by uncovering anionic sites on albumin. Therefore, a slightly elevated anion gap is normal when the pH is very high. The anion gap can be decreased in conditions such as hypoproteinemia, hypophosphatemia, and multiple myeloma (the latter due to an increase in cationic monoclonal IgG levels).

There are five common causes of an increased anion gap metabolic acidosis and two common causes of a normal anion gap metabolic acidosis:

Note that aspirin overdose can cause both a respiratory alkalosis (by direct stimulation of the brain’s respiratory drive center) and a metabolic acidosis (by accumulation of acetylsalicylic acid in the blood).

Increased anion gap metabolic acidoses can be further subdivided into those that cause an increased osmolar gap (> 10 mOsm/L) and those with a normal osmolar gap (< 10 mOsm/L). The osmolar gap is the difference between the measured and the calculated osmolality of the blood and this is normally reported out by the lab when a plasma osmolality test is ordered. The two most common causes of an increased osmolar gap are (1) methanol poisoning and (2) ethylene glycol poisoning. These are critical diagnoses to make because neither ethylene glycol nor methanol blood levels are able to measured quickly and so the arterial blood gas is usually the only way to establish an early diagnosis in order to direct life-saving treatment. All of the other causes of metabolic acidosis result in a normal osmolar gap.

Metabolic Alkaloses:

There are two subcategories of metabolic alkalosis: (1) chloride responsive metabolic alkaloses and (2) chloride unresponsive metabolic alkaloses. Chloride responsiveness is defined by the urine chloride level: if the urine chloride is < 10 mEq/L, the metabolic alkalosis is chloride responsive and if the urine chloride is > 10 mEq/L, the metabolic alkalosis is chloride unresponsive. There are three common causes of a chloride responsive metabolic alkalosis. Although there are also three causes of a chloride unresponsive metabolic alkalosis listed below, the most common is corticosteroid medication.

Step 3: Determine if the main acid-base disturbance is compensated

Very frequently, there will be more than once acid-base disturbance simultaneously. For example, a patient with pneumonia can have both a respiratory acidosis (from respiratory failure) and a metabolic acidosis (from lactic acidosis due to sepsis). To determine if there is more than than one acid-base disturbance, there are compensation rules. If a patient meets the criteria for these rules, then there is a simple acid-base disturbance (i.e., only one acid-base disturbance). Many of these rules are cumbersome and involve using nomograms or complex formulas. The following are the compensation rules that I have used throughout my career that are simple, require minimal calculations, and easy to use:

  • Metabolic acidosis: The last 2 digits of the pH will equal the PCO2
  • Metabolic alkalosis: For every 10 mEq increase in the HCO3, there will be a 6 mm increase in the PCO2
  • Respiratory acidosis:
    • Acute: For every 10 mm increase in the PCO2, there will be a 1 mEq increase in the HCO3
    • Chronic: For every 10 mm increase in the PCO2, there will be a 3.5 mEq increase in the HCO3
  • Respiratory alkalosis:
    • Acute: For every 10 mm decrease in the PCO2, there will be a 2 mEq decrease in the HCO3
    • Chronic: For every 10 mm decrease in the PCO2, there will be a 5 mEq decrease in the HCO3

If the patient fails the simple acid-base disorder compensation rule, then there is more than one acid-base disturbance. The direction of change from the expected compensation in PCO2 (metabolic disorders) or HCO3 (respiratory disorders) will indicate what that second acid-base disorder is.

Although patients can rarely have three or even four different acid-base disorders occurring at the same time, most patients will only have one or have two occurring simultaneously. The table below describes the findings when there are two acid base disturbances:

Step 4: Check the anion gap

Always, always, always calculate the anion gap! If the anion gap is elevated, then there is an increased anion gap metabolic acidosis, even if the pH, PCO2, and HCO3 are all normal.  The combination of a metabolic acidosis plus a metabolic alkalosis can cause the ABG to appear normal and the only clue that the patient has acid base disorders will be the increased anion gap.

The “delta-delta” rule. The Greek letter delta (Δ)is often used in medical shorthand to mean ‘change in’. In a simple, compensated increased anion gap metabolic acidosis, the Δ anion gap should always be equal to the Δ bicarbonate. In other words, the increase in the anion gap in mEq/L from normal should equal the decrease in the HCO3 in mEq/L from normal. Once again, assume that the normal anion gap is 12 mEq/L and the normal HCO3 is 24 mEq/L. If these two values for Δ are not equal, then there is a second acid-base disturbance. For example, if the anion gap is 20 mEq/L (8 mEq/L above normal), then the bicarbonate should be 16 mEq (8 mEq/L below normal). If the change in bicarbonate is larger than the change in the anion gap, then there is a concurrent metabolic acidosis. On the other hand, if the change in bicarbonate is smaller than the change in anion gap, then there is a concurrent metabolic alkalosis.

Questions containing a completely normal ABG with an increased anion gap are a favorite of those who write questions for board examinations, and with good reason. A common scenario where this occurs is the patient with diabetic ketoacidosis (causing an increased anion gap metabolic acidosis) who is vomiting (causing a chloride responsive metabolic alkalosis). In this case, the decrease in the HCO3 from the metabolic acidosis can be offset by the increase in the HCO3 from the metabolic alkalosis – the ABG can look normal but the patient will still be very sick. The Δ bicarbonate will be less than the Δ anion gap. In this situation, the increased anion gap will be the only prompt for the emergency room physician to immediately start the patient on IV fluids and insulin.

There is a wealth of information contained in those four numbers: the pH, PCO2, HCO3, and anion gap. During emergent situations, such as during a cardiopulmonary arrest, there is not time to look up ABG interpretation in a book or on-line reference. By being able to rapidly analyze the acid-base status, the clinician can use that information to direct life-saving treatments. Memorization of the differential diagnosis of each of the four primary acid-base disturbances and memorization of the compensation rules is essential to the practice of emergency medicine, anesthesia, and critical care medicine.

May 9, 2022

Categories
Emergency Department Intensive Care Unit Medical Education

Physiology Of Arterial Blood Gases

Part 1 of this post will cover the physiology behind arterial blood gases and part 2 will cover clinical interpretation of arterial blood gases. Arterial blood gases (ABGs) are an essential part of the evaluation of unstable patients. In unconscious patients who are unable to give a history, the blood gas can provide key data that can lead to a diagnosis long before other test results come back. In the intensive care unit and in the operating room, the ABG can provide critical results that can direct life-saving treatment. But optimal use of the arterial blood gas requires the physician to be able to rapidly interpret the results of the ABG. The two main components of the arterial blood gas are (1) oxygenation and (2) acid-base status. This post will focus on the background physiology of the acid-base components of the ABG. If you are primarily interested in the use of ABGs in clinical decision making of acid-base disorders, skip ahead to the next post.

Components of the ABG

Fundamentally, there are 5 main results in an arterial blood gas report: pH, PO2, PCO2, HCO3, and O2%. The pH is measured directly and indicates whether the patient is acidemic (pH < 7.40) or alkalemic (pH > 7.40). The PO2 is the partial pressure of dissolved oxygen in the blood. The PCO2 is the partial pressure of dissolved carbon dioxide in the blood. The HCO3 is the bicarbonate concentration which is very similar to the serum CO2 reported in an electrolyte panel (the serum CO2 is the total of everything that can be converted into CO2 in the blood including bicarbonate, carbonic acid, and dissolved carbon dioxide – it should not be confused with the PCO2 from the arterial blood gas which is a completely different value). The O2% is the oxygen saturation which is the percentage of hemoglobin binding sites that contain bound oxygen molecules. The normal values for each of these results are usually listed as a range of normal but for the purposes of analyzing the acid-base status, consider normal to be single numbers: pH = 7.40, PCO2 = 40 mm Hg, and HCO3 = 24 mEq/L.

Many ABG analyzer machines can also measure other values such as methemoglobin, carboxyhemoglobin, potassium, lactate, hemoglobin, etc. However, these tests usually need to be ordered separately and if only an ABG is ordered, then you will just get the 5 results as described above.

Acid-base regulation

Our bodies try to keep the pH as close to 7.40 as possible. The two ways that we regulate the pH are by (1) increasing or decreasing carbon dioxide excretion by the lungs and (2) increasing or decreasing bicarbonate excretion by the kidneys. When the carbon dioxide level of the blood is too high or too low, the kidneys compensate by increasing or decreasing the bicarbonate level of the blood by altering bicarbonate excretion in the urine. On the other hand, when the bicarbonate level is too high or too low, the lungs compensate by increasing the carbon dioxide level using hypoventilation or by decreasing the carbon dioxide level using hyperventilation.

Our tissues are constantly producing acids (in the form of hydrogen ions) and acid production can increase very rapidly with exercise. Therefore, there has to be an efficient way to get rid of acid as quickly as it is produced. This is done by converting hydrogen ions into carbon dioxide. In the blood, this is done by the enzyme carbonic anhydrase that first converts hydrogen ions into carbonic acid and then converts carbonic acid into carbon dioxide and water. The carbon dioxide is then excreted by the lungs in the form of exhaled carbon dioxide. When more acid (and thus carbon dioxide) is produced, for example, during exercise, the lungs can immediately dispose of that carbon dioxide by hyperventilation. In order to keep the pH at 7.40, we have to maintain a constant ratio of bicarbonate:dissolved carbon dioxide, as dictated by the Henderson-Hassalbach equation.

During conditions resulting in hyperventilation, the lungs get rid of more carbon dioxide and as a consequence, the blood PCO2 can become lower. Conversely, during conditions resulting in hypoventilation, the lungs are not able to get rid of carbon dioxide adequately and the blood PCO2 will rise.

There are other acids that are produced by metabolism that cannot be converted into carbon dioxide. These are called non-volatile acids and must be excreted by the kidneys. The kidneys can also excrete bicarbonate into the urine and can thus respond to a change in the blood carbon dioxide level by either eliminating or retaining bicarbonate. Unlike the lungs which can respond to increased carbon dioxide within seconds, it takes the kidneys 2-3 days to raise or lower bicarbonate levels with the result that the kidney’s full compensatory response to an acid-base disorder takes several days. However, the blood does have the ability to have a small but immediate effect on a changing carbon dioxide level by a chemical buffering mechanism. The result of this is that there are two responses to a high or a low carbon dioxide level: an acute compensation by chemical buffering and a chronic compensation from excretion of bicarbonate by the kidney. The buffering mechanism of the blood is fairly limited and can only result in a mild/limited degree of compensation compared to kidney excretion of bicarbonate.

Base deficit and base excess

In some situations, the ABG report will be resulted as “base deficit” or “base excess”. This is commonly used in the operating room by anesthesiologists. A base deficit refers to the amount that the bicarbonate level is too low and a base excess refers to the amount that the bicarbonate is too high. For practical purposes, base excess can be used synonymously with metabolic alkalosis and base deficit can be used synonymously with metabolic acidosis.

Acid-base disorders

Acid-base disorders can be divided into those that make the pH go up (alkaloses) or make the pH go down (acidosis). Each of these can be dividing into respiratory disorders that affect the carbon dioxide level and metabolic disorders that affect the bicarbonate level. Thus, there are 4 main groups of acid-based disturbances:

In a respiratory acidosis, the primary problem is that the blood carbon dioxide level is too high and the kidneys compensate by retaining bicarbonate. In a respiratory alkalosis, the primary problem is that the blood carbon dioxide level is too low and the kidneys compensate by increasing bicarbonate excretion into the urine. In a metabolic acidosis, the primary problem is that the blood bicarbonate level is too low and the lungs compensate by hyperventilating to reduce the blood carbon dioxide level. In a metabolic alkalosis, the primary problem is that the blood bicarbonate level is too high and the lungs compensate by hypoventilating to increase the blood carbon dioxide level.

As noted previously, the lungs can compensate to a metabolic acidosis or alkalosis within seconds but the kidneys take 2-3 days to fully compensate for a respiratory acidosis or alkalosis. However, there is a partial compensation to a respiratory acidosis or alkalosis by the buffering chemistry within the blood that happens immediately. For this reason, metabolic acidoses and alkaloses can be divided into those that are acute (occurring in minutes to hours) that are partially compensated by buffering and those that are chronic (occurring more than 2-3 days previously) that are more fully compensated by renal bicarbonate excretion.

It is important to note that a person can have more than one acid base disturbance at the same time. For example, a person can have a condition causing a metabolic acidosis and also simultaneously have another condition causing a metabolic alkalosis. Or, a person can have both a metabolic acidosis and simultaneously have a  respiratory acidosis. If there is a single acid-base disturbance, it is called a simple acid base disorder and if there are more than one acid-base disturbances, it is called a complex acid base disorder.

The next post will review the causes of acid-base disturbances and how interpretation of the arterial blood gas can be used to diagnose these disorders.

May 9, 2022

Categories
Intensive Care Unit

Your Right To Get COVID Stops Where Our ICU Begins

This post is on behalf of all physicians, nurses, and respiratory therapists who work in U.S. intensive care units.

To all anti-vaxxers and anti-maskers:

For months, you have been telling us that you deserve the freedom to choose: to choose whether or not to get a COVID-19 vaccine and to choose whether or not to wear a face mask in public places. In other words, you have been saying that it is your right to get infected with COVID and that measures to prevent it are an assault to your freedoms as an American. Although it is true that you do have the right to do a lot of dangerous things that jeopardize your health and your lives, you do not have the right to do dangerous things that jeopardize our health and our lives. And when you get COVID, you are doing just that.

  • You have the right to smoke cigarettes. But when you get lung cancer, your metastases are not contagious to the oncologist.
  • You have the right to promiscuous unprotected sex. But when you get gonorrhea, your sexually-transmitted disease is not contagious to the nurse in the emergency department who takes care of you.
  • You have the right to use intravenous heroin and fentanyl. But when you overdose, your respiratory failure is not contagious to the respiratory therapist.

You say you have the freedom to choose to not wear face masks and to not get a vaccination. But as healthcare workers, we do not have the freedom to refuse to take care of you when you become infected with COVID and need us to care for you in our ICUs.

Currently in the United States, 30% of all patients in our ICUs have COVID. In many parts of Texas, Florida, Louisiana, and other southern states, the majority of patients in ICUs have COVID. Although nearly two-thirds of American adults have gotten a COVID vaccine, 98% of all of the hospitalized COVID patients are unvaccinated. In many U.S. cities, there are no empty ICU beds left and that means that when a patient comes in with a heart attack, pneumonia, or a stroke, we do not have an ICU bed to care for that patient.

Your self-professed freedom to get COVID means that we have to work extra shifts, sometimes 24 or 36 hours straight, because there are too many COVID patients in our ICUs to take care of with our normal number of staff. Every time we walk through the door into an ICU room to care for a patient with COVID, we are exposing ourselves to the deadly contagious virus and we are risking our lives to take care of that patient.

In the beginning of the pandemic, before vaccines were available, we worked tirelessly when our ICUs were overwhelmed with sick and dying COVID patients. We did it because it was our duty to take care of all of the innocents who could not prevent their viral infections. It is what we signed up for. The emotions of sadness, fear, and exhaustion that we felt in the summer of 2020 have been replaced by the emotion of resentment because in the summer of 2021, almost all COVID ICU admissions were avoidable.

Like the intravenous drug users who occupy beds in our ICU because of an overdose, you are occupying our ICU beds because of your bad life choices. Unlike those intravenous drug users who will wake up and get out of our ICUs after a day or two, you will spend an average of 14 days in our ICUs and 20% of you will die in our ICUs. During those 14 days, you are taking up beds needed by other patients with diseases that were not caused by bad life choices.

The average cost of a hospitalization for COVID is $20,000 and if that hospitalization includes admission to the ICU, the cost is 5-10 times that much. In July 2021 alone, the hospitalization costs of unvaccinated COVID patients in the U.S. was $1.5 billion. Those costs are paid by health insurance companies and passed on to all of the rest of us by increased health insurance premiums and Medicare payroll taxes. In other words, your self-declared freedom to get COVID is paid for by higher insurance costs to those of use who got vaccinated and wear face masks. We are tired of paying for your bad life choices.

We watch on the news as you angrily demonstrate against vaccines and face masks at our statehouses. We read on social media about your delusions that vaccines cause disease. We hear you call us fascists because you are required to wear face masks when you enter the restaurants we eat in, stores we shop in, and hospitals we work in. And all the time, we are desperately trying to save your lives when you get sick from COVID infections that you could have prevented. It is as if Satan has taken over your minds and now our entire country needs an exorcism.

But we will continue to take care of you in our hospitals and in our intensive care units. The code of ethics that we are bound by dictates that we must. We only wish that your code of ethics was as virtuous.

August 29, 2021

Categories
Intensive Care Unit

How Many ICU Beds Does A Hospital Need?

When a new hospital is built or an existing hospital plans to expand, a key question is “How many ICU beds will we need?“. There is not a one-size-fits-all answer to that question but there are some general principles that guide the number of ICU beds that a hospital requires.

Data from the American Hospital Association’s 2020 publication on U.S. hospital resources reveals that there are 6,146 hospitals in the U.S. Excluding the psychiatric hospitals and federal hospitals, there are 5,198 community hospitals in the United States, of which, 51.4% have intensive care units. Overall, there are 792,417 community hospital beds in the U.S., of which 13.5% are ICU beds. The overall make-up of U.S. community hospital beds is:

  • 792,417 total hospital beds
  • 55,663 medical/surgical ICU beds
  • 15,160 cardiac care unit beds
  • 7,419 other ICU beds
  • 22,721 neonatal ICU beds
  • 5,115 pediatric ICU beds
  • 25,157 step down unit beds

Location, Location, Location

Intensive care units are not uniformly distributed in the United States. Many smaller hospitals lack ICUs and consequently, more than 50% of U.S. counties do not have any ICU beds. Most ICU beds are found in metropolitan areas (defined as > 50,000 population) or micro metropolitan areas (defined as 10,000 – 49,999 population:

  • 94% of ICU beds are in metropolitan areas
  • 5% of ICU beds are in micro metropolitan areas
  • 1% of ICU beds are in rural areas

There are a number of reasons for the paucity of ICU beds in rural areas but perhaps the most important reason is that an ICU is more than just a bed and a ventilator, an ICU requires critical care-trained nurses, advanced pharmacy support, 24-hour respiratory therapy, and physicians with critical care skills. Smaller hospitals in rural areas generally cannot support all of these specialized personnel to provide care for a relatively small number of ICU beds.

Although the overall average percentage of hospital beds in the U.S. that are ICU beds is 13.5%, because many rural hospitals lack ICUs, the percentage of ICU beds in metropolitan hospitals is necessarily higher than 13.5%. This is particularly true for academic medical centers and pediatric hospitals that function as tertiary care facilities with the result that these hospitals admit more complex patients who more often require ICU services. So, for example, in Columbus, Ohio, between the 3 major hospital systems plus the children’s hospital, there are 3,873 hospital beds. Of these, 572 (15%) are ICU beds.

Another way of analyzing ICU bed use is by expressing the number of ICU beds per 10,000 population. This can be misleading, however, because many rural areas will send most of their ICU-level patients to nearby metropolitan areas with the result that the larger metropolitan areas will have more ICU beds per capita. Nevertheless, in an analysis by the Washington Post, the major metropolitan areas in Ohio varied significantly in ICU beds per 10,000 population:

  • 6.3 Toledo
  • 5.3 Cleveland
  • 5.0 Cincinnati
  • 5.0 Dayton
  • 4.7 Akron
  • 4.4 Canton
  • 3.6 Columbus

What About Utilization?

The Society of Critical Care Medicine recently analyzed ICU occupancy. Overall in the United States, the ICU occupancy rate is 66.6% for adult ICUs, 61.6% for pediatric ICUs, and 67.7% for neonatal ICUs. One of reasons that these percentages seem low is that there can be wide swings in occupancy and a hospital needs to have sufficient resources to accommodate high-census times. Furthermore, ICU occupancy is generally based on the midnight census in a hospital, that is, the number of patients in a bed at midnight. Because patients usually do not get transferred out of ICUs until early afternoon (after the physicians make morning rounds) but patients get transferred into ICUs continuously throughout the day, the 66.6% occupancy rate at midnight for adult ICUs underestimates the peak occupancy for ICUs at noon which is considerably higher.

When a hospital’s ICU occupancy rate is low, the ICU tends to harbor less acute patients. Conversely, when a hospital’s ICU occupancy rate is high, higher acuity patients often get admitted to non-ICU locations such as step-down units. Consequently, a patient with a COPD exacerbation requiring non-invasive ventilation with BiPAP but not requiring intubation with mechanical ventilation would be admitted to an ICU bed when there is adequate ICU capacity but might be admitted to a step-down bed when there is insufficient ICU capacity.

So, how many ICU beds does a hospital need?

If we start with the U.S. average, then a hospital needs 13.5% of its beds to be ICU beds. Hospitals in larger cities need a higher percentage whereas hospitals in small towns need a lower percentage. Within larger cities there will also be variation: tertiary care hospitals and children’s hospitals will require a higher percentage than other hospitals in metropolitan areas.

In deciding whether to expand ICUs, a hospital should also look at its ICU occupancy rate. If the average occupancy rate is < 66% then the hospital likely does not need additional ICU beds. However, if the occupancy rate is > 66%, then ICU bed expansion may be warranted.

Lastly, the hospital should examine the acuity of patients in the ICU when determining whether ICU beds should be increased. A 2013 study of ICU occupancy and ventilator use in the U.S. found that the mean percentage of ICU patients on a ventilator at any given time was 40%. If a hospital’s ICU ventilated patient percentage averages less than this, then it may not need additional ICU beds. However, if the percentage of ICU patients on a ventilator is > 40%, then more ICU beds may be needed.

A hospital needs to have the correct number of intensive care unit beds to support its operating rooms and general nursing units. There also needs to be sufficient ICU beds regionally to support the community’s need to care for the sickest patients. ICUs are expensive and the specialized staff it takes to care for patients in ICUs are even more expensive. However, the DRG reimbursement for these patients is high and so ICUs can be financially lucrative for a hospital. When hospitals plan bed expansion, it must be done with the right balance of ICU to non-ICU beds in mind.

October 10, 2020