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

Categories
Intensive Care Unit

The Pandemic Of Dogma Within The Pandemic Of COVID-19

Our generation of physicians prides itself on the practice of evidence-based medicine. Ideally, this means making medical decisions based on peer-reviewed clinical studies and randomized, controlled clinical trials. It means getting away from the “this-is-the-way-you-do-it-because-this-is-the-way-we’ve-always-done-it” approach to medicine to ensure that patients get the best known treatment for any given medical condition.

But what happens when you face a disease and there are no peer-reviewed publications and randomized controlled clinical trials? In that situation, physicians’ definition of what constitutes evidence can vary considerably. Thus enters dogma and nowhere in recent memory has there been a greater pandemic of dogma than in our intensive care units managing patients with COVID-19. As critical care physicians, we hold our convictions about how to best treat patients with COVID-19 respiratory failure more tightly than we hold religious convictions or political convictions. And given that many of these convictions are diametrically opposed, we can’t all be right. Forty years ago, in my first week of medical school, one of the professors told me that 50% of everything I was about to learn was going to ultimately be proven to be wrong. I think those words could be just as easily applied to our approach to managing patients with COVID-19 in the ICU today.

To Ventilate or Not To Ventilate?

That  is the question… or is it? For decades, we have defined patients as having ARDS (acute respiratory distress syndrome) if they have acute onset of diffuse pulmonary infiltrates with severe hypoxemia in the absence of heart failure and in the presence of something known to cause non-cardiogenic pulmonary edema, such as infection. And ever since 1967 when surgeon David Ashbaugh and pulmonologist Tom Petty first described the ARDS in the medical literature, it has been well-accepted that mechanical ventilation with PEEP (positive end-expiratory pressure) is the first line treatment.

But in the era of COVID-19, we read on-line news articles about a hospital in New York that reported 88% of their patients placed on mechanical ventilators died. And then all of a sudden, some critical care physicians are having second thoughts about intubating COVID-19 patients in respiratory failure and instead letting them be hypoxic. On the other hand, we read a blog post from a physician in Europe that he observed hospitalized COVID-19 patients develop sudden severe hypoxemia and go from needing 4 L oxygen by nasal cannula to having respiratory arrest despite 100% oxygen by face mask in just 30 minutes. And all of a sudden, some critical care physicians are intubating every COVID-19 patients who needs 4 L oxygen by nasal cannula.

Maybe COVID-19 really is different from ARDS from any other infection. But until someone proves that, I know that mechanical ventilation can bridge patients through life-threatening ARDS until time heals the lungs, that PEEP helps, and that low tidal volume ventilation is better than high tidal volume ventilation. We should not throw out everything that we’ve learned about the management of ARDS over the past 53 years because of a blog post.

Steroids Yes or Steroids No?

Over the past 35 years, the steroid pendulum has swung back and forth several times with respect to treating ARDS. First, studies showed steroids were beneficial, then studies showed they were not beneficial, and now studies again suggest they might be beneficial again. Similarly, you can find studies that show steroids improve the mortality rate of other coronaviruses and influenza; you can also find that steroids have no effect on the mortality rate of viral pneumonia. Some critical care physicians believe that steroids are the cure to the “cytokine storm” attendant to COVID-19 respiratory failure. Other critical care physicians believe that steroids paralyze the body’s immune defenses against COVID-19 resulting in increased viral replication. Our resident and fellow trainees are often caught in the middle, hearing that “You’re going to kill your patients if you don’t give then steroids” from one critical care attending physician on Monday and then hearing “You’re going to kill your patients if you give them steroids” from another critical care attending physician on Tuesday.

Hydroxychloroquine?

A non-randomized, non-placebo-controlled study from France suggested that 20 COVID-19 patients who got anti-malaria drug hydroxycholorquine had lower levels of detectable virus than patients previously published in the literature. This made immediate news in the lay press and the U.S. President called the drug a “game changer”. Within 3 days, pharmacies all across the country were sold out of hydroxychlorquine and I had patients calling in and asking me to prescribe it for them to prevent getting COVID-19 infection. Physicians throughout the world began prescribing it for any of their patients sick enough to be admitted to the intensive care unit. But then other studies showed that patients who received hydroxychloroquine actually did worse than those did not receive it because of potential fatal heart rhythm disturbances brought on by hydroxychloroquine. Once again, you’ll find critical care physicians who think it is the standard of care and others who think that it is nonsense.

Tocilizumab?

Patients with COIVD-19 have high levels of the cytokine, IL-6. This occurs during the “cytokine storm” that these patients can get when their macrophages and monocytes produce enormous quantities of pro-inflammatory cytokines. This is also called the “macrophage activation syndrome”. Tocilizumab is an inhibitor of IL-6 and so some physicians believe that by inhibiting IL-6, the cytokine storm can be attenuated. It is one of those “makes sense, no data” treatments that might make patients better, might not do anything at all, or might actually make them worse. But in the absence of randomized, placebo-controlled clinical trials, you can find critical care physicians who are staunch proponents and others who are staunch opponents.

And Everything Else?

Across the United States, there are some critical care physicians who believe that because D-dimer levels are high, that anticoagulation helps by preventing clotting; other critical care physicians thing that empiric anticoagulation just makes patients bleed more. Some physicians believe that inhaled vasodilators such as nitric oxide or epoprostenol improve oxygenation in COVID-19 patients by redirecting blood flow to less affected parts of the lungs; other physicians believe that these drugs can cause patients to become hypotensive and develop cardiac arrest. Other treatments that might or might not work include transfusion of plasma from patients who recover from COVID-19 infection, the anti-viral drug lopinavir/ritonavir, another anti-viral drug remdesivir, and the complement inhibitor eculizumab.

As humans, for thousands of years we have sought ways to control nature. And we base a lot of our attempts at control on anecdotal experience that leads to superstition. For example, a child falls into a volcano and the next day it rains so the village starts throwing lots of children into the volcano the next year when there is a drought. As physicians, we are no different. We see or hear about a patient who got one treatment or another and got better and then that one patient or small group of patients becomes the evidence that we base our practice on when there is a vacuum of randomized, placebo-controlled clinical trials. COVID-19 has overtaken the world suddenly, too fast for science to give us direction about how to best treat patients and so we fall back on medical superstition. Some of those superstitions will ultimately be proven to be right and others will ultimately be proven to be wrong.

So, all of a sudden, what constitutes evidence in evidence-based medicine today is a lot different than what constituted evidence last year.

April 25, 2020

Categories
Emergency Department Inpatient Practice Intensive Care Unit

With COVID-19, Hope For The Best But Prepare For The Worst

In August 2004, my family was vacationing on the North Carolina Outer Banks. I had been following Tropical Storm Alex as it came north from the Caribbean toward the island that we were staying on. On August 3rd, it was looking like the storm was going to head out over the Atlantic the next afternoon and miss Cape Hatteras. Not wanting to take any chances, I decided to get up early the next morning, pack up the kids, and head inland for the day, just to be sure. When I woke up at 5 AM, the first thing I heard on TV was that overnight, the storm had picked up wind speed, was moving across the ocean faster than expected, and had turned inland – directly toward our rental house in the town in Salvo. The second thing that I heard was that there was that storms overnight had caused sand and water to block the only road on the island leading to the bridge to mainland. The news announcer said to all of the people now stuck on Hatteras Island “Hope for the best but prepare for the worst.”

Having 4 children, my wife and I were used to buying in bulk and since this was at the beginning of our planned 2-week vacation, we were already pretty well stocked with food and supplies. We filled up all of the bathtubs with water for bathing and filled up as many bottles as we could find with drinking water.

By the time the storm hit us, Alex was now a level 2 hurricane. The eye wall passed over our rental house and as the wind changed direction with the passage of the eye, we moved all of the kids from a bedroom in one corner of the house to bedrooms in other corners. As the power went out, the wind sounded like a freight train and I watched as siding and parts of roofs were torn off of houses around us. A 2×4 board flew through the air like a missile across the street. Picnic tables, bicycles, and and lawn furniture were flung a hundred yards like toys. The roads all turned into rivers. Meanwhile, we played games with the kids and fed them Cheerios to keep them distracted.

It seemed like the end of the world and I wanted to be almost anywhere other than where we were.

But by afternoon, the wind died down, the clouds cleared, and the sun came out. All of a sudden, it was just another beautiful day on the Outer Banks. Over the next 3 days, the power returned, the flood waters subsided, and the sand was cleared from the roads. The bridge re-opened and the people staying in Salvo came out and cheered when one of the first vehicles that crossed the bridge to the island was a Budweiser truck.

COVID-19 is a lot like Hurricane Alex. The patient surge is coming and we can’t just wish it away. Just as the news announcer said on TV in the morning of August 4, 2004, we should hope for the best but prepare for the worst. But also like Hurricane Alex, the COVID-19 surge is going to pass; the clouds and pandemic storm is going to eventually subside; and life will be back to normal once more.

April 1, 2020

Categories
Inpatient Practice Intensive Care Unit

Reducing Hospital Employee Exposures To COVID-19 Patients

Having patients with COVID-19 in the hospital can be disturbing to the doctors, nurses, and respiratory therapists who take care of them. The good news is that isolation procedures work and proper use of personal protective equipment can dramatically reduce the chance of getting healthcare workers infected. Even though that risk is low, there are certain simple steps you can take that will reduce the risk even further. By taking these steps, you not only reduce healthcare worker exposures but you can also conserve personal protective equipment (masks, gowns, gloves). Here are a few:

  1. Use the right personal protective equipment (PPE) and be sure that it is used correctly.
  2. Minimize blood draws. If you don’t need daily labs, don’t send the nurses in to draw them. When you do get labs, try to cluster all of the lab tests that you need in a single phlebotomy.
  3. To anticoagulant a patient, use oral apixaban, oral rivaroxaban, or subcutaneous enoxaparin instead of a heparin drip. The problem with heparin drips is that you have to do frequent PTT blood tests. Other anticoagulants do not require testing.
  4. Use a sliding scale of subcutaneous insulin rather than an insulin drip. Insulin drips require the nurse to check the patient’s blood glucose every 1-2 hours whereas the SQ insulin sliding scale may only need to be done every 6 hours.
  5. Synchronize medications. Ordering a Q6 hour medication plus a Q8 hour medication means that a nurse has to go into a patient room 7 times a day. If that Q6 hour medication can be stretched out to be given Q8 hours, then a nurse only has to enter a patient’s room 3 times a day. Even better, use medications that only have to be given once a day whenever possible. This is particularly true of empiric antibiotics where there may be multiple equally appropriate antibiotic choices – some that have to be given 3 or 4 times a day and some that only have to be administered once a day.
  6. Use meter dose inhalers instead of nebulizer treatments. Nebulizers can result in aerolsolization of viral particles, at least in theory. Meter dose inhalers for bronchodilator treatments reduce the amount of time that a respiratory therapist has to be in a room to deliver a bronchodilator treatment.
  7. Have patients self-administer meter dose inhalers (or nebulizer treatments). The respiratory therapist can often observe the patient from a door window or a video monitor to ensure that the patient uses proper technique.
  8. Minimize the rounding team. If bedside rounds normally consist of the attending physician, a nurse, a resident, and a physician assistant, then reduce that to just the attending physician and just once a day.
  9. Don’t use physical and occupational therapy if you don’t need it. Frequently, admission order sets will include PT and OT for nearly every admission. Only order it if you really need it.
  10. Don’t order tests that you don’t need. “Routine” daily chest x-rays are usually unnecessary.
  11. Don’t order tests that can be done later. If a chest x-ray shows a suspicious pulmonary nodule and a chest CT is recommended for confirmation, that CT can wait a few weeks.
  12. Empiric treatment is OK. If a patient has epigastric pain, rather than ordering an endoscopy right away, give the patient some empiric omeprazole to minimize procedures.
  13. Utilize inpatient telemedicine for consults. There are two ways to do this, by a regular telemedicine visit or by an eVisit.
    1. CPT 99451 is for an eVisit and reimburses at 1.04 RVUs. There has to be an order for the consult and the consultant has to put a note in the medical record. The consultant must document his/her time and it must be > 5 minutes. This is a way to get reimbursed for the so-called “curbside consult”. An example would be “What follow up should occur for the incidental 5 mm pulmonary nodule that was seen on my patient’s CT scan?”
    2. CPT G0425 (30 minutes ), G0426 (50 minutes), and G0427 (70 minutes) are for initial inpatient telemedicine consults. For follow up inpatient consult visits, use CPT G0406 (15 minutes ), Go407 (25 minutes), and G0408 (35 minutes). These codes are based on the amount of time communicating with the patient
  14. Can you run your pumps outside of the patient’s door? continuous infusion pumps are forever alarming or needing infusion rates to be frequently adjusted. If the infusion pumps can be placed outside of a door with the tubing running under the door then the pumps can be adjusted without the nurse having to enter the room.
  15. Eliminate visitors. Visitors can bring COVID with them and many visitors have often had close contact with COVID patients before they were admitted, making them especially high risk. By eliminating visitors, there are fewer members of the public in patient care areas who can infect hospital staff. Furthermore, there are fewer times that the patient’s door is opened and no additional personal protective equipment consumed by the visitors.
  16. Be sure that the healthcare personnel are getting enough rest. When a nurse, RT, or physician works too long of a shift or too many shifts, fatigue can set in and with fatigue brings mistakes. Mistakes with isolation procedures can create infection risks.

March 31, 2020

Categories
Epidemiology Intensive Care Unit

Re-Using N-95 Masks In The Time Of COVID-19

The geniuses at Battelle have done it again. This time, they have invented a process for sterilizing and re-using N-95 masks using vaporized hydrogen peroxide. Battelle Memorial Institute is a non-profit scientific research and development institute here in Columbus, Ohio that is located about 3 blocks from the OSU hospital. Researchers at Battelle were the ones who invented the photocopier (and then launched Xerox Corporation), the cruise control for automobiles, the first nuclear fuel for nuclear-powered submarines, and the reusable insulin pen for injecting insulin for diabetics. In full disclosure, about 25 years ago, I had a grant from Battelle to assist with development of inhaled chemotherapy for lung cancer and that led to my receipt of the endowed Battelle Professorship in Inhalational Therapeutics that I held until assuming my position as the medical director of our hospital.

N-95 refers to a mask that can filter 95% of airborne particles. In medicine, we use N-95 masks when we care for patients with infectious diseases that are transmitted by airborne routes, such as tuberculosis, disseminated varicella, and measles virus. The virus that causes COVID-19 is the SARS-CoV-2 virus and this is believed to be transmitted by droplet spread rather than by airborne spread. Normally, viruses spread by droplets do not require the use of N-95 masks; a simple surgical mask with a plastic face shield will suffice. However, certain medical procedures, such as endotracheal intubation, can result in aerosolization of droplets containing viral particles and that is when the N-95 masks are needed.

For an N-95 mask to work properly, a healthcare worker must be fit tested to determine which specific type of N-95 mask fits tightly against the face. If a type of mask does not pass the fit test, then it will not filter out 95% of airborne particles and is no better than a regular surgical mask. Everyone’s face is shaped a little differently so different people will need different N-95 mask types. All healthcare workers who use these masks are required to get fit tested once a year to ensure that the mask that they are wearing actually does what it is supposed to do. Recently, OSHA declared that men who wear beards should not be fit tested because beards can interfere with a tight fit of the masks. For many years, I always passed my fit test with a specific type of N-95 mask despite my beard but because of OSHA’s rules, I was not able to be fit tested last year. Two weeks ago, our hospital required all men who could be involved in the care of a COVID-19 patient to shave their beards (so that they can be fit tested for N-95 masks) and thus, I shaved for the first time in 37 years!.

N-95 masks have come to the forefront of public consciousness recently because the COVID-19 outbreak is causing many hospitals to run low on N-95 masks. A misconception has arisen that N-95 masks are safer than regular surgical masks plus a face shield. For day-to-day care of patients with COVID-19, this really is not true because unless you are performing a procedure such as endotracheal intubation, an N-95 mask is unnecessary. Overuse of N-95 masks in situations when they are not necessary now will result in inadequate supples of these masks in situations when they are necessary in the future. In addition, the over emphasis on N-95 masks could lead the public to overlook the single most important way to prevent the spread of viruses spread by droplets, namely washing one’s hands after they touch various surfaces that those droplets land on (such as door handles and elevator buttons).

With supplies dwindling, Battelle invented a process for sterilizing N-95 masks so that they can be reused up to 20 times. They built the equipment to process 160,000 masks per day and this would greatly improve the nation’s N-95 mask inventory. However, medical equipment is overseen by the Food and Drug Administration. The FDA would only grant Battelle’s mask sterilization equipment limited approval, meaning that they are only permitted to sterilize 10,000 masks per day and only here in Central Ohio. That’s good news for our hospital because now we can count on a steady supply of masks in the upcoming weeks of the COVID-19 surge. But it is bad news for every other hospital in the United States.

Desperate times call for desperate measures. This may be a time for the FDA to take the desperate measure of cutting through bureaucracy.

March 29, 2020