Avoiding both overdiagnosis and undertreatment in critical care
Pulmonary hypertension and VAP require a complex balancing act by Deborah Gesensway
Published in the June 2008 issue of Today's Hospitalist
This is the first in a three-part update on critical care medicine for hospitalists
Whether they work alongside critical care subspecialists or on their own, hospitalists are picking up much of the care of critically ill patients nationwide.
What that means, said experts during the critical care presession at the Society of Hospital Medicine annual meeting this spring, is that hospitalists face a complicated balancing act. On the one hand, they must be able to recognize life-threatening diseases without overdiagnosing them. But they also have to manage diseases while not erring on the side
“We sometimes have to remind echocardiographers that there are two ventricles, not just the left one.”
–Richard N. Channick, MD University of California, San Diego
of either overusing drugs and tests or undertreating patients.
Two conditions that hospitalists commonly see in ICUs—pulmonary hypertension and ventilator-associated pneumonia (VAP)—exemplify those challenges of doing too much or too little.
When it comes to pulmonary hypertension, Richard N. Channick, MD, professor of medicine at the University of California, San Diego Medical Center, noted that hospitalists “may be the first people to think about this diagnosis. You are going to see a lot of patients admitted to the hospital with pulmonary hypertension who were never diagnosed.”
Consider the following scenario, which is fairly common: A patient, who has had noted shortness of breath for years and has possibly been told that he or she has asthma, is admitted because of worsening symptoms. With testing, it becomes clear that the patient does not have asthma, but pulmonary hypertension.
Because many symptoms of pulmonary hypertension—shortness of breath, fatigue, syncope, swelling, chest pressure, cyanosis or heart palpitations—mimic those of other diseases, Dr. Channick recommended that hospitalists keep known risk factors in mind when deciding whether to order an echocardiogram and work up the patient for pulmonary hypertension.
Key risk factors include a family history; a concomitant connective tissue disease such as scleroderma, Lupus or rheumatoid arthritis; chronic liver disease; HIV/AIDS; sleep apnea; a history of pulmonary embolism or deep vein thrombosis; congenital heart disease; left-sided heart failure; or a history of methamphetamine use.
When sending a patient for an echocardiogram, Dr. Channick said, make sure you specifically ask the technician to look for right-sided chamber size and function and to give an estimate for pulmonary artery pressure.
“Be specific about what you want,” he said. “We sometimes have to remind echocardiographers that there are two ventricles, not just the left one.”
And while the echo itself is important, it will not be enough to make the diagnosis; you’ll also need a right heart catheterization to confirm the diagnosis and determine severity. Pulmonary hypertension exists if the resting mean pulmonary artery pressure is greater than 25 mmHg or the exercise mean pulmonary artery pressure exceeds 30 mmHg.
A common misconception, he said, is that the mean pressure has to be 70 or 80 to warrant attention. “It really takes very little pressure in the pulmonary artery to cause significant right ventricular dysfunction,” he said, noting that the right ventricle is not meant to pump against very much pressure.
“A mean pressure of 25 or 26 is quite elevated and needs to be addressed.” In addition, he said, remember that a number of people will have increased pressure only during exertion.
Once you make the diagnosis, the next step is to figure out its cause. Dr. Channick recommended thinking it through anatomically: “Where is the triggering lesion that leads to the elevated pulmonary artery pressure?” (See “Pulmonary hypertension: parsing out the cause,” below.)
That’s the only way to know which treatment to go with. “We have effective therapies, but only in the right patient,” he said. “If you take a patient with severe left ventricular dysfunction and prescribe a medication to treat pulmonary hypertension, you are probably going to make that patient worse, not better. So you need to rule out significant left heart disease.”
Another mistake is putting a patient with thromboembolic pulmonary hypertension on medication rather than recommending a special clot-busting operation called a thromboendarterectomy.
“You are missing a chance of curing pulmonary hypertension in that patient,” Dr. Channick said. While hospitalists may not be the ones to order a specific therapy, “you need to know about them, and you need to know that without therapy, pulmonary hypertension is typically progressive and usually fatal.”
(See below for more information on pulmonary hypertension)
While hospitalists have to conquer the risks of underdiagnosis in pulmonary hypertension, they face the opposite dilemma with VAP, said R. Scott Harris, MD, of the pulmonary and critical care unit at Massachusetts General Hospital and Harvard Medical School in Boston. With VAP, the danger lies more with overdiagnosis, overtesting and overtreatment with antibiotics.
VAP will develop in 20% of all critically ill patients, he explained, and it is more likely to occur the longer a patient is in the ICU.
But one challenge of treating patients in the ICU, Dr. Harris said, is that fever plus an infiltrate does not always equal an infection. He cited one study that found that only 31% of ICU patients diagnosed with pneumonia actually had the infection. As a result, he said, antibiotics are often overused.
A major quandary, however, is that several methods of diagnosing pneumonia—from invasive techniques like bronchoalveolar lavage or protected specimen brush to non-invasive strategies like endotracheal aspirate—have problems with specificity and sensitivity.
Unfortunately, Dr. Harris pointed out, “evidence-based medicine does not support one technique over another.”
Antibiotic choice: “location, location, location”
Studies do show, however, that delayed administration of appropriate antibiotics for VAP increases mortality. “It doesn’t matter if you change the antibiotic in a few days,” Dr. Harris said. Study after study has shown that mortality is significantly higher if the initial selection was wrong.
But while the rationale behind using an invasive technique is to better pick the right antibiotic as soon as possible, he said, studies do not support that strategy. So far, using one technique over another does not seem to strike the right balance between avoiding delays in initiation and reducing the inappropriate use of broad-spectrum antibiotics.
So how can hospitalists caring for critically ill VAP patients do better? First, said Dr. Harris, understand that the bacteria involved are affected by the old real estate adage: location, location, location. In the ICU, the bacteria are likely to be the same whether or not patients are intubated. “Where you are determines what you get,” he said. “And mostly, it’s staph and pseudomonas.”
When trying to decide which bacteria to suspect and whether those may be multi-drug resistant, Dr. Harris advised thinking about how long patients have been in the ICU and on mechanical ventilation, and whether they were previously on antibiotics.
“Over time, we are seeing an increase in resistance to gram negatives,” he said. Plus, each hospital will exhibit different patterns. “This points to the importance of an antibiogram for your institution.”
For patients with multi-drug resistant organisms, Dr. Harris urged hospitalists to treat patients according to American Thoracic Society/Infectious Diseases Society of America guidelines. These recommend starting VAP patients on two antibiotics plus something to fight methicillin-resistant Staphylococcus aureus in those patients at risk for multi-drug resistance.
“Some people have misinterpreted this as double-covering pseudomonas,” Dr. Harris said. “But that’s not right. We’re just trying to get it right the first time. If you have pseudomonas and it turns out to be sensitive to one antibiotic, stop the other.”
The risk factors Dr. Harris outlined for multi-drug resistance include previous hospitalization (within 90 days); recent antibiotics (within 90 days); nursing home residence; home infusion therapy; chronic dialysis; home wound care; a family member with a multidrug resistant pathogen; current hospitalization of more than five days; and the presence of high-risk pathogens in the hospital or community.
Just as getting it right the first time is important in picking an antibiotic, Dr. Harris said, stopping antibiotics that are not working quickly is critical too. Excess antibiotic use, especially durations of longer than a week in mechanically ventilated patients, have been linked with subsequent multi-drug resistant infections.
Studies have shown, Dr. Harris pointed out, no difference in eight vs. 15-day courses, so “we are moving toward using shorter regimens.” He recommended following a protocol that focuses on the third day, when you can often decide whether to stop, deescalate or change antibiotics, depending on patient response.
“If the patient is responding and the culture is negative,” said Dr. Harris, “consider stopping the antibiotic because maybe the patient didn’t have an infection. If the patient is not getting better, think about dosing or search for other causes.”
Deborah Gesensway is a freelance writer who covers U.S. health care from Toronto, Canada.
Pulmonary hypertension: parsing out the cause IN A CRITICAL CARE PRESESSION COURSE held at the Society of Hospital Medicine annual meeting this spring, Richard N. Channick, MD, told hospitalists to think of all pulmonary hypertension as falling into one of four groups determined by the location of the lesion:
● Pulmonary arterial hypertension. The first group, which Dr. Channick identified as pulmonary arterial hypertension, is caused by intrinsic arteriopathies.
Something happened, he explained, to damage the small arteries and veins going in and out of the lungs. The reason can be familial or idiopathic, or it may be related to connective tissue disease, congenital heart disease or the use of illicit drugs.
A number of drugs either on the market or being investigated can improve symptoms and survival, and reduce the need for hospitalizations and transplants. These include iloprost (Ventavis), bosentan (Tracleer) and sildenafil (Revatio). Dr. Channick pointed out, however, that the drugs do not dramatically improve pulmonary artery pressure. New studies recommend against using calcium channel blockers, except for the occasional patient who is “acutely reactive to a vasodilator in the cath lab.”
● Left heart disease. The second group includes patients whose pulmonary hypertension is triggered by left heart disease, said Dr. Channick, who is professor of medicine at the University of California, San Diego (UCSD) Medical Center. Although it’s the most common cause of pulmonary hypertension, left heart disease is often missed until the patient has significant pulmonary hypertension.
The current thinking, he explained, is that chronic venous congestion in some patients leads to remodeling of the pulmonary arteries to such an extent that even when the left side of the heart is repaired and left-sided pressure is returned to normal, the pulmonary artery pressure doesn’t equally improve.
● Respiratory disease. The third group includes patients whose trigger is a respiratory disease. This includes concomitant COPD, interstitial lung disease, sleep apnea or restrictive lung disease.
For the most part, said Dr. Channick, these patients will have mild pulmonary hypertension that is sometimes reversible. An example is the classic, obese Pickwickian patient.
“If you get that patient and diurese the heck out of them—you get 40 to 50 pounds of fluid out of them—and treat their sleep apnea with CPAP, you may see dramatic improvement and even resolution of the pulmonary hypertension,” he noted.
● Thromboembolism. The fourth group encompasses patients whose trigger is thromboembolic. These individuals have nonresolved pulmonary emboli, which look more like fibrotic scar tissue sitting in the vessels and less like a true clot. About half the time, Dr. Channick said, these patients never have a history of pulmonary embolism. There tends to be a three-year delay in diagnosis.
The good news is that this form of pulmonary hypertension is curable. A few places in the world, including UCSD, perform pulmonary thromboendarterectomies. Dr. Channick advised referring patients in this group to such centers.