In Texas, trauma centers lose, on average, $20 million each year. In California, losses total at least $400 million for the state’s major trauma centers, and the California Medical Association is calling for a $300 million infusion of cash into the state’s trauma system just to maintain the services.
“Trauma care in Texas is imperiled,” claims Amir Rubin, chief operations officer at Hermann Hospital in Houston. “Texas’ trauma centers are currently delivering the highest levels of critical services to all Texans around the clock, regardless of HMO plan restrictions, regardless of insurance status. These trauma centers however, cannot sustain losses year after year and remain viable.”
In Texas, where motorists rack up the highest number of annual motor vehicle accidents (3901 in 1999), trauma centers often mean the difference between life and death for accident victims, who make up the majority of their patients. However, according to a survey of the state’s Level I and II trauma centers by Mr Rubin, most centers are losing large amounts of money.
Trauma in the uninsured population accounts for much of the increase during the past decade, according to Mr Rubin’s study. Twenty-one percent of Texans are without health insurance, he reported, with 31% of the population of Harris County (which includes Houston) and 25% of Dallas County uninsured. During the past year, the volume of trauma increased 5.4%, with concurrent increases in operating losses. At the same time, the federal government cut the funding that goes into state Disproportionate Share Payments. These payments were designed to help defray deficiencies between Medicaid payments and the cost of delivering Medicaid and indigent care (for which there is no reimbursement). Payments to private, nonprofit trauma centers declined 23% and those to public, district facilities dropped 11%.
“The survey results reveal not only a bleak financial picture for the state’s trauma centers, but also a financial situation that is worsening,” Mr Rubin wrote. County hospitals must receive sufficient tax support to keep trauma centers open. However, that is not enough. Federal disproportionate share payments need to be restored to levels consistent with those of 2 years ago or even increased.
The best answer, of course, is to address the problem of the large population of insured citizens. In the short term, simplifying Medicaid enrollment and reducing the frequency of re-enrollment requirements will allow those who qualify for the program to enroll. “Texas should also look to raise the income level under which residents qualify for Medicaid,” he said.
However, those measures may not prove adequate. “Targeted state and federal financial support is needed for Texas’ Level I and II trauma centers to ensure their viability in the near term,” he wrote. “Specifically, the state legislature and the governor have taken an essential step in this direction of targeted support by creating a tertiary care and indigent care fund” during the last legislative session. Now, the state needs to fund that proposal, “which should then be focused on maintaining the viability of Texas’ Level I and II trauma centers.”
In addition, the federal government needs to evaluate the financial plight of trauma centers nationwide and contribute to keeping the vital safety net open. “I think it is a nationwide phenomenon,” said Guy Clifton, MD, professor and chairman of neurosurgery at The University of Texas Medical School at Houston. The Bush administration will have to deal with the problem within 2 years, Dr Clifton predicted. “Indigent care is an issue that will drag the trauma center down. However, solving the indigent care problem will take too much time to save trauma centers.” Trauma financing needs to be a designated fund, carved out of the healthcare budget.
Perhaps the funds could come from a tax on people convicted of driving under the influence of drugs or alcohol or it could be spread more broadly as a surcharge on license plates, said Dr Clifton. He favors the former because “it makes the people who cause the accidents pay for them.”
Saving trauma centers will require an ongoing source of funding, but Dr Clifton said funding each patient’s care at a Medicaid reimbursement level might take care of the problem. “The trauma centers would lose some money, but we don’t want to invent an inflated payment system.”
Dr Clifton noted that if private hospitals continue to lose money, they will get out of the trauma business. “The public hospitals are where the meltdown will come. That trauma volume cannot be offloaded. If the infrastructure in these hospitals goes down, it will affect the quality of and access to health care. All the beds will be full.”
He said the situation in Houston has been close to meltdown for the past year. “Our service, for the first time in 10 years, was turning down emergency patients,” he said of the Hermann Hospital center he supervises. “This requires more than a Band-Aid approach.”
Texas is not the only example of trauma meltdown. Emergency departments in California lost $400 million in 1999, according to the California Medical Association. Since 1990, 12% of California emergency departments have closed, and patients in the 335 that remain have to wait longer for care to be delivered by fewer nurses, doctors, and technicians.
Almost 80% of the 335 open California emergency departments lost money in 1999, according to the state medical society report, and more than 9 million patients were treated that year at an average loss of $46 per visit. Emergency physicians gave an additional $100 million in uncompensated care.
Two bills pending before the California Legislature seek to solve the crisis by infusing $300 million in cash into the system—$200 million for hospitals that deliver trauma care and $100 million to doctors who would otherwise go uncompensated—and by requiring HMOs to pay doctors and hospitals directly for emergency services. Currently, the HMOs pay different health plans, which can then delay or refuse to pay bills, causing dramatic cash-flow problems.
The situation in San Francisco and the Bay area is bad, said Michael Callaham, MD, chief of the division of emergency medicine at the University of California at San Francisco. Much of the furor surrounding it has been directed at ambulance diversion, but “that is just a tiny bit of the problem. The inpatient side of the hospital is stuffed.”
The inability of managed care patients to see a primary physician contributes to the problem, he said. Usually, when a patient comes in for this reason, he or she is a reasonable person “with significant disease, who says, ‘I tried to get in to see my primary care doctor and he can’t see me.’”
The result is emergency departments bulging at the seams. The volume in the hospital where Dr Callaham practices has doubled in the past 6 years. “It is now customary to treat patients in the hallways for their entire stay. We routinely have people waiting for beds.”
Even if hospitals had the money to absorb the losses associated with such care, they do not have the physical space in which to provide it. “I’m not an alarmist, but I would say that we are pretty close to a breaking point,” said Dr Callaham.
Robert Derlet, MD, chairman of emergency medicine at the University of California at Davis, sees the same sorts of stresses. On a recent weekday, his hospital was on diversion. “Our intensive care units are filled, and beds in the hospital, the operating rooms, and the recovery rooms are filled.” His department provides life-saving services only to have insurance companies downgrade payment, arguing that the services did not meet the coding the hospital put on them. Without those funds, the hospitals cannot expand services.
“People wait hours and hours in the waiting rooms,” said Dr Derlet. “People wait in the hallways. Some may have complained of abdominal pains, but they really have a heart attack. Others have been brought in by people who told the emergency department staff that they were drunk, but they really had a head injury. They lay in the hallways with a worsening subdural (hematoma). It is absolutely abominable. I am sorry for the patients. These patients need care; they need emergency care; they are sick.”
80 Nobel Laureates Urge Support for Embryonic Stem Cell Research
Eighty Nobel laureates sent President Bush a letter February 22, 2001, urging that he reconsider his opposition to research involving embryonic stem cells. They also asked that he allow the federal government to fund research into the field.
President Bush has been quoted as saying he does not think the federal government should pay for such work because the stem cells derived from human embryos use tissue from aborted fetuses. Many in the research community fear that Bush will use the power of the executive order to prohibit public financing for such studies.
The Clinton administration had approved work with the stem cells as long as it complied with requirements set by the National Institutes of Health. Those regulations require researchers to use tissue from embryos that are created in fertility clinics but not needed by the couples seeking to have children. The guidelines specifically say the embryos cannot have been created for the purposes of research.
Scientists say the stem cells could lead to therapies that would repair damaged tissues (including brains) and even cure many diseases considered almost untreatable today. Among those who signed the letter was James D. Watson, PhD, who, along with Francis Crick, PhD, first described the double helix structure of DNA.
Three Groups Identify Gene for DiGeorge Syndrome
The race to find the gene that causes the DiGeorge syndrome associated with facial and heart defects has resulted in a virtual tie among 3 groups at the following institutions: Baylor College of Medicine (Nature. 2001;410:97–101), Columbia University School of Physicians and Surgeons (Nat Genet. 2001;27:286–291), and the University of Pennsylvania Medical Center (Cell: 2001;104:619–627). A fourth group implied that another gene might be implicated in some aspects of the syndrome (Nat Genet. 2001;27:293–298).
One gene, TBX1, was identified by all 3 groups as a candidate for the cause of DiGeorge syndrome, the most frequent contiguous-gene deletion syndrome in humans. It occurs in 1 in 4000 live births. Loydie Jerome and Virginia Papaionnou, who wrote in Nature Genetics, suggested that TBX1, a transcription factor, may be critical to the aortic arch malformations seen in DiGeorge syndrome. However, in a study by Deborah Guris that was also reported in Nature Genetics, researchers saw similar defects in mice with a homozygous deletion in a gene called CRKL. Most people with DiGeorge syndrome have heart defects that demonstrate an abnormal pattern in the arteries of the aortic arch, improper alignment and septation of the aortic and pulmonary outflow vessels, and defects in the septation of the 2 ventricular chambers. In the 1980s, DiGeorge syndrome was likened to chromosomal translocations and deletions on chromosome 22.
The case for TBX1 is strong because, although deletion of both alleles is lethal in mice, the embryos demonstrate all features of the syndrome, including the cardiac outflow abnormalities. When the deletion is heterozygous, the malformations vary, depending on the genetic background, but most mice show absent or reduced aortic arches. The case for CRKL is less strong than that for TBX1 said Martina Schinke and Seigo Izumo of the Cardiovascular Division of Beth Israel Deaconess Medical Center and Harvard Medical School in a News and View article that accompanied the 2 articles in Nature Genetics (2001;27:239–240). “That TBX1 haploinsufficiency is likely to be the major determinant of aortic arch abnormalities in people with DiGeorge syndrome comes as welcome news. It should be noted, however, that point mutations in the coding sequence of TBX1 have not been found in people who present with the syndrome but lack 22q11 deletions. The new studies of TBX1 will undoubtedly reopen the search for such point mutations,” the authors said. Schinke and Izumo also said the other gene might act independently or in conjunction with this one to affect the same developmental pathways.
Antonio Baldini, MD, an associate professor of cardiology at Baylor College of Medicine in Houston, said that he and his team feel strongly that TBX1 is the cause of DiGeorge syndrome. “Because this gene is a transcription factor that regulates other genes, we think that by studying what it controls, we should be able to get a handle on a number of birth defects,” he said. “Now that we know what the gene is, we can look at patient populations to see if they carry mutations in that gene. This could help with diagnosis and possible prevention strategies in the future.”
Jump in Sudden Cardiac Deaths Reported in Younger People During Past Decade
In 1989, 2719 teenagers and young adults fell victim to sudden cardiac death. By 1996, the number had jumped almost 10% to 3000, according to researchers at the American Heart Association’s 41st Conference on Cardiovascular Disease Epidemiology and Prevention that began in San Antonio on March 1, 2001.
“Explaining these trends will require more scientific studies. But we can speculate that some of the increase may be related to the increased prevalence of cardiovascular risk factors, such as obesity among adolescents. It may also be due to a poor rate of recognizing sudden cardiac death in younger patients and applying cardiopulmonary resuscitation,” said Zhi-Jie Zheng, MD, PhD, lead author of the study and an epidemiologist at the Cardiovascular Health Branch of the National Center for Chronic Disease Prevention and Health Promotion at the Centers for Disease Control and Prevention in Atlanta.
A total of 21% of the deaths occurred among those aged 15 to 24, and 79% were in people aged 25 to 34, said Dr Zheng. The data for people aged 15 to 34 who experienced sudden cardiac death between 1989 and 1996 showed that 71% were men and 29% were women. Although the rate of the disease among men was double that of women, the rate of increase in women was 30%, higher than the 10% rate of increase seen in men. Dr Zheng said this was a matter worthy of further study. \.
- Copyright © 2001 by American Heart Association