Restraining the Unsustainable

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lation, and mucosal integrity) may contribute to its pathogenesis.1– 8 _{Enteric bacteria may ferment}

mal-absorbed carbohydrates to various gases, producing distension and increased intraluminal pressure, which could decrease mucosal blood flow. Short chain fatty acid products of fermentation could be toxic to enterocytes. Alternately, nutritionally in-duced inflammation (increased growth of bacteria with release of endotoxin) together with impaired mucosal barrier function and an imbalance between inflammatory versus antiinflammatory mediators could contribute to NEC. Poor gastrointestinal mo-tility (from immaturity, ileus, inflammation) may produce stasis and bacterial overgrowth, thus exac-erbating the abnormal states discussed above.

Nonetheless, randomized trials have not demon-strated that fast versus slow or early versus delayed feedings have altered the incidence of NEC.9 –11

In-deed, the incidence of NEC was not affected in one randomized study, which achieved full enteral feed-ings within 7 or 10 days. However, no study has fed infants at the rates or volumes present before the onset of NEC.4

In an attempt to improve gastrointestinal function and avoid the risk of intravenous alimentation, many neonatologists use gut stimulation protocols. Also called gut priming, minimal enteric feedings, hy-pocaloric feeds, or trophic feeds, this method has demonstrated important benefits when compared with infants kept nothing per os.8,12–15_{These studies}

reported no effect on the incidence of NEC, but have demonstrated a decreased incidence of direct and indirect hyperbilirubinemia as well as signs of os-teopenia. In addition, glucose tolerance and feeding tolerance were improved as well as the maturation of antral-duodenal motility. Theoretically, gut stimula-tion could also prevent fasting-induced mucosal at-rophy, thus preventing bacterial translocation and episodes of endotoxemia, mucosal inflammation, or sepsis.

In an exciting and novel approach to the disap-pointment that previous gut stimulation protocols did not prevent NEC, Berseth and colleagues16

com-pared their gut stimulation protocol with a tradi-tional enteral feeding protocol using standard rates of volume advancement. The authors had to close the study early because the incidence of NEC in the advancing volume group was 10% versus 1.4% in those receiving the gut stimulation protocol.

This study raises several important questions, such as is gut stimulation protective or do early advancing protocols contribute to the development of NEC? Both may be correct. Regardless, the study reinforces previous conclusions that gut stimulation protocols are beneficial to very low birth weight infants and should be routine in all neonatal intensive care units. There are very few contraindications to using these protocols, even in infants weighing 500 to 600 g with indwelling umbilical catheters while on ventila-tors.12,14_{The initiation of a gut stimulation protocol}

for 7 to 10 days followed by modest advancement of feedings, particularly with human milk, may greatly reduce the incidence of NEC.13,16

Robert M. Kliegman, MD Department of Pediatrics Medical College of Wisconsin Milwaukee, WI 53226

REFERENCES

1. Kliegman RM, Walker WA, Yolken RH. Necrotizing enterocolitis: re-search agenda for a disease of unknown etiology and pathogenesis.

Pediatr Res.1993;34:701–708

2. Brown EG, Sweet AY. Preventing necrotizing enterocolitis in neonates.

JAMA.1978;240:2452–2454

3. Uauy RD, Fanaroff AA, Korones SB, et al. Necrotizing enterocolitis in very low birth weight infants: biodemographic and clinical correlates.

J Pediatr.1991;119:630 – 638

4. Anderson DM, Kliegman RM. The relationship of neonatal alimentation practices to the occurrence of endemic necrotizing enterocolitis.Am J Perinatol.1991;8:62– 67

5. Kamitsuka MD, Horton MK, Williams MA. The incidence of necrotizing enterocolitis after introducing standardized feeding schedules for in-fants between 1250 and 2500 grams of less than 35 weeks of gestation.

Pediatrics.2000;105:379 –384

6. McKeown RE, Marsh TD, Amarnath U, et al. Role of delayed feeding and of feeding increments in necrotizing enterocolitis.J Pediatr.1992; 121:764 –770

7. Patole SK, Kadalraja R, Tuladhar R, Almonte R, Muller R, Whitehall JS. Benefits of a standardized feeding regimen during a clinical trial in preterm neonates.Int J Clin Pract.2000;54:429 – 431

8. La Gamma EF, Browne LE. Feeding practices for infants weighting less than 1500 g at birth and the pathogenesis of necrotizing enterocolitis.

Clin Perinatol.1994;21:271–306

9. Rayyis SF, Ambalavanan N, Wright L, Carlo WA. Randomized trial of “slow” versus “fast” feed advancements on the incidence of necrotizing enterocolitis in very low birth weight infants.J Pediatr.1999;134:293–297 10. Kennedy KA, Tyson JE, Chamnanvanikij S. Early versus delayed initi-ation of progressive enteral feedings for parenterally fed low birth weight or preterm infants. Cochrane Neonatal Group.Cochrane Database Syst Rev.2002 (Issue 4)

11. Kennedy KA, Tyson JE, Chamnanvanikij S. Rapid versus slow rate of advancement of feeding for promoting growth and preventing necro-tizing enterocolitis in parenterally fed low birth weight infants. Co-chrane Neonatal Group.Cochrane Database Syst Rev.2002 (Issue 4) 12. Kliegman RM. Experimental validation of neonatal feeding practices.

Pediatrics.1999;103:492– 493

13. Schanler RJ, Shulman RJ, Lau C, O’Brian Smith E, Heitkemper MM. Feeding strategies for premature infants: randomized trial of gastroin-testinal priming and tube-feeding method.Pediatrics.1999;103:434 – 439 14. Dunn L, Hulman S, Weiner J, et al. Beneficial effects of early hypocaloric enteral feeding on neonatal gastrointestinal function: preliminary report of a randomized trial.J Pediatr.1988;112:622– 629

15. Williams A. Early enteral feeding of the preterm infant.Arch Dis Child Fetal Neonatal Ed.2000;83:F219 –F220

16. Berseth CL, Bisquera JA, Paje VU. Prolonging small feeding volumes early in life decreases the incidence of NEC in very low birth weight infants.Pediatrics.2003;111:529 –534

Restraining the Unsustainable

Medical care the world over stands on the brink of a huge expansion of investment in health care in two possible directions: either need-driven coordinated expansion of labor-intensive continuing care and health maintenance for whole populations. . .or profit-driven independent ex-pansion of capital-intensive technical repair, as an

ulti-Received for publication Dec 4, 2002; accepted Dec 4, 2002.

Address correspondence to William A. Silverman, MD, 501 Via Casitas, Apt 421, Greenbrae, CA 94904-1947. E-mail: [email protected].

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mately false alternative to continuing care, directed at profitable sub-groups in the population.

—Julian Tudor Hart1

S

everal years ago, Daniel Callahan (Director of the Hastings Center, founded in 1969 for the study of value and the sciences) examined the implications of a frequently noted observation: “No matter how much money is spent, and no matter what the health gains, they never seem enough.”2

This worrisome image of insatiable demands led him to ask some fundamental questions about the “ap-propriate goals of medicine.” Callahan2 _was

inter-ested to see similar issues in debates about the envi-ronment, and he concluded there is a “need for a view of medicine that would be at once equitable and sustainable.” Despite all of its excitement, he opined, modern medicine has become “increasingly and painfully unaffordable.” “Just as we need a sustain-able environment, we need a sustainsustain-able medicine.” Conservationists have argued that nature must be protected to serve human needs. With wise manage-ment of natural resources, according to this line of reasoning, there is no reason to expect that these assets will not be available to serve human ends indefinitely. However, as Callahan noted, the “belief of scientific medicine—like the corresponding belief of many conservationists—that nature is infinitely plastic and repairable, that technology can solve the problems of technology, and that progress can move forward in a straight line should now be seen as. . . patently self-deceptive.” Callahan recommended against adopting “the kind of conservationism that sees nature as the kind of stuff for human manipu-lation, even in the name of health.” In the end, he predicted, “medicine will need to find a benign equivalent of the conservationists’ view of nature.” And, he stressed, medicine should “adopt their long-term perspective, recognizing that the great impera-tive is sustainability over generations, not just for the next few years.”

Our country’s $1.3 trillion-per-year disorganized approach to the provision of health care provides the most apposite current example of unsustainability. And there has been no dearth of critics of the confu-sion that resulted from a series of historical acci-dents. For example, the American job-based form of health insurance began fortuitously during World War II when wages were frozen by government edict. This stricture led employers to offer medical benefits in an effort to attract scarce employees. J. D. Kleinke,3_{an economist, has recently charged that this}

and similar unplanned events were largely respon-sible for the beginning of “a pernicious effect on consumers because it denies them choice and uncou-ples them from any awareness of the costs of treat-ment.” The economic behavioral effects of the Amer-ican arrangement, Kleinke asserts, are “deeply perverse and go a long way in explaining why the United States spends far more per-capita on medical care than any other nation in the world.”

As currently structured, Kleinke charges, health care in the United States “is so rife with economic conflict that every attempt to simplify it actually

complicates it further.” And American doctors have been rendered relatively powerless amid dozens of layers of health care administration. Moreover, con-trol is often in the hands of patients and their fami-lies, few of whom behave rationally during a medical crisis. “Even if physicians’ clinical behavior could be analyzed and modeled fairly,” Kleinke continues, “the sheer irrationality woven into the experience of major disease or injury produces chaotic perturba-tions in every patient’s action and reaction.”

“The creation of a standard benefits plan for health care in the United States,” Kleinke asserts, “would result in enormous economies of scale.” Unfortu-nately, he notes, “legions of benefits-consultants, brokers, claims-processing software companies, re-imbursement-vendors and entrepreneurs of all shapes and sizes divert billions of dollars [every year] that are earmarked for medical care, as they preside over the oxymoron that is the US health care ‘system’.”

A notable example of the conspicuous and even-tually unsustainable disconnect between input and outcome is found in neonatal medicine. This rela-tively new specialty invented itself in the 1960s and grew very rapidly, particularly in the United States, with no thought given to overall limits and goals. And the expense of neonatal intensive care has grown enormously (the outlay of this for-profit in-dustry in our country was estimated in 1992 at $5.6 billion per annum).4 _{Now that the very smallest,}

marginally viable neonates are rescued routinely, troubling questions have surfaced about the long-term biological and social consequences of the im-mediate technical triumphs.5 _{For example, parents,}

struggling to rear severely retarded children born after extreme prematurity, protest6 _{that they were}

“made to feel like criminals for questioning” heroic medical treatment. Doctors are “out of touch with the harsh realities of our children’s lives,” they com-plain. “Where,” they ask, “is a description of the months or years of grueling hospitalization with the associated gastrostomy tubes, jejunostomy tubes, and fundoplications; the tracheostomies, shunts, or-thopedic, eye, and brain surgeries; hyperalimenta-tion, oxygen tanks, and ventilators?” Similarly, med-ical accounting fails to recognize the frequency of emotional and financial breakdown in families caused by the extreme burdens of caring for devel-opmentally retarded children with superimposed se-vere medical problems.

In addition to these disturbing long-term results of unrestrained rescue, it is also clear that we have too many highly trained experts and an oversupply of technical resources when compared with other de-veloped countries.7,8 _{Some leaders in neonatology}

are now asking “Is more neonatal intensive care always better?” A way forward is suggested by a declaration in the Netherlands,9 _{where it has been}

decided on the basis of humane concerns to stop active intensive treatment of the most immature in-fants (those born before 25 weeks’ gestation).

Callahan concluded his discourse with the asser-tion that a “sustainable medicine is necessary not simply because we cannot afford any other but also

COMMENTARIES 673

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because it could help displace the goal-less, progress driven, never-happy medicine that grew out of [its] embrace of modernism.” We need to understand “the social meaning of medicine and health care,” he declared, “and the relationship of medicine to the cultures of which it is a part.” In this regard, J. Kirby10 _{of Australia also made some relevant}

com-ments (concerning the need to slow the headlong rush of modern medicine),

“My hope is that it won’t be the epitaph of our generation that people will say: ‘Here was a commu-nity which developed the most amazing, dazzling fields of science and yet proved themselves so indif-ferent or incompetent, that they didn’t address the serious social and ethical consequences of what they were up to.’”

William A. Silverman, MD Greenbrae, CA 94904-1947

REFERENCES

1. Hart JT. Two paths for medical practice.Lancet.1992;340:772–775 2. Callahan D.False Hopes.New Brunswick, NJ: Rutgers University Press;

1999

3. Kleinke JD.Oxymorons: The Myth of a U. S. Health Care System.New York, NY: Jeffrey-Bass; 2001

4. Winslow R. Infant health problems cost business billions.Wall Street Journal.May 5, 1992

5. Jobe AH. Predictors of outcomes in preterm infants: which ones and when?J Pediatr.2001;138:153–156

6. Culver G, Fallon K, Londner R, et al.Informed decisions for extremely low-birth-weight infants [letter].JAMA.2000;283:3201

7. Lorenz JM, Paneth N, Jetton JR, den Ouden L, Tyson JE. Comparison of management strategies for extreme prematurity in New Jersey and The Netherlands: outcomes and resource expenditure.Pediatrics.2001;108: 1269 –1274

8. Thompson LA, Goodman DC, Little GA. Is more neonatal intensive care always better? Insights from cross-national comparison of reproductive care.Pediatrics.2002;109:1036 –1043

9. Sheldon T. Dutch doctors change policy on treating preterm babies.

BMJ.2001;322:1383

10. What rules for embryology? [editorial].Manchester Guardian Weekly.

February 7, 1981

Thimerosal and Autism?

C

oncern has been expressed over the possibility that the mercury-containing compound thi-merosal in vaccines may cause autism.1– 4

Thimerosal is sodium ethylmercury thiosalicylate, an organic compound of ethyl mercury, included in certain vaccines to protect multiple dose ampules from bacterial and fungal contamination. Mercury in sufficient dose is neurotoxic, and probably more toxic in the immature brain. It is reasonable to ask whether thimerosal in childhood vaccine increases risk of chronic childhood neurologic disability and specifically of autism. The available data with which to address the question are very limited and largely inferential. Most of the information we have about

mercury toxicity is related to exposure to methyl rather than ethyl mercury.

Bernard et al1_{offered an hypothesis that autism is}

an expression of mercury toxicity resulting from thimerosal in vaccines. They base this hypothesis on their views2_{that the clinical signs of mercury toxicity}

are similar to the manifestations of autism, that the onset of autism is temporally associated with immu-nization in some children, that the recent increase in diagnosis of autism parallels exposure to thimerosal, and that there are higher levels of mercury in per-sons with than without autism.

This review will examine these issues and others to ask whether, according to evidence now available, thimerosal is a probable cause of autism. We will not discuss which, if any, of the differing guidelines designed to limit exposure to mercurials is appropri-ate for deciding whether thimerosal in vaccines is in all regards safe for children. Our focus is on a nar-rower but important question: whether current evi-dence indicates that mercury at any known dose, form, duration, age, or route of exposure leads to autism.

ARE THE CLINICAL MANIFESTATIONS OF AUTISM SIMILAR TO THOSE OF RECOGNIZED

MERCURY TOXICITY?

Bernard et al1 _{present a table listing} _⬃_{95 clinical}

findings they consider to be shared by autism and mercury poisoning. Their table does not distinguish typical and characteristic manifestations of either disorder from the rare, unusual, and highly atypical. In mercury poisoning, the characteristic motor findings are ataxia and dysarthria (Table 1).5,6_These

signs, along with tremor, muscle pains, and weak-ness, are noted on relatively high-dose exposure, acute or chronic. In 3 Romanian children accidentally exposed to ethyl mercury in a fungicide, these same symptoms were prominent.7 _{The outcome of fetal}

methyl mercury poisoning in severe form also in-cluded spasticity.8 _{In contrast, in autism, the only}

common motor manifestations are repetitive behav-iors (stereotypies) such as flapping, circling, or rock-ing. Persons with Asperger syndrome may be clumsy, and hypotonia has been noted in some in-fants with autism; the frequency of clumsiness and hypotonia in autism spectrum disorders is not estab-lished. No other motor findings are common in au-tism, and indeed the presence of ataxia or dysarthria in a child whose behavior has autistic features should lead to careful medical evaluation for an al-ternative or additional diagnosis.

The most characteristic sensory finding of mercury poisoning is a highly specific bilateral constriction of visual fields.5,6,9_{With lesser exposure there may be}

compromise of contrast sensitivity.10,11 _{In addition,}

there may be paresthesias or, in infants, erythema and pain in hands and feet because of peripheral neuropathy. In autism, decreased responsiveness to pain is sometimes observed along with hypersensi-tivity to other sensory stimuli, including hyperacu-sis. The “sensory defensiveness” of autism seems to reflect altered sensory processing within the brain rather than peripheral nerve involvement.12–14

Received for publication Dec 2, 2002; accepted Dec 2, 2002.

Reprint requests to (K.B.N.) NEB/NINDS/NIH, Building 10, Room 5S221, Bethesda, MD 20892-1447. E-mail: [email protected].

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DOI: 10.1542/peds.111.3.672

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William A. Silverman

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