Rh disease (also Rhesus disease, Haemolytic Disease of the Newborn (HDNB) or Morbus haemolyticus neonatorum or erythroblastosis) is a condition that occurs when a Rh negative mother has given birth to a Rh positive baby and subsequently becomes pregnant with another Rh positive child. About 5% of at-risk pregnancies would result in still births or extremely sick babies. Many who managed to survive would be severely retarded. Once a woman gives birth to a baby with the disease, all subsequent babies would also have it. The connection between the Rh antigen and erythroblastosis was made in 1941 by Dr. Philip Levine. The treatment that came to be developed for the disease was blood transfusion, which was often ineffective or only partially ameliorative because the damage had already been done. Severely retarded children often resulted.

During the first pregnancy and the act of birth a small amount of the baby's blood may enter the mother's body. If the mother is Rh negative, her body produces antibodies (including IgG) against the Rhesus antigens on her baby's erythrocytes, if the baby is Rh positive. During the second pregnancy the IgG is able to pass through the placenta into the fetus, where it leads to agglutination and destruction of erythrocytes. The means to prevent this harmful disease is to vaccinate the mother immediately after the birth of her first child: she is treated with anti-Rh antibodies, so that the fetal erythrocytes are destroyed before her immune system can discover them.

This explanation of the etiology of the disease was first worked in 1960 out by Dr. Ronald Finn, a Liverpool, England native, who applied a microscopic technique for detecting fetal cells in the mother's blood. It lead him to propose that the disease might be prevented by injecting the at-risk mother with an antibody against fetal red blood cells. He proposed this for the first time to the public on February 18, 1960. A few months later, he proposed at a meeting of the British Genetical Society, that the antibody be anti-Rh. Nearly simultaneously with him, a group of researchers from New York City Columbia-Presbyterian Medical Center, John Gorman, Vince Freda, and Bill Pollack came to the same realization, and set out to prove it by injecting a group of male prisoners at Sing Sing Correctional Facility with anti-body supplied by Ortho Pharmaceutical Corporation. Dr. Gorman's daughter-in-law was the first at risk woman to receive a prophylactic injection on January 31, 1964. Clinical trials by the two rival groups, and others quickly confirmed their hypothesis, and the vaccine was finally approved in England and the United states in 1968. Within a year or so, it had been injected with great success into more than 500,000 women. Time magazine picked it as one of the top ten medical achievements of the 1960's. By 1973, it was estimated that in the US alone, over 50,000 baby's lives had been saved.

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Extracorporeal membrane oxygenation and pulmonary disease
From CHEST, 1/1/05 by Robert R. Kirby

To the Editor:

The case report by Mimed and colleagues (July 2004) (1) and the accompanying editorial by Weber (2) were interesting, but the conclusions appear to be questionable. Ahmed et all reported a ease of Wegener granulomatosis with diffuse alveolar hemorrhage in a 26-year-old woman, who was emergently intubated. Mechanical ventilation and positive end-expiratory pressure were utilized as treatment, but her condition continued to deteriorate and she sustained bilateral tension pneumothoraces. Four hours following tracheal intubation, venovenous extracorporeal membrane oxygenation (ECMO) was initiated. Ultimately treatment was successful, and the patient was discharged home on day 58.

The final paragraph of this article stated, "In conclusion, ECMO should be considered for supportive therapy in patients with DAH [diffuse alveolar hemorrhage] from ANCA [antineutrophil cytoplasmic antibody]-associated vasculitis when conventional ventilation has failed." Perhaps this conclusion was warranted, but the article did not mention the levels of positive end-expiratory pressure and the specific modes of ventilation that were used prior to the initiation of ECMO therapy. Thus, the reader cannot be sure that there really was no response to conventional therapy.

Conversely, in the accompanying editorial, Weber (2) took his conclusion too far, in our estimation. After presenting a succinct and informative history of ECMO therapy in neonatal, pediatric, and adult patients, he concluded "... ECMO should at least be considered for all patients with potentially reversible pulmonary failure, even if there is little or no literature support and common sense argues against its use." Thus, he jumped from a single pulmonary disease entity that had been treated successfully with ECMO in a single patient to the potential application of ECMO in all types of pulmonary failure in all patients.

This conclusion is not warranted and seems to discard the concept of evidence-based medicine that is a mainstay of current research and teaching. Although therapeutic paradigm shifts, by definition, challenge conventional medicine, they do so based on our evolving pathophysiologic knowledge. If readers were to follow the advice of Weber, many patients who might recover using conventional therapy would be needlessly subjected to ECMO, an approach that in adults is, at the least, questionable, invasive, and unproven. Regardless of his obvious enthusiasm for ECMO, we do not believe that his approach in this setting is justified, and we wonder at the rationale behind it.

Robert R. Kirby, MD, FCCP

Emilio B. Lobato, MD

North Florida/South Georgia Veterans Health System

Gainesville, FL

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: permissions@chestnet.org).

Correspondence to: Robert R. Kirby, MD, FCCP, Department of Veterans Affairs, North Florida/South Georgia Veterans Health System, 1601 SW Archer Rd, Gainesville, FL 32608; e-mail: rkirby@anest.ufl.edu

REFERENCES

(1) Ahmed SH, Aziz T, Cochran J, et al. Use of extracorporeal membrane oxygenation in a patient with diffuse alveolar hemorrhage. Chest 2004; 126:305-309

(2) Weber TR. Extending the use of ECMO [editorial]. Chest 2004; 126:9-10

To the Editor:

We would like to convince Drs. Kirby and Lobato that conventional mechanical ventilation was inadequate in our patient with Wegener granulomatosis and diffuse alveolar hemorrhage (DAH). Immediately after intubation, our patient was sedated, paralyzed, and maintained on 100% fractional expired oxygen. Positive end-expiratory pressure was titrated to 18 cm [H.sub.2]O, and the mode of ventilation was transitioned from pressure-regulated volume control, to pressure control with an inverse inspiratory/expiratory ratio, to high-frequency oscillatory ventilation. Prone positioning was not attempted due to hemodynamic instability, ongoing apheresis, and the presence of multiple lines and bilateral chest tubes. The decision was made to begin extracorporeal membrane oxygenation (ECMO) because of persistent hypoxemia (saturation, < 80%) and concern for impending morbidity and mortality.

We acknowledge the lack of evidence-based literature on ECMO, particularly in regard to the patient with DAH. We also believe that the readers of CHEST have a general understanding of the concept behind evidence-based medicine and the limitations of a single case report. ECMO has been generally accepted as the "standard of care" in neonatology. This is largely based on two small trials (1,2) involving a total of 51 infants, 40 of whom received ECMO. These trials employed adaptive randomization schemes because conventional randomized controlled trials were considered to be unethical. Likewise, a randomized controlled trial of ECMO for the patient with DAH who does not respond to conventional mechanical ventilation would also be unethical and is simply not feasible. If evidence-based medicine is required before using ECMO for unconventional indications, we will be permanently handcuffed in using this potentially life-saving therapy. Furthermore, we believe that it is our ethical duty to add our single ease report to the existing body of literature and would like to remind Drs. Kirby and Lobato that there has been a ease series and several sporadic case reports describing the use of ECMO in both the pediatric and adult populations for respiratory failure secondary to DAH.

We drink that Dr. Weber's editorial (3) does not advocate the indiscriminate use of ECMO in the patient with DAH and that there is an emphasis on the very real complication of fully anticoagulating a patient with preexisting hemorrhage. Fortunately, most patients with DAH can be maintained with conventional mechanical ventilation. In conclusion, we agree with Dr. Weber that "ECMO should at least be considered for all patients with potentially reversible pulmonary failure" when conventional therapy fails, "even if there is little or no literature support and common sense argues against its use." We contend that this is the art of medicine.

Kristin B. Highland, MD, FCCP Medical University of South Carolina Charleston, SC

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: permissions@chestnet.org).

Correspondence to: Kristin B. Highland, MD, FCCP, Medical University of South Carolina, Division of Pulmonary and Critical Care Medicine, Allergy and Conical Immunology, 96 Jonathan Lucas St, Suite 812 CSB, PO Box 250630, Charleston, SC 29425; e-mail: highlakb@musc.edu

REFERENCES

(1) Bartlett RH, Roloff DW, Cornell RG, et al. Extracorporeal circulation in neonatal respiratory failure: a prospective randomized study. Pediatrics 1985; 76:479-487

(2) O'Rourke PP, Crone RK, Vacanti JP, et al. Extracorporeal membrane oxygenation and conventional medical therapy in neonates with persistent pulmonary hypertension of the newborn: a prospective randomized study. Pediatrics 1989; 84:957-963

(3) Weber TR. Extending the use of ECMO [editorial]. Chest 2004; 126:9-10

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