SIDS and respiratory acidosis

October 23, 2006 (Las Vegas) — Sudden infant death syndrome (SIDS) may be a result of shock, metabolic acidosis, and loss of homeostasis, according to findings presented here at the annual meeting of the American Society for Clinical Pathology.

These data challenge the notion that respiratory acidosis is the etiology of most, if not all, SIDS cases, the study's author, Hazel L. McGaffey, MD, told Medscape. "Our belief is that it's the metabolic acidosis that causes the heart to stop," said Dr. McGaffey, a retired pathologist at Sacred Heart Hospital in Idaho Falls, Idaho, and a former coroner.

It was in her capacity as coroner that Dr. McGaffey conducted laboratory studies on SIDS cases that occurred between 1965 and 1987. Venous blood drawn from the superior sagittal sinus and cerebrospinal fluid from the cisterna cerebellomedullaris was analyzed from 40 infants who died between 1 and 8 months of age. All of the samples were collected an average of 7 hours after the children were last seen alive, and the results were compared with findings taken from children and adults who died from other causes, including respiratory and cardiac illness, acute trauma, and various chronic diseases.

The SIDS cases showed extreme acidosis, with an average pH of 6.15 compared with an average of 6.65 among children who died of respiratory causes. The SIDS bicarbonate buffer was decreased to an average of 6.31 mEq/L compared with an average of 15.8 mEq/L among cases of respiratory death.

These findings suggest that the brainstem respiratory center may have shut down secondary to severe metabolic acidosis, Dr. McGaffey said. "The elevation in carbonic acid [averaging 5.24 mEq/L in SIDS cases compared with 2.33 mEq/L in cases of respiratory death] suggests that metabolic acidosis was the cause of death," she explained. "As our findings indicate, respiratory acidosis is associated with lower, not higher, carbonic acid."

Electrolyte levels were also severely imbalanced. Extreme hyperkalemia was one of the most striking findings: the SIDS babies had an average potassium concentration of 24.4 mEq/L compared with a normal range of 4.1 to 5.3 mEq/L, according to Dr. McGaffey. They also had hyponatremia, with an average sodium level of 127.9 mEq/L compared with a normal range of 139 to 146 mEq/L; anoxia, as reflected in a lactic acid level of 22.6 mMol/L; and the presence of nucleated red blood cells. Elevated uric acid and blood urea nitrogen levels suggested early renal failure.

"All of this may reflect metabolic acidosis that began developing several days before death," Dr. McGaffey said. "If we look for that in future cases, we may be able to prevent some deaths." She cited one case of a 2-month-old male admitted with a low-grade fever and a croupy cough. His pH was 7.2, and his HCO₃- was 16.52 mEq/L. However, his potassium was slightly elevated, at 6.1 mEq/L, and he had anemia and a relative lymphocytosis, among other findings. The patient was given penicillin, improved, and was discharged, but his symptoms returned and about 10 days later he was found dead in his crib. A full autopsy, including postmortem clinical laboratory testing, revealed findings typical of SIDS at 7 to 8 days after the original tests. "This suggests that the development of metabolic acidosis in SIDS may take considerable time," Dr. McGaffey said. "If we look for that, we might be able to prevent death."

"I think this is a very significant paper," said Martin Kroll, MD, professor of pathology at the University of Texas Southwestern School of Medicine in Dallas. "It certainly points a finger in a different direction than we considered before," he told Medscape.

Currently, healthy babies seldom undergo metabolic testing after the first month of life, "but it is extremely doable," said Dr. Kroll, who was not involved in the study. "Maybe we should do more laboratory tests on children. It certainly takes time for these conditions to develop; with testing, we might be able to intercept the problem."

This study did not receive commercial support. The authors did not report any relevant financial relationships.

Am J Clin Pathol. 2006;126:636. Abstract 34; presented October 19, 2006.