Rubeola

During the 2-year period, 1989 to 1990, the United States experienced a resurgence in the number of measles cases reported to the Centers for Disease Control (CDC). In 1989, the CDC reported 17,862 cases of measles, which represented a fivefold increase in incidence from 1988.[1] By the peak of the epidemic, in 1990, more than 25,000 cases had been reported, representing the largest increase in measles cases since 1978.[2] More importantly, this epidemic refocused interest on the potential morbidity and mortality of this disease. More measles-related deaths were reported in the United States in 1990 than in any year since 1971.[3]

The most dramatic rise in new cases and related deaths was seen in major metropolitan areas, such as New York, Chicago, and Los Angeles. In our encatchment area of San Bernadino County, which borders on Los Angeles County, we noted a particularly severe epidemic. During the period january 1989 and january 1990, 17 deaths were reported. While the causes of death and complications have been reported,[4,5] we relate on our experience during the most recent epidemic.

MATERIALS AND METHODS

We reviewed the charts of 19 pediatric patients admitted to the pediatric ICU (PICU) with the diagnosis of rubeola (made by clinical and serologic evidence) and respiratory failure (hypoxemia requiring intubation and mechanical ventilation). Patients studied were admitted to the hospital during the period June 1989 to June 1990. The mean age of the study group was 19 months, with a range of 3 months to 51 months. The study group included 14 male and 5 female patients.

During the study period, 560 cases of measles were reported in the San Bernadino County (the encatchment area of the PICU) and 168 patients were hospitalized.

RESULTS

Measles was diagnosed by clinical examination in all 19 cases reviewed (ie, recent contact with measles; characteristic morbilliform rash; temperature >38.6[degrees] C; and antecedent upper respiratory tract infection symptoms). Of the 19 patients studied, 13 had standard serologic tests for rubeola performed and all 13 demonstrated positive rubeola titers.

Respiratory failure was the result of two causes: (1) bacterial tracheitis with upper airway obstruction, 53 percent (10/19); (2) pneumonitis with refractory hypoxemia, 47 percent (9/19).

The diagnosis of pneumonitis was made by characteristic chest radiographic changes. Hypoxemia was based on a Pa [O.sub.2] of 60 mm Hg or less by arterial blood gas analysis with a delivered FI[O.sub.2] of 1.0 Patients in this group were intubated for a mean of 28 days and showed a mortality of 56 percent (5/9). The overall mortality of the entire study group was 26 percent (5/19). In the pneumonitis group, an oxygenation index (01) of greater than 40 for 4 h or more separated the survivors from the nonsurvivors (Table 1):

0I = ([MAP x FI[O.sub.2]/Pa[O.sub.2]) X 100.

The diagnosis of tracheitis was based on evidence of upper airway obstruction (eg, stridor; increased upper airway secretions; tachypnea) and descriptions of the upper airway at the time of intubation. Of the ten patients included in this group, all were noted to have audible stridor with increased tipper airway secretions. However only four charts made note of tracheal erythema or swelling during intubation. The patients in this group all survived and were intubated for a mean of 9 days. All patients in the tracheitis group had tracheal aspirates performed between 0.5 and 6 h after intubation. All but one of the cultures grew out a specific organism, and no culture isolated more than one organism. In 70 percent (7/10) of the patients Staphylococcus aureus was the organism isolated. Of the three remaining patients, one culture grew Pseudomonas aeruginosa, another grew Escherichia coli, and the third culture showed no growth (possibly of viral cause).

Two of the patients who had document d Staphylococcus tracheitis developed signs and symptoms of toxic shock syndrome and toxic shock syndrome toxin 1 (TSST-1) was later isolated from each patient.

Finally, Table 2 lists the complications that were documented in the study group. While most of these complications have been reported,[6] no data were available on pericardial effusions in this clinical setting.

COMMENT

Between 1977 and 1988, there were sporadic epidemics of measles in the United States. However, the dramatic increases in 1989 and 1990, respectively, represent the worst epidemic in more than 10 years. This increase was due in large part to unimmunized children in large metropolitan centers, who receive much of their primary care in emergency departments where their exposure risk was the highest.[7]

In the present series, most of the children came from lower socioeconomic backgrounds and lacked proper immunizations. This is of particular note since children in this group have a higher morbidity and mortality related to measles.[8]

Previous reviews of the literature have suggested a high mortality in patients with measles complicated by, pneumonia or respiratory failure.[8-10] In this study, the presence of respiratory failure complicating measles was associated with a 26 percent mortality Furthermore, in patients with documented pnuemonitis the 56 percent mortality was higher than previously reported.[4]

While no statistical correlation could be found regarding the 0I, it is of interest that we were able to predict survivors from nonsurvivors based on OI criteria used previously in patients undergoing extracorporeal membrane oxygenation (ECMO).[11,12] This may add support to the use of nonconventional modes of ventilation (eg, high-frequency oscillators and ECMO) in patients with severe, refractory hypoxemia.

While the common denominator in those patients who died was pneumonitis, respiratory failure alone was more often associated with bacterial tracheitis. This finding is consistent with published reports,[13] both in terms of course and prognosis. Of interest, however, is the concomitant development of toxic shock. While certainly described in association with bacterial tracheitis, a link to rubeola infections has not been reported.

CONCLUSION

Recent epidemics of measles continue to be a significant public health issue in the United States. While for the most part, the disease is self-limiting, it does carry a risk for significant morbidity and mortality In particular, pneumonitis carries a very high risk of mortality. Treatment of this illness is best accomplished by adequate immunization rather than secondary treatment of its complications.

REFERENCES

[1] Centers for Disease Control. Measles -- United States, 1989 and first 20 weeks of 1900. MMWR 1990; 39:353-63 [2] Adcock LM, Bissey JD, Feigin RD. A new look at measles. Infect Dis Clin North Am 1992; 6:134-47 [3] Brunell PA. Measles one more time. Pediatrics 1990; 86:474-78 [4] Dover AS, Escobar JA, Duenal AL, Leal EC. Pneumonia associated with measles. JAMA 1975; 234:612-14 [5] Beckford AP, Kaschula ROC. Stephen C. Factors associated with fatal cases of measles. S Afr M ed J 1985; 68:858-63 [6] Halsey NA. Current status of measles in the United States 1973-1977. J Infect Dis 1978; 137:847-52 [7] Goldsmith MF. Long past date set for its disapperance, measles remains a threat to many children. JAMA 1989; 262:1156 [8] Kaschulla ROC, Druker J, Kipps A. Late morphological consequences of measles: a late and debilitating lung disease among the poor. Rev Infect Dis 1983; 5:395-403 [9] Pather M, Wesley AG, Scholand M, Thambiran AK. Severe measles-associated pneumonia treated with assisted ventilation. S Afr Med J 1976; 50:1600-03 [10] Barkin RM. Measles Mortality-analysis of the primary cause of death. AJDC 1975; 129:307-09 [11] Rivera RA, Butt W, Shan F. Predictors of mortality children with respiratory failure: possible indications for ECMO. Anaesth Intensive Care 1990; 18:385-89 [12] Lillehei CW, O'Rourke PP, Vacant JP, Crone RK. Role of extracorporeal membrane oxygenation in selected pediatric respiratory problems. J Thoric Cardiovasc Surg 1989; 98:968-71 [13] Manning SC, Ridenour B, Brown OE, Squires J. Measles: an epidemic of upper airway obstruction. Head Neck Surg 1991; 105:415-18 (*) From the Division of Pediatric Critical Care, Department of Pediatrics, Loma Linda University Medical Center, Loma Linda, Calif. Manuscript received January 21, 1993; revision accepted April 30. Reprint requests: Dr. Swift, Pediatric Critical Care, Harbor-UCLA Medical Center, Bldg N-4, Torrance, CA 90509

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