Why Does Child Mortality Decrease With Age? Modeling the Age-Associated Decrease in Mortality Rate Using WHO Metadata From 25 Countries.

Background: Our previous study analyzed the age trajectory of mortality (ATM) in 14 European countries, while this study aimed at investigating ATM in other continents and in countries with a higher level of mortality. Data from 11 Non-European countries were used. Methods: The number of deaths was extracted from the WHO mortality database. The Halley method was used to calculate the mortality rates in all possible calendar years and all countries combined. This method enables us to combine more countries and more calendar years in one hypothetical population. Results: The age trajectory of total mortality (ATTM) and also ATM due to specific groups of diseases were very similar in the 11 non-European countries and in the 14 European countries. The level of mortality did not affect the main results found in European countries. The inverse proportion was valid for ATTM in non-European countries with two exceptions. Slower or no mortality decrease with age was detected in the first year of life, while the inverse proportion model was valid for the age range (1, 10) years in most of the main chapters of ICD10. Conclusions: The decrease in child mortality with age may be explained as the result of the depletion of individuals with congenital impairment. The majority of deaths up to the age of 10 years were related to congenital impairments, and the decrease in child mortality rate with age was a demonstration of population heterogeneity. The congenital impairments were latent and may cause death even if no congenital impairment was detected.

Why Does Child Mortality Decrease With Age? Modeling the Age-Associated Decrease in Mortality Rate Using WHO Metadata From 14 European Countries.

Background: Mortality rate rapidly decreases with age after birth, and, simultaneously, the spectrum of death causes show remarkable changes with age. This study analyzed age-associated decreases in mortality rate from diseases of all main chapters of the 10th revision of the International Classification of Diseases. Methods: The number of deaths was extracted from the mortality database of the World Health Organization. As zero cases could be ascertained for a specific age category, the Halley method was used to calculate the mortality rates in all possible calendar years and in all countries combined. Results: All causes mortality from the 1st day of life to the age of 10 years can be represented by an inverse proportion model with a single parameter. High coefficients of determination were observed for total mortality in all populations (arithmetic mean = 0.9942 and standard deviation = 0.0039). Slower or no mortality decrease with age was detected in the 1st year of life, while the inverse proportion method was valid for the age range [1, 10) years in most of all main chapters with three exceptions. The decrease was faster for the chapter "Certain conditions originating in the perinatal period" (XVI).The inverse proportion was valid already from the 1st day for the chapter "Congenital malformations, deformations and chromosomal abnormalities" (XVII).The shape of the mortality decrease was very different for the chapter "Neoplasms" (II) and the rates of mortality from neoplasms were age-independent in the age range [1, 10) years in all populations. Conclusion: The theory of congenital individual risks of death is presented and can explain the results. If it is valid, latent congenital impairments may be present among all cases of death that are not related to congenital impairments. All results are based on published data, and the data are presented as a supplement.

Modeling the Age-Associated Decrease in Mortality Rate for Congenital Anomalies of the Central Nervous System Using WHO Metadata From Nine European Countries.

Background: In humans, the mortality rate dramatically decreases with age after birth, and the causes of death change significantly during childhood. In the present study, we attempted to explain age-associated decreases in mortality for congenital anomalies of the central nervous system (CACNS), as well as decreases in total mortality with age. We further investigated the age trajectory of mortality in the biologically related category "diseases of the nervous system" (DNS). Methods: The numbers of deaths were extracted from the mortality database of the World Health Organization (WHO) for the following nine countries: Denmark, Finland, Norway, Sweden, Austria, the Czech Republic, Hungary, Poland, and Slovakia. Because zero cases could be ascertained over the age of 30 years in a specific age category, the Halley method was used to calculate the mortality rates in all possible calendar years and in all countries combined. Results: Total mortality from the first day of life up to the age of 10 years and mortality due to CACNS within the age interval of [0, 90) years can be represented by an inverse proportion with a single parameter. High coefficients of determination were observed for both total mortality (R2 = 0.996) and CACNS mortality (R2 = 0.990). Our findings indicated that mortality rates for DNS slowly decrease with age during the first 2 years of life, following which they decrease in accordance with an inverse proportion up to the age of 10 years. The theory of congenital individual risk (TCIR) may explain these observations based on the extinction of individuals with more severe impairments, as well as the bent curve of DNS, which exhibited an adjusted coefficient of determination of R¯2 = 0.966. Conclusion: The coincidence between the age trajectories of all-cause and CACNS-related mortality may indicate that the overall decrease in mortality after birth is due to the extinction of individuals with more severe impairments. More deaths unrelated to congenital anomalies may be caused by the manifestation of latent congenital impairments during childhood.

Occipitocervical stabilization using bilateral laminar C2 screws in children with mucopolysaccharidosis IVA.

PURPOSE: Mucopolysaccharidosis IVA (MPS IVA) is a multisystemic storage disorder. Patient's disability and life expectancy depends upon skeletal complications, including cervical myelopathy due to upper cervical compression or instability. Posterior decompression followed by occipitocervical fixation or C1-2 fusion are the most frequently recommended surgical interventions. The bony elements of C1 and C2 are often inadequately developed making routine screw insertion difficult. The main purpose of this work was to present novel technique of occipitocervical fixation using two C2 laminar screws. METHODS: Four children with MPS IVA underwent decompression and C0-C2 instrumented fusion using two C2 bilateral laminar screws. The dimensions of the C2 lamina were measured. Clinical and radiological results were monitored prospectively for a minimum 3 years. RESULTS: The mean laminar length was 24 ± 1.15 mm, width 6.15 ± 0.55 mm and height 7.4 ± 0.6 mm. Patients remained in a stable neurological condition. The mean antero-posterior diameter of the spinal canal on the pre-operative MR was 6.2 ± 0.74 mm and it was enlarged to 11.4 ± 0.8 mm after 3 years. All screws were placed adequately. In all patients, the control CT scan 2 years post-operatively revealed a stable position of the treated segments, but solid bony fusion was not registered in any patient. CONCLUSIONS: Decompression and fusion of the upper cervical spine is a generally accepted approach to treat upper cervical spine instability and myelopathy in MPS IVA patients. The feasibility and the suitability of the technique of C0-C2 stabilization using bilateral C2 laminar screws have been presented.

The relationship between S100B protein serum levels, injury severity and Glasgow Outcome Scale values in children with CNS injuries.

OBJECTIVES: The S100B protein subgroup is a thermolabile acidic calcium-binding protein, which was first described in association with the central nervous system. Destruction of nerve tissue results in S100B protein release from astrocytes and elevation of its levels in cerebrospinal fluid. If the blood-brain barrier is also damaged, S100B can pass into the systemic circulation and elevated blood levels of S100B can be detected. High S100B serum levels in patients with head injuries are predictive of possible development of secondary brain injury and may be related to the extent of permanent injury to the CNS . MATERIAL AND METHODS: The authors present results obtained from a group of 39 children aged 0 (newborns) to 17 years with an isolated craniocerebral injury. RESULTS: In our group of 39 children (aged 0-17 years) we observed excellent GOS group (GOS - Glasgow Outcome Scale 4 or 5) in 33 patients at the time of transfer from our intensive care unit to the neurological department. There were no deaths and only 6 children were in the poor GOS group (GOS 2 or 3). A second GOS evaluation was performed 6 months later: at this time 36 children were in the excellent GOS group and only 3 children remained in the poor GOS group. CONCLUSIONS: Due to high variability in S100B protein serum levels in children (dependent on age and gender) no correlation between initial S100B levels and GOS was observed for our group of patients. Our results indicate that the rate of decrease of S100B protein levels back to normal values is more meaningful than its absolute value.