|Year : 2021 | Volume
| Issue : 2 | Page : 149-154
Association of developmental lumbar spinal canal stenosis and stunting
Jamlick Micheni Muthuuri
Department of Orthopaedic/Trauma, The Mombasa Hospital, Mombasa, Kenya
|Date of Submission||16-Mar-2020|
|Date of Decision||12-Jun-2020|
|Date of Acceptance||11-Sep-2020|
|Date of Web Publication||24-May-2021|
Jamlick Micheni Muthuuri
The Mombasa Hospital, P.O. Box 84074-80100, Mombasa.
Source of Support: None, Conflict of Interest: None
Objective: To determine a possible relationship between developmental lumbar spinal canal stenosis (DLSS) and stunting. Background: Stunting is due to failure of longitudinal length with shortened long bones. Stunted individuals have failure of growth of long bones implying a possibility of involvement of short and flat bones. The hypothesis in this study is that DLSS is part of a generalized skeletal dysplasia. Materials and Methods: This is a cross-sectional study (CSA) of 400 patients looking at the association of DLSS with stunting. The study compares the size of the spinal canal in individuals with stunting and those without stunting. Stunting was defined according to the WHO/UNICEF criteria of −2SD of the median height of the same population. The participants were divided into two types: those who were deemed stunted and those who were not. DLSS was similarly defined as −2SD of the relevant measured parameter. The study included skeletally mature patients between 18 and 60 years. All syndromic individuals, those with spine tumors and previous spine surgery, were excluded. Results: Four hundred individuals were sampled from a pool of 597 participants. One hundred and eight or 27% were stunted. The stunted individuals had statistically significantly shallow canal depths or anteroposterior diameters (11.2 ± 2.0 mm vs. 14.6 ± 2.6 mm, t(398) = −11.1, P < 0.001), and narrower canal widths (transverse diameters) (14.6 ± 3.3 mm vs. 18.8 ± 4.5 mm, t(398) = −8.1, P < 0.001) and smaller CSAs (134.0 ± 49.4 mm vs. 220.2 ± 82.0, t(398) = −9.4, P < 0.001) when compared to individuals with normal heights. Odds ratio was 10. Conclusions: Stunted individuals have smaller lumbar spinal canals when compared to nonstunted individuals. It can be concluded that developmental lumbar spinal canal stenosis is part of a generalized skeletal dysplasia.
Keywords: Developmental, lumbar–spinal–canal, stenosis, stunting
|How to cite this article:|
Muthuuri JM. Association of developmental lumbar spinal canal stenosis and stunting. Indian Spine J 2021;4:149-54
| Introduction|| |
Undernutrition in children has strongly been associated with shorter adult height because most stunted children remain stunted to adulthood. Therefore, the adult height of an individual is influenced by early nutrition. Stunting has traditionally been used as an indicator of longitudinal bone growth, particularly during childhood. Stunting is defined by World Health Organization (WHO/UNICEF) as “length below minus two standard deviations (SD) from median height for age of reference population.” A “reference population” here refers to that population whose disease experience during some period is the source of the study data.
According to Pollit et al., a third of all young children in developing countries are affected by stunting. Sereebutra et al. studied 131 children in Guatemala and found the overall prevalence of stunting to be 34.4% in the study population. Data from nearly 3000 Filipino children followed after birth to 2 years of age showed stunting occurred in 69% of rural and 60% of urban children by 24 months of age. A systematic review by De Onis et al. on the global magnitude of protein-energy malnutrition found the global prevalence of stunting as 38.6%. That study found the prevalence rate in Kenya to be 32.2%. Recent studies from sub-Saharan Africa showed different levels of stunting, for example in Burundi stunting was reported to be 57.7%, Malawi 47.1%, Comoros 11.1%, and 8.7% in Ethiopia. In 2017, the prevalence of stunting in Kenya was recorded as 23.3%.
Stunting has been associated with smaller lumbar vertebra with smaller canal size, particularly the anteroposterior (AP) diameter and consequently, the cross-sectional area (CSA). These were found to be significantly reduced in low-birth-weight babies. Therefore, dysplasia of the lumbar vertebrae may present as a smaller vertebra body with short pedicles and shallow spinal canals. In this study, the phenomenon is referred to as developmental spinal canal stenosis (DLSS). This concept is not new as evidenced by an etiological classification presented by Arnoldi et al. which attempted to distinguish the congenital, developmental, and acquired forms of spinal stenosis. Congenitally undeveloped vertebral canals tend to be syndromic, particularly associated with dwarfism and achondroplasia.
Developmental lumbar spinal stenosis may or may not be symptomatic. Symptoms occur earlier than in the degenerative patients and become more severe with degeneration. Therefore, lumbar spinal canal stenosis is an important aetiological factor in chronic low back pain syndromes.
Since the depth of the canal or the AP diameter is almost fully grown by 5 years of age, it is vulnerable to being dysplastic with early childhood malnutrition. Unfortunately, there is minimal chance to catch up, even when nutrition status improves. On the other hand, the width of the spinal canal or the transverse diameter (TRD) continue to grow until around 17 years. This allows the width of the canal to grow when nutritional circumstances improve. Therefore, in DLSS, the depth is more affected than width, giving an ovoid-shaped canal.
Various modalities have been used to measure the dimensions of the spinal canal including ultrasonography, plain X-rays, computed tomography (CT) scans, and MRI scans. The radiological modality of choice for evaluation of spinal canal stenosis and its pathology is MRI. The CT axial views are as accurate method of measuring the canal dimensions as the MRI. In both CT and MRI scans, measurements are done at the interpedicular level where the canal is spared the vagaries of degenerative processes that generally affect the junctional levels, particularly the disc level. This study used CT scans due to the paucity of MRI scanners in the study region.
This study hypothesizes that there is increased prevalence of DLSS in stunted individuals than in those with normal heights. The study used the CSA of the vertebral canal as the outcome variable with stunting as the determinant variable.
| Materials and Methods|| |
The study was a cross-sectional survey, with all data collected in a single short period, between October 2017 and January 2018 from three radiological centers. Permission for the study was granted by the Ethics Review Committee (ERC) of the University, and by the National Commission for Science, Technology and Innovation (NACOSTI). Written informed consent was obtained from each participant, without any form of coercion or monetary inducement. Confidentiality was maintained and patient information de-identified.
The procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional or regional) and with the Helsinki Declaration of 1975, as revised in 2000.
All the study participants were mature adults referred for abdominal or lumbar spine CT scan for diagnostic purposes. The referrals for CT scans were from other physicians who were not part of the study. All the participants were skeletally mature (18–60 years). The inclusion criterion was an ambulant individual with an adequate CT scan of the lumbar-sacral spine. The exclusion criterion was syndromic individuals, nonambulant patients, and those patients with gross spine deformity, previous spine/hip surgery, vertebral fractures, tumors, and infections or severe degeneration.
This study enrolled consecutive patients with an adequate CT scan of the lumbosacral spine. Each patient was sequentially given a serial number as they were recruited.
A semistructured questionnaire was used to record patient details. A detailed history of illness, including LBP, was taken followed by a thorough medical examination. Gender and age were recorded. Measurements of height, weight, and basal mass index (BMI) were done. The scans were done on Siemens Perspective128 slice CT scanners (Frankfurt, German). Measurements of the lumbar spinal canal were done digitally on all the scans by three radiographers trained specifically on the study requirements. The dimensions of the spinal canal were marked anteriorly by the posterior edge of the vertebral body, posteriorly by the anterior edge of the spinous process and laterally by the medial borders of the pedicles. The measurements of the spinal canal were done at the interpedicular level on the axial scans of each lumbar vertebra from L1 to L5. The values were recorded on the data collection sheet attached to the questionnaire. The canal parameters measured were the AP diameter (APD) for canal depth and the TRD for canal width. These dimensions were used to calculate the CSA using the mathematical formula for calculating the area of an oblong (A = πxy, where A is the cross-sectional area, x is half the TRD, and y half the anteroposterior diameter) [Figure 1].
|Figure 1: Canal measurement, APD (r), and TRD (R). Measurements made at the pedicular level|
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Measurement of height was done using a stand-meter to the nearest millimeter. After the height was determined, the sample mean, and median were determined. Using the −2SD of the median as a cut-off, those who were stunted were grouped together as Group 1 and those who were not statistically stunted as Group 2. Comparisons of the lumbar spinal canal size were made between these groups.
Stunting was used as the predictor or independent variable. The canal measurements were used as the primary outcome. The CSA was used for the final data analysis.
Data was analyzed using SPSS 20.0 (SPSS, Inc., Chicago, IL). The means were compared between the groups and the significance of the differences tested with independent t-test and nonparametric tests. Pearson correlation moment was performed to establish relationships between the parameters and the odds ratio (OR) for the association. Linear regression was applied to model the relationship between stunting and DLLS (CSA). Data was presented as the mean value ± standard deviation with a statistical significance set at P < 0.05.
| Results|| |
From October 2017 and January 2018, a total of 597 patients met the inclusion criteria. Seventeen declined to participate, 16 were excluded for spine or hip defects, and 164 were randomly sampled out. Four hundred were enrolled for the study, 108 in Group 1, and 292 in Group 2. The sampling frame is shown in [Figure 2].
|Figure 2: Sampling frame. The figure shows exclusions, sampling, and grouping. Group 1 indicates those who are statistically stunted and Group 2 indicates those who are not|
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The study had 174 males and 226 females (n = 400) with a mean age of 41.3 years. One hundred and eight participants or 27% were stunted, 292 (73%) were of normal height according to the study population median height. The differences in gender population were not statistically significant, P = 0.1034, [Table 1].
The key variables tested in the sample included age, height, lumbar spinal canal depth, canal width, and CSA. The means and statistical significance are shown in [Table 2]. The mean rank averages for the APD for both groups are shown in diagrammatically in [Figure 3].
|Table 2: Means of various variables tested in the sample and groups with standard deviation and statistical significance|
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|Figure 3: Mean rank averages for the AP diameter of both groups (the stunted and nonstunted individuals|
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Seventy-eight or 19% of all participants had DLSS, 52 (48%) were in the stunted group (N1 = 108) and 26 (9%) in the nonstunted individuals (N2 = 292). The OR between the two groups was 10. The differences in case distribution between the two groups was statistically significant, χ2P < 0.001, [Table 3].
|Table 3: Frequency of stunting and DLSS in the sample (−2SD, sample mean)|
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Pearson correlation moment between stunting and DLSS showed a strong positive linear relationship (r = 0.65) [Table 4].
Distribution was normal in both groups. One-sample statistics was used in order to compare the study population means against other populations means reported in the literature [Table 5].
|Table 5: One-sample statistics with test value for canal depth (APD) of 16 mm, canal width (TRD) of 22 mm, and CSA of 280 mm2 (n = 400)|
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| Discussion|| |
Stunting is a process that can begin early, soon after conception, or any time thereafter until about the fourth year of life. During this period, the nutrition of the mother and the child are essential determinants of the child’s growth. Stunting can, therefore, arise consequent to either infant or fetal/maternal factors. The common denominator in these factors is failure to meet the nutrition requirement for optimal growth of the child. The point at which nutritional deficiency occurs and its duration determines the physiological consequences and the future disease burden. The first 6 to 24 months of life is a particularly critical period for linear growth. This period has been noted to be the time of peak stunting prevalence in developing countries. This is due to a high demand for nutrients coupled with limited quality and quantity of complementary foods. It is reported that almost 200 million children under 5 years of age are affected globally.
Stunting is a phenotypic manifestation of a complex syndrome with multiple physiological outcomes. Stunting or linear growth deficit is the most used indicator of early life undernutrition and is used as an important public-health tool for monitoring nutrition in populations.,
This study has used stunted growth as a phenotypic characteristic of generalized skeletal growth failure, with consequences in most skeletal tissues. The underdevelopment of the lumbar spinal canal would have far-reaching clinical manifestations. With the onset of degenerative changes in the disc, facet joint, and spinal ligaments which further compromise the canal space. The prevalence of stunting in the study population was 27%. This compares with studies done by Shinsugi et al. and M’Kaibi et al. that showed the prevalence of stunting in Kenya as 34.7% and 23.3%, respectively.,
The overall prevalence of DLSS in the study population was 19%. The prevalence is much higher than reported in other studies; Schroeder et al. reported a prevalence rate of developmental lumbar stenosis of 9.3% in the American population. Kalichman et al. reporting in the Framingham study concluded that the prevalence of “congenital stenosis” was 7.3%. Both authors studied populations in the developed world with very low rates of undernutrition and, therefore, stunting.
The cut-off in this study population for radiological diagnosis of DLSS was −2SD of mean parameter measurement, yielding the following values, APD <10 mm, TRD <12.6 mm, and CSA <90 mm2. CSA of <90 mm2 was used in this study to discriminate those with DLSS and those without. For diagnosis of DLSS, Ullrich et al., in a US-based study, suggested a CSA value of <145 mm2 as a measure of “developmental stenosis” at L3, and Griffith et al. recommended a mid-vertebral spinal canal CSA of <212 mm2 in males and <213 mm2 in females.
The average canal dimensions found in the sample population were depth (APD) of 13.8±2.9 mm, width (TRD) of 17.8 ± 4.6 mm, and CSA of 201.0 ± 83.9 mm2.
The means of measured parameters are also lower in the stunted group than those with normal heights; APD of 10.3 ± 1.5 mm vs. 14.6 ± 2.6 mm, P < 0.001; TRD of 12.9 ± 2.6 mm vs. 18.8 ± 4.5 mm, P < 0.001; CSA of 107.1 ± 32.9 mm2 vs. 220.4 ± 82.0 mm2, P < 0.001. This clearly shows reduced or narrowed lumbar spinal canal in stunted individuals.
Alvarez et al., studying a Caucasian population, reported average lumbar spinal canal depth to be 16–20 mm with a mean of 18 mm, and the width of 22–28 (mean = 25 mm) yielding a CSA of 276–440 mm2 (mean = 350 mm2). Griffith et al., reporting a study from a Korean population, found a mean APD of 15.8 ± 1.96 mm, canal width of 23.6 ± 4.25 mm, and a CSA of 278.5 ± 50.3 mm3.
Therefore, using the global averages for comparison, the means in this study are 78% for depth, 72% for width, and 57% for CSA of the Caucasian population values. There are few published values from the indigenous African population for purposes of comparison.
The canal dimensions in this study population are, therefore, lower than in better nourished populations and also very varied.
This study shows that individuals with stunting have a higher frequency of DLSS (48%) compared to 9% of those without stunting. The OR was 10, indicating a high association between stunting and DLSS. There was also significant correlation between stunting and DLSS (R = 0.7).
The weaknesses in this study which is also its strength was the use of height (stunting) as a measure of nutrition. Short height is also attributable to other causes that include genetics and other severe stresses during peak growth periods. That is why the prevalence of stunting and DLSS in this study population is not equal population (27% and 19%, respectively). Secondly, the screening process for both stunting and DLSS may be specific but not sensitive as there are short people who are not stunted and some relatively tall people who are stunted (as they may not have reached their full-length potential).
Thirdly, screening for DLSS with the mean of the parameter measurement averaged for all the five lumbar vertebrae leaves out many individuals with stenosis at one or two segments.
| Conclusion|| |
Individuals with stunting have increased frequency and prevalence of DLSS than those with normal heights. Developmental lumbar spinal stenosis can be safely assumed to be part of generalized skeletal dysplasia caused chiefly by undernutrition.
I wish to acknowledge with gratitude the administration of The Mombasa Hospital, Aga Khan Hospital and Coast General Hospitals and their radiographers for allowing me to use their facilities. I have special thanks to my supervisors (Prof Eliab Seroney Some and Dr. Peter Chege for guiding me through the research and final dissemination. Lastly, I wish to pay tribute to the research assistants who tirelessly strived to collect the data over the period of time.
Financial support and sponsorship
Conflicts of interest
There is no conflict of interest of any form.
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[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]