A retrospective case-control cohort analysis of comorbidity and health expenditure in hospitalized adults diagnosed with obesity utilizing ICD-10 diagnostic coding.

The cost and comorbidity of obesity in hospitalized inpatients, is less known. A retrospective study of patients presenting to a large district hospital in Western Sydney (April 2016-February 2017) using clinical, pathological as well as diagnostic coding data for obesity as per ICD-10. Of 43 212 consecutive hospital presentations, 390 had an obesity-coded diagnosis (Ob, 0.90%), of which 244 were gender and age-matched to a non-obesity coded cohort (NOb). Weight and BMI were higher in the Ob vs NOb group (126 ± 37 vs 82 ± 25 kg; BMI 46 ± 12 vs 29 ± 8 kg/m2 , P < .001) with a medical record documentation rate of 62% for obesity among Ob. The Ob cohort had 2-5× higher rates of cardiopulmonary and metabolic complications (P < .001), greater pharmacologic burden, length of stay (LOS, 225 vs 89 hours, P < .001) and stay in intensive care but no differences in the prevalence of mental disorders. Compared with BMI <35 kg/m2 , inpatients with BMI >35 kg/m2 were 5× more likely to require intensive care (OR 5.08 [1.43-27.3, 95% CI], P = .0047). The initiation of obesity-specific interventions by clinical teams was very low. People with obesity who are admitted to hospital carry significant cost and complications, yet obesity is seldom recognized as a clinical entity or contributor.

Motor neuron disease: a primary disorder of corticomotoneurons?

It has been suggested that the primary site of damage in motor neuron disease (MND) is the cortical motor neuron, with secondary degeneration of spinal motor neurons. To test this hypothesis, we sought to determine if loss of corticomotoneurons in MND precedes spinal motor neuron loss. The density of corticomotoneurons was measured in 18 MND and 9 control cases using 10-microns horizontal sections of motor cortex in the hand/arm region. The density of spinal motor neurons was measured in 10-microns transverse sections of the lower cervical spinal cord. Corticomotoneuron and spinal motor neuron densities were decreased in MND cases compared to controls, but in MND cases there was poor correlation (r2 = 0.06) between corticomotoneuron and spinal motor neuron densities. The results indicate that corticomotoneuron and spinal motor neurons are lost at different rates in different MND patients, and that corticomoteneuron loss is unlikely to be a primary event in MND.