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Hidden costs, hidden lives: Financial effects of fatal work injuries on families
- Lynda R Matthews, Michael Quinlan, Glenda M Jessup, Philip Bohle
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- Journal:
- The Economic and Labour Relations Review / Volume 33 / Issue 3 / September 2022
- Published online by Cambridge University Press:
- 01 January 2023, pp. 586-609
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Although workplace death is known to have profound social and psychological effects on families, the economic consequences have not been explored. This pioneering study investigated families’ financial situations following fatal workplace injuries. An online survey explored the impact of post-death financial change on 142 participants from Australia, Canada, the USA, and the UK using a scale from the economic strain model. Half of the participants experienced financial loss, and the proportion struggling financially increased from 24% to 62% after the death. Workers’ compensation claims were made by 74% of participants, but they reported problems with delays, levels of entitlement, and satisfaction with the scheme. Other key sources of assistance were family and friends or support groups and services. Participants who were older, next-of-kin, and partner/spouses were significantly more likely to experience financial loss as were those whose deceased relative worked 51+ hours per week, possibly because the deceased was self-employed or worked significant overtime not covered by compensation settlements. Those experiencing financial loss sought short- and long-term financial help, accessed social security, re-entered the workforce, acquired mental disorders, and experienced declines in physical health, at significantly higher rates than participants without financial loss, and their children developed mental health problems significantly more often. Findings highlight the detrimental, and potentially intergenerational, effects of financial loss on the health and wellbeing of families bereaved by traumatic workplace deaths. Policy issues flowing from the results are discussed, including how this informs wider debates on refashioning regulatory protection.
104 Valproate-Induced Hyperammonemic Encephalopathy: Case Studies
- Dan Matthews, Glenda Matthews
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- Journal:
- CNS Spectrums / Volume 23 / Issue 1 / February 2018
- Published online by Cambridge University Press:
- 15 June 2018, pp. 68-69
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BACKGROUND
Hyperammonemia and carnitine deficiency with concomitant encephalopathy have been reported to result from valproic acid administration (Coulter DL, J Child Neurol 1991Jan; 6(1); 7-14 and Mock, CM, et al, Am J Health Syst Pharm, 2012 Jan; 69(1):35-9). Although there have been numerous publications regarding this adverse event in the neurology literature, there have been very few reports published in the psychiatric literature. The reported incidence of hyperammonemia in children treated with valproate is 19%. It is important that prescribers be aware of the risk of valproic acid induced hyperammonemic encephalopathy, as well as its diagnosis and management.
OBJECTIVEThe current study explores the feasibility of reversing Valproate Induced Hyperammonemic Encephalopathy (VHE) by discontinuing valproic acid and normalizing the carnitine level via L-carnitine supplementation.
METHODSThree males (ages 10-16 years), are reported with 12 - 24 month histories of cognitive decline during treatment for “Bipolar Disorder of Childhood” with valproate. All were referred with multi-year histories of explosive/impulsive aggression and multiple unsuccessful psychopharmacological regimes. The one consistent medication throughout treatment was sodium valproate. The subjects received serial neuropsychological testing, complex EEG, MRI, valproic acid, carnitine, and ammonia blood levels. Oxcarbazepine titrated to 30-50 mg/kg/day was substituted for valproate after initial testing was completed. Normative reference laboratory levels were as follows: (1) ammonia (reference interval 15-45 mcg/dl), (2) total carnitine (reference interval 34-77 nmol/ml), and (3) valproic acid (reference interval 50-125 mcg/ml).
RESULTSCase Study 1: Male, 10 years old, ammonia 78 mcg/dl; carnitine 17 nmol/ml; valproic acid 92 mcg/ml. IQ 79 (compared to 105 one year earlier); MRI cerebral atrophy; EEG - left temporal aberrancies.
Case Study 2: Male, 12 years old, ammonia 76 mcg/dL; carnitine 14 nmol/ml; valproic acid 104 mcg/ml. IQ 89 (compared to 109); MRI normal; EEG - left temporal aberrancies.
Case Study 3: Male, 16 years old, ammonia 72 mcg/dl; carnitine 24 nmol/ml; valproic acid 125 mcg/ml. IQ 45 (compared to 65); MRI normal; EEG - left temporal aberrancies.
In all three subjects, after valproate was removed (oxcarbazepine substituted) and supplemental L-carnitine added, ammonia and total carnitine levels normalized. At one year follow up, IQ’s returned to previous baselines, and MRI atrophy (Case 1) normalized. EEG aberrancies were unchanged. Patients were mood and behaviorally stable on oxcarbazepine.
CONCLUSIONEvidence of cognitive decline while on valproate warrants ammonia and carnitine level testing. If these levels are abnormal, VHE should be diagnosed and valproate should be removed as rapidly as feasible; L-carnitine supplementation (the lesser of 100 mg/kg/day or 2 grams/day) should be implemented to normalize the carnitine level.
Funding AcknowledgementsNo funding.