Organophosphate poisoning-induced acute renal failure.

BACKGROUND: Acute kidney injury as a direct complication of organophosphate poisoning has rarely been described and its etiology is unclear. CASE: A 17-year-old adolescent girl was admitted to the pediatric intensive care unit after a suicidal attempt with chlorpyrifos, an organophosphate insecticide compound. The patient developed acute kidney injury followed by renal failure, necessitating renal replacement therapy. She was treated with continuous venovenous hemofiltration with full resolution of her renal function. CONCLUSIONS: Organophosphate poisoning can lead to renal failure, which, with proper treatment, may be reversible but, if left unattended, might aggravate the clinical course of the disease. Physicians should be aware of this rare complication.

Severe neurotoxicity associated with exposure to the solvent 1-bromopropane (n-propyl bromide).

BACKGROUND: 1-bromopropane was recently substituted for traditional ozone-depleting solvents in the industrial setting. CASE SERIES: We report a cohort of six cases of 1-bromopropane neurotoxicity occurring in foam cushion gluers exposed to 1-bromopropane vapors from spray adhesives. Patients 1-5 were exposed 30-40 hours per week over three years; patient 6 had been employed for the previous three months. Exposure had peaked over the previous month when ventilatory fans were turned off. All patients complained of subacute onset of lower extremity pain or paresthesias. Five of six complained of difficulty walking and on examination had spastic paraparesis, distal sensory loss, and hyperreflexia. Three patients initially had nausea and headache. Serum bromide concentrations ranged from 44 to 170 mg/dL (reference 0-40 mg/dL). Apparent hyperchloremia was present with serum chloride concentrations of 105 to 139 mmol/L (reference 98-107 mmol/L). Air samples taken at the workplace during gluing operations revealed the mean air concentration of 1-bromopropane to be 130 ppm (range 91-176 ppm) with a seven hour time-weighted average of 108 ppm (range 92-127 ppm), well above the EPA-proposed limit of 25 ppm. Two years after exposure, the two most severely affected patients had minimal improvement of function and they, with a third patient, continued to experience chronic neuropathic pain. CONCLUSION: This report supports the growing recognition of 1-bromopropane neurotoxicity in humans consisting most commonly of headache, nausea, and subacute spastic paraparesis with distal sensory loss. The pathogenesis of 1-BP neurotoxicity in humans has yet to be fully elucidated but may reflect a central distal axonopathy syndrome.

[Spinal cord protection and opioids].

Opioids, when administered in large doses, were reported to produce brain damage primarily in limbic system and association areas in animals. We recently found the result that intrathecal (IT) morphine after a short interval of aortic occlusion in the rodent model induced transient spastic paraparesis via opioid receptor-coupled effects in the spinal cord. Histopathological analysis revealed the possibility that IT morphine could induce degeneration of spinal ventral neurons even after a short lasting of spinal cord ischaemia in rats, and this degeneration was associated with the activation of spinal N-methyl-D-aspartate receptors by elevation of glutamate release in cerebrospinal fluid after IT morphine. Therefore, we would like to emphasize that all anesthesiologists should be aware of the possibility of morphine-induced paraplegia after thoracic aortic surgery and that we should carefully select appropriate analgesic agents from the several available opioids for these patients.

Intrathecal nicorandil and small-dose morphine can induce spastic paraparesis after a noninjurious interval of spinal cord ischemia in the rat.

We investigated the interaction between nicorandil, a K(+)ATP channel opener, and morphine on motor function after a noninjurious interval of spinal cord ischemia in the rat. Spinal ischemia was induced by aortic occlusion for 6 min with a balloon catheter in Sprague-Dawley rats. All animals received intrathecal (IT) injection of morphine (1-60 microg) 1 h after ischemia. In addition to IT injection of morphine, group M (control), group MN (combination of morphine and nicorandil), and group MNG (combination of morphine, nicorandil, and glibenclamide) received IT saline, nicorandil (10 microg), and both glibenclamide (10 microg) and nicorandil (10 microg) after 150 min of reperfusion, respectively. A quantal bioassay for the effect of IT morphine on neurological function after ischemia was performed to calculate 50% effective dose values (ED50) for inducing paraparesis at 3 h of reperfusion. The ED50 in group M and group MN was 15.1 +/- 4.9 microg and 2.9 +/- 1.0 microg of IT morphine, respectively (P < 0.05). In Group MNG, the dose-response curve shifted back to the right and the ED50 for inducing paraparesis was 11.6 +/- 4.7 microg of IT morphine. The present study demonstrates that IT small-dose morphine combined with nicorandil induces spastic paraparesis after noninjurious interval of spinal cord ischemia in the rat.

Mu and delta, but not kappa, opioid agonists induce spastic paraparesis after a short period of spinal cord ischaemia in rats.

BACKGROUND: Intrathecal (IT) morphine given after a short interval of aortic occlusion in a rodent model induced transient spastic paraparesis via opioid receptor-predicted actions in spinal cord. To determine the role(s) of spinal opioid receptor subtypes we investigated whether IT administration of various selective opioid receptor agonists can induce paraparesis following a short period of spinal cord ischaemia in rats. METHODS: In Sprague-Dawley rats implanted with an IT catheter, spinal cord ischaemia was induced for 6 min using an intraaortic balloon. Mu ([D-Ala2, N-Me Phe4, Gly-ol5] enkephalin), kappa (U50488H) or delta ([D-Pen(2,5)] enkephalin) selective agonists were injected intrathecally 30 min after reperfusion. A separate group of animals was used to investigate the dose-response effect on this motor dysfunction. For this purpose, three doses of mu, kappa, or delta agonists were injected intrathecally after ischaemia. After IT injection, recovery of motor function was assessed periodically using the motor deficit index (0=complete recovery; 6=complete paraplegia). RESULTS: IT administration of mu and delta but not kappa agonists produced dose-dependent effects in the induction of spastic paraparesis. In addition, this spasticity induced by IT mu and delta agonists was reversed completely by IT naloxone and naltrindole, respectively. CONCLUSION: These results suggest that the effect of various opioids on motor function after a short period of spinal cord ischaemia depends upon individual opioid receptor subtypes.

Enfermedades neurológicas asociadas al consumo de variedades de mandioca con alto contenido en gluconitrilos / Neurological diseases associated with intake of cassava varieties with high gluconitrile content

Los alimentos vegetales contienen, con frecuencia, compuestos tóxicos. En condiciones normales, el procesamiento de dichos alimentos está adaptado para permitir su consumo seguro. Sin embargo, en determinadas circunstancias, estos tóxicos provocan la aparición de enfermedades, entre las que destacan las de tipo neurológico. Un caso importante es el de la mandioca o yuca, la principal fuente de fécula en múltiples regiones tropicales. La mandioca contiene los gluconitrilos linamarina y lotaustralina, cuya degradación genera cianuro. Datos epidemiológicos asocian el consumo de mandioca a hipotiroidismo y a 2 enfermedades neurológicas muy diferentes entre sí: la neuropatía atáxica tropical, una polineuropatía periférica que cursa con sordera sensitivoneural y atrofia óptica, y el konzo, una paraparesia espástica. La neuropatía atáxica tropical y el konzo se asocian a 2 patrones diferentes de consumo de mandioca. La neuropatía atáxica tropical es una enfermedad crónica, que se presenta en personas de más de 40 años en determinadas regiones de Nigeria en las que se da una dieta monótona predominada por la mandioca. El konzo es una enfermedad que afecta preferentemente a niños y mujeres y que aparece de forma abrupta en períodos de crisis alimentaria, en los que la mandioca se mantiene prácticamente como el único alimento disponible. La patogenia de ambas enfermedades sigue sin esclarecerse. Para la neuropatía atáxica tropical, su origen alimentario no está suficientemente demostrado. En el caso del konzo, el origen tóxico-nutricional y la vinculación con la mandioca parecen indudables; sin embargo, la hipótesis más simple, la que supone un papel causal del cianuro, no parece cierta (AU)

Combination of cassava flour cyanide and urinary thiocyanate measurements of school children in Mozambique.

The maximum daily cassava flour intake of children may be calculated from determination of the total cyanide content of cassava flour and urinary thiocyanate levels of school children in samples collected at the same time and place. Four sites, two with and two without recent konzo cases, were chosen for study. In two sites with recent konzo cases, 84% and 93% of school children consumed cassava the previous day, and the calculated maximum daily consumption of cassava was over 700 g. In two sites without recent konzo cases, about 50% of school children consumed cassava the previous day and the calculated daily consumption of cassava flour was less than 150 g. By measurements of cyanide in flour and urinary thiocyanate we are therefore able to distinguish between communities whose diet is almost totally reliant on cassava, and who are therefore susceptible to konzo, and those who have a broader diet and are free from konzo. In another calculation it is shown that 4-23% of the essential S-containing amino acids in the cassava flour consumed by children is used up to detoxify and flour cyanide to thiocyanate. This depletion of methionine and cystine may leads to protein deficiency and may contribute to onset of konzo.

Intrathecal administration of morphine, but not small dose, induced spastic paraparesis after a noninjurious interval of aortic occlusion in rats.

UNLABELLED: We sought to investigate the dose-response relationship for the effect of intrathecal morphine on the transient spastic paraparesis after short-lasting spinal ischemia in rats. Spinal ischemia was induced by aortic occlusion for 6 min with a balloon catheter in rats previously implanted with an intrathecal catheter for drug delivery. After ischemia, the animals were allowed to recover, and 3, 10, or 30 microg of morphine or saline was injected intrathecally at 30 min after reperfusion. In a separate group, the quantal bioassay for the effect of intrathecal morphine on neurological function after ischemia was performed to calculate 50% effective dose values for inducing paraparesis at 2 h of reperfusion. Subsequently, histopathology of the spinal cord was assessed at 48 h of reperfusion. Intrathecal injection of 30 or 10 micro g of morphine, but 3 micro g of neither morphine nor saline, caused a progressive development of hindlimb spasticity. The 50% effective dose values for inducing paraparesis were 16.1 +/- 1.5 microg in assessing behavioral analysis at 2 h after intrathecal morphine. Histopathological analysis of spinal cords in the 30- microg group revealed the presence of dark-staining alpha-motoneurons in lumbosacral segments. We conclude that spinal administration of a large dose of morphine after transient aortic occlusion may be associated with a potential risk of paraparesis and the corresponding development of neurological dysfunction. Careful attention should be paid when intrathecal morphine is used for pain control after thoracoabdominal aortic aneurysm repair. IMPLICATIONS: Spinal administration of large-dose morphine after transient aortic occlusion may be associated with a potential risk of irreversible spinal neuronal degeneration and the corresponding development of neurological dysfunction.