ABSTRACT
Deaths due to poisonous snakebite are a significant health related problem especially the rural heartland of in tropical countries. Renal involvement in snakebite is well documented especially so in bites by the Viperidae group. The Elapidae family consisting of cobra and kraits among other varieties are mainly considered neurotoxic. The venom of neurotoxic variety predominantly has direct depressing action on the respiratory center and neuromuscular junction. We investigated the renal changes at autopsy and histology of fatal cobra bites. This series included autopsy examination of 14 cases of fatal cobra bite in our hospital-based study. Dissected kidneys were sectioned, stained with hematoxylin & eosin stain and histological examination was done under light microscope. Five cases from head injury subject were used as control. The study reveals renal involvement in 64.28 %of fatal bites by Indian cobra (Naja naja) primarily considered neurotoxic. The major renal changes were tubular necrosis 1(7.14%), cortical necrosis 3 (21.42%) and interstitial nephritis 3(21.42%). This fact is worth giving due consideration during management and monitoring of cases of envenomation by cobra.
Subject(s)
Autopsy , Cause of Death , Elapid Venoms/toxicity , Elapidae , Fatal Outcome , Glomerulonephritis, Membranous/pathology , Humans , India , Kidney/pathology , Kidney Cortex Necrosis/pathology , Kidney Glomerulus/pathology , Snake Bites/complications , Snake Bites/epidemiology , Snake Bites/mortality , Snake Bites/statistics & numerical dataABSTRACT
There are more than 3000 species of snakes in the world but only about 350 are venomous. With approximately 10000 deaths occurring annually in India, a large proportion of snake bites occur when people work barefoot in the fields or while walking at night or early morning through fields or along roads. Although, nearly all snakes with medical relevance can induce nephropathy, leading to Acute Renal Failure (ARF), it is unusual except with bites by Russell‟s Viper, E. Carinatus and members of the genera Crotalus and Bothrops. In India, ARF is mostly associated with Russell‟s Viper and E. Carinatus bites. The incidence of ARF following Russell‟s Viper or E. Carinatus bites is 13-32% in India. A histopathological study was conducted on renal autopsy specimens from those subjects who were admitted to IPGME&R and SNP Hospital, Kolkata as a result of development of acute renal failure following poisonous snake bite. Acute tubular necrosis (100%) and Acute cortical necrosis (25%) were the most significant renal histopathological changes. Glomerular lesions were also present in 30% of cases.
Subject(s)
Acute Kidney Injury/etiology , Acute Kidney Injury/mortality , Acute Kidney Injury/pathology , Autopsy , Humans , India , Kidney/pathology , Kidney Cortex Necrosis/etiology , Kidney Cortex Necrosis/mortality , Kidney Cortex Necrosis/pathology , Kidney Tubular Necrosis, Acute/etiology , Kidney Tubular Necrosis, Acute/mortality , Kidney Tubular Necrosis, Acute/pathology , Snake Bites/complications , Snake Bites/mortality , Snake VenomsABSTRACT
Previous studies have shown ocular haemorrhages in choline-deficient rats. The aim of this paper is to study further the relationship between ocular and renal lesions and biochemical alterations in rats fed a choline-deficient diet. Fifty one weanling male Wistar rats, were divided into two groups. Thirty one ofthem were fed a choline-deficient diet and the rest was fed a choline- supplemented diet ad libitum. Animalsfrom both groups were killed between the fifth and the eighth day. Urea, creatinine and homocysteine concentrations in blood were determined. Eyes were used for light microscopy study; high resolution lightmicroscopy and the study of the retina as rétine a plat. Kidneys were studied by light microscopy. Cholinesupplementedrats did not show ocular or renal lesion. Choline-deficient rats that showed renal lesions, tubular or cortical necrosis, did not always have ocular changes. There were no ocular changes in the only cholinedeficient rat without renal lesion. The ocular changes consisted mainly in haemorrhage in both cameras andciliary and vitreous bodies. Correlations between ocular and renal lesion (r=0.72, p<0.0001, CI 95%: 0.48-0.86); ocular lesion and creatinine (r=0.86, p<0.0001, CI 95%: 0.72-0.93) and ocular lesion and urea (r=0.70, p<0.0001, CI 95%: 0.44-0.85) were positive. Choline-deficiency induces ocular haemorrhagic lesions after the development of renal necrosis. The ocular pathology could be due to the immaturity of the ocular vasculature at this age. The hyaloid, choroid and retinal system are involved
Estudios previos han demostradohemorragia ocular en ratas deficientes en colina. El objetivo de este trabajo es profundizar en la relación entre las alteraciones oculares, renales y bioquímicas en ratas deficientes en colina. Cincuenta y una ratas Wistar macho recién destetadas fueron divididas en dos grupos: treinta y una fueron alimentadas con una dieta colino deficiente y el resto con colina suplementada ad-libitum. Los animales de ambos grupos fueron sacrificados entre el quinto y el octavo día. Se midió la concentración de urea, creatinina y homocisteína en sangre. Los ojos fueron estudiados por microscopía de luz, microscopía óptica de alta resolución y para el estudio de la retina como retina plana. Los riñones fueron estudiados por microscopía de luz. Las ratas suplementadas con colina no mostraron lesiones oculares o renales. Las colino deficientes que mostraron lesiones renales, necrosis tubular o cortical, no siempre tuvieron cambios oculares. No se encontraron cambios oculares en la única rata deficiente en colina sin lesión renal. Los cambios oculares consistieron principalmente en hemorragia enambas cámaras, cuerpo ciliar y vítreo. La correlación entre la lesión ocular y renal (r=0.72, p<0.0001, CI 95%:0.48-0.86), lesión ocular y creatinina (r=0.86, p<0.0001, CI 95%: 0.72-0.93) y lesión ocular y urea (r=0.70,p<0.0001, CI 95%: 0.44-0.85) fue positiva. La deficiencia de colina induce lesiones oculares luego del desarrollode la necrosis renal. La patología ocular podría ser debida a la inmadurez de los vasos oculares. El sistemahialoide, coroideo y retinal están involucrados
Subject(s)
Animals , Male , Rats , Choline Deficiency/pathology , Diet , Eye Injuries/pathology , Eye/ultrastructure , Kidney Cortex Necrosis/pathology , Kidney Tubular Necrosis, Acute/pathology , Analysis of Variance , Choline Deficiency/complications , Creatinine/blood , Disease Models, Animal , Eye Injuries/complications , Eye/blood supply , Homocysteine/blood , Kidney Cortex Necrosis/etiology , Kidney Tubular Necrosis, Acute/etiology , Rats, Wistar , Retinal Hemorrhage/etiology , Retinal Hemorrhage/pathology , Severity of Illness Index , Urea/bloodABSTRACT
La necrosis renal cortical aguda (NRCA) es la destrucción parcial o total de todos los elementos de la corteza renal. Se caracteriza por oliguria prolongada y recuperación incompleta de la función renal. Se ha implicado al vasoespasmo y a la liberación de toxinas en los eventos fisiopatológicos que producen esta enfermedad. Las causas más comunes de ARCN son complicaciones del enbarazo, síndrome urémico hemolítico, pancreatitis, sepsis, quemaduras, trauma, mordeduras de serpientes, shock y rechazo de injertos. La mortalidad es muy alta y muchos de los sobrevivientes requieren substitución permanente de la función renal
Subject(s)
Humans , Diagnosis, Differential , Kidney Cortex Necrosis/diagnosis , Kidney Cortex Necrosis/pathology , Kidney Cortex Necrosis/physiopathology , Kidney Cortex Necrosis/therapy , Kidney Tubular Necrosis, Acute/diagnosis , Oliguria/etiologyABSTRACT
Se presentan dos casos de pacientes mordidos por serpientes del género Bothrops con evolución diferente que tuvieron paralelismo con su biopsia que mostraron necrosis cortical difusa (fallecido) y el otro caso necrosis tubular aguda (recuperado)