Surto de intoxicação por sal em ovinos no estado do Pará / Salt poisoning outbreak in sheep in the state of Pará

O presente trabalho relata um surto de intoxicação por sal em ovinos no Brasil, em uma propriedade no estado do Pará. De um total de 545 ovinos, oito animais adoeceram (1,46%) e quatro destes morreram (50%). A avaliação das instalações e do manejo indicaram como fatores predisponentes a ingestão excessiva de mistura mineral e a restrição hídrica. Os principais sinais clínicos foram decúbito, diminuição ou ausência da sensibilidade cutânea, ausência dos reflexos de ameaça, palpebral e auricular, midríase, nistagmo, opistótono, espasticidade de membros, sonolência e estupor. Havia ainda, timpanismo, diarreia, taquipneia, taquicardia, desidratação e poliúria. A evolução do quadro clínico nos animais que morreram variou de duas horas e meia a 48 horas. As médias das concentrações séricas de sódio e de potássio de 31 ovinos do mesmo lote afetado pela intoxicação, em amostras colhidas durante o surto, revelaram hipernatremia (190mEq/l) e hipercalemia (8,2mEq/l). À necropsia, observou-se em um animal, achatamento das circunvoluções cerebrais. Microscopicamente, neste animal, evidenciou-se vacuolização moderada do neurópilo, particularmente nas lâminas intermediárias do córtex cerebral, com aumento dos espaços perineural e perivascular. Nessas áreas foram observados ainda, acentuada tumefação e edema dos astrócitos e necrose neuronal aguda. A dosagem de sódio no encéfalo de um ovino, revelou-se elevada com valor de 3.513ppm. O diagnóstico foi realizado com base na epidemiologia, nos sinais clínicos, nas lesões macro e microscópicas e nas dosagens de sódio no soro e no encéfalo dos ovinos.(AU)

This paper reports an outbreak of salt poisoning in sheep on a farm in the state of Pará, northern Brazil. Eight (1.46%) animals were affected from a total of 545 sheep and four (50%) of them died. The evaluation of the facilities and the handling indicated as predisposing factors excessive intake of the mineral supplement and water restriction. The main clinical signs were recumbency, decrease or absence of cutaneous sensibility, absence of auricular, palpebral and menace reflex, mydriasis, nystagmus, opisthotonus, spasticity of limbs, somnolence and stupor. Beside these signs bloat, diarrhea, tachypnea, tachycardia, dehydration and polyuria were observed. The course of the disease in animals that died ranged from two hours and a half to 48 hours. The medium of serum concentration of sodium and potassium of 31 sheep from the same group affected on samples collected during the outbreak revealed hypernatremia (190mEq/l) and hyperkalemia (8.2mEq/l). At necropsy, there was flattening of the cerebral gyri in one sheep; in this animal was found vacuolization of the neuropil in the cerebral cortex with moderate intensity in the intermediary and mild on the superficial layers, with increased perineural and perivascular spaces. In these areas there were markedly swollen nucleus of astrocytes with acute neuronal necrosis. The dosage of sodium in the brain of a sheep revealed a high value of 3.513ppm. The diagnosis was made based on the epidemiology, clinical signs, macro and microscopic lesions and in the dosages of sodium in serum and brain.(AU)

Watering cattle (young bulls) with brackish water--a hazard due to its salt content?

OBJECTIVE: The aim of this experimental study was primarily to test the effects and reactions of cattle offered salty water as the only source of drinking water. MATERIAL AND METHODS: Mineral balance studies were carried out on three bull, continuously fed a ration based on hay, hay cobs, barley, soybean meal and a vitamin/mineral supplement. The salt content of the drinking water varied between the trials (trials I/II/III: 0.10/5.00/10.0 g/l; town water supplemented by different amounts of an additive containing 95.4% sodium chloride and 4.6% potassium chloride). RESULTS: Rising salt concentration of the drinking water led to significantly higher sodium, potassium and chloride intake (sodium: trial I/II/III = 5.42/59.5/ 157 g/day; potassium: trials I/II/III = 108/117/121 g/day; chloride: trials I/II/III = 22.8/112/266 g/day) mainly caused by a significantly higher water intake (trials I/II/III: 21.8 ± 2.03/30.4 ± 3.08/41.5 ± 5.89 kg/day). Amounts of urine increased significantly (trials I/II/III: 3.99 ± 0.46/ 9.66 ± 1.34/20.2 ± 3.14 kg/day). The concentrations of minerals in the urine (sodium: trials I/II/III = 123/3729/6705 mg/kg; potassium: trials I/II/III = 17345/9996/ 5496 mg/kg; chloride: trials I/II/III = 2020/ 9672/11870 mg/kg) and faeces (sodium: trials I/II/III = 1299/6544/ 7653 mg/kg; potassium: trials I/II/III = 6343/3719/3490 mg/kg; chloride: trials I/II/III = 3851/4580/4693 mg/kg) also changed significantly over time. Serum values of sodium tended to decrease (trials I/II/III: 142/137/137 mmol/l) within the physiological range, whereas those of chloride increased (trials I/II/III: 91.5/95.6/97.5 mmol/l) at higher salt concentrations in drinking water. The haematocrit, pH-value as well as urea content in blood were not affected by the higher salt intake. In balance trial III (highest salt load: 10.0 g/l), sodium intake of the bulls reached 0.57 ± 0.03 g/kg BW (~22.1 ± 0.9 g sodium/kg dry matter feed). CONCLUSION AND CLINICAL RELEVANCE: An increase of salinity in drinking water up to 10 g/l--with otherwise harmless water quality--had no measurable negative effects on animal health in the investigation period and subsequent periods (total of 58 days with more than 5.00 g of salt per litre drinking water).

Intoxicação por sal em suínos: aspectos epidemiológicos, clínicos e patológicos e breve revisão de literatura / Salt poisoning in swine: epidemiological, clinical and pathological aspects and brief review of the literature

Salt poisoning occurs commonly in pigs by excessive intake of sodium chloride or by a period water deprivation for followed by free access to water. The objective of this work is to aggregate data from cases of salt poisoning, combining existing data in the literature and describe the main clinical and pathological features observed. We reviewed five outbreaks, one of which was carefully monitored. In three of them the intake of sodium chloride had been determined. Clinical signs were basically seizures with the lateral decubitus with paddling movements. Circling was observed in some cases. Sodium determination in muscle of and liver fragments, serum, cerebrospinal fluid and aqueous humor showed increased concentrations of this ion. There was eosinopenia characterizing increased recruitment eosinophils from the circulation into the brain. In all outbreaks eosinophil infiltration was observed in the meninges and the Virchow-Robin space of the cerebral cortex. Cortical laminar necrosis was more pronounced in the brain of pigs from one of the outbreaks in which animals were sick for six days. The combination of these two lesions characterizes the disease. The changes observed result from high concentrations of sodium in the brain causing cause edema that leads to increased intracranial pressure and decreased perfusion to the brain tissue causing diffuse ischemia and neuronal necrosis, with consequent malacia.

Intoxicação por sal ocorre comumente em suínos por ingestão excessiva de cloreto de sódio ou por privação de água por um período de tempo, seguido de um livre acesso a água abundante. O objetivo deste trabalho é agregar dados de casos de intoxicação por sal, diagnosticados, compilar dados já existentes na literatura e caracterizar as principais alterações clínicas e patológicas observadas. Foram revisados cinco surtos, sendo que um deles foi minuciosamente acompanhado. Em três deles a ingestão de cloreto de sódio foi determinada. Os sinais clínicos eram basicamente convulsões, com intensos tremores musculares e desenvolvimento de opistótono. Os animais permaneciam em decúbito lateral, fazendo movimentos de pedalagem. Alguns andavam em círculos. Dosagens de sódio em fragmentos de músculo e de fígado, no soro, líquor e humor aquoso revelaram concentrações aumentadas do íon. A quantidade de eosinófilos circulantes foi baixa caracterizando grande recrutamento dessas células para o encéfalo. Em todos os surtos foi observada infiltração de eosinófilos nas leptomeninges e no espaço de Virchow-Robin do córtex cerebral. Necrose cortical laminar foi observada mais detalhadamente em um dos surtos onde os suínos estavam doentes há seis dias. A combinação dessas duas lesões caracteriza a doença. Todas as alterações observadas podem ser explicadas pela provável patogenia da doença em que as elevadas concentrações de sódio causam edema cerebral que leva ao aumento da pressão intracraniana e decréscimo da perfusão para o cérebro causando isquemia difusa e necrose neuronal, com consequente malacia.

Etoricoxib attenuates effect of antihypertensives in a rodent model of DOCA-salt induced hypertension.

While it is known that non-steroidal anti-inflammatory drugs including selective cyclooxygenase-2 (COX-2) inhibitors influence BP, the exact relationship and underlying mechanisms are still unclear. We investigated the effect of etoricoxib, a selective COX-2 inhibitor on the antihypertensive efficacy of atenolol; beta-blocker, ramipril; angiotensin converting enzyme inhibitor and telmisartan; angiotensin receptor blocker in deoxycorticosterone acetate (DOCA)-salt hypertensive rats, a mineralocorticoid volume expansion model. Etoricoxib attenuated the antihypertensive-induced reduction of systolic (atenolol; P < .001, ramipril; P = .011, telmisartan; P = .003) and mean arterial pressure (atenolol; P < .001, ramipril; P = .032, telmisartan; P = .023). These results demonstrate that COX-2 dependent mechanisms play a significant role in blood pressure regulation, and etoricoxib-induced COX-2 inhibition blunts the therapeutic effect of different classes of antihypertensives in this mineralocorticoid volume expansion model of hypertension.

Surto de intoxicação por sal em suínos em Santa Catarina / Outbreak of salt poisoning in pigs in Santa Catarina

Descreve-se a ocorrência de surto de intoxicação por sal em suínos de duas propriedades, onde 70 porcos morreram. Soro de leite proveniente da salga de queijo era servido no cocho como única fonte hídrica aos animais. Não havia bebedouros nas instalações. Um dia após o fornecimento do soro, os porcos começaram a adoecer e apresentaram salivação excessiva, movimentos de pedalagem, opistótono e tremores cíclicos. Na necropsia, dois suínos apresentaram achatamento das circunvoluções do córtex telencefálico e um outro, edema no córtex telencefálico. Na histopatologia, observou-se necrose neuronal laminar difusa acentuada no córtex telencefálico, astrócitos de Alzheimer tipo II (AIIA), infiltrado multifocal perivascular de eosinófilos e linfócitos e edema perivascular. Outros achados incluíram marcação imuno-histoquímica fraca ou ausente para proteína glial fibrilar ácida (GFAP), mas intensa marcação positiva no citoplasma dos AIIA para S-100. As concentrações de sódio sérico e do líquor mensuradas nos porcos estudados foram de 140 e 156mmol/L, respectivamente.

A total of 70 pigs were affected and died due to salt poisoning in two farms in southern Brazil. The only source of drinking water available to the pigs was whey from cheese salting process. One day after receiving the whey, animals started getting sick and showed excessive salivation, opisthotonus, paddling, and cyclic tremors. At necropsy of three pigs, two of them presented flattening of gyri and the other one presented cortical telencephalon edema. Microscopically, severe diffuse neuronal necrosis in telencephalic laminar cortex, Alzheimer type II astrocytes (AIIA), eosinophilic and lymphocytic perivascular cuffing apart of perivascular edema were observed. Weak or absent anti-glial fibrillary acidic protein (GFAP) immunolabeling was associated with positive immunostaining for S-100 in AIIA cytoplasm. Concentration of sodium in serum and liquor samples from dead pigs resulted 140 and 156mmol/L, respectively.

Alzheimer type II astrocytes in the brains of pigs with salt poisoning (water deprivation/intoxication).

The finding of Alzheimer type II astrocytes, in addition to the pathognomonic combination of laminar cerebrocortical necrosis and eosinophil infiltration, in the brains of pigs is reported for the first time in cases of indirect salt poisoning following water deprivation.

[Plasma hypertonicity in children]. / Hipertonia plasmática na criança.

The plasma hypertonicity is a severe and quite frequent disorder in children. The most frequent causes are hypernatremia related conditions, even though other causes of hyperosmolarity, such as hyperglycaemia and exogenous solutes accumulation also occur. The management and treatment of this condition is delicate and requires a thorough understanding of the underlying hydro electrolytic disorder. The authors perform a theoretical review of plasma hypertonicity in children, focusing on the three most frequent associated conditions: hypernatremic dehydration, salt poisoning and hyperosmolar coma.

Acute salt poisoning due to different oral rehydration solution (ORS) packet sizes.

The packing and composition of ORS has undergone a change since its introduction. In India, some companies are manufacturing smaller pouches (4.2 g) to be dissolved in 200 ml of water. Therefore, out of confusion some prescribers routinely advise the patients to dissolve the standard formulation ORS pouch (21 g) in a glass (200 ml) of water. Two cases are discussed. First patient developed salt poisoning due to improper dilution and recovered after rapid correction. In the second patient improper reconstitution led to hypernatremia and death.

Fatal voluntary salt intake resulting in the highest ever documented sodium plasma level in adults (255 mmol L-1): a disorder linked to female gender and psychiatric disorders.

Excessive ingestion of salt is a well-recognized cause of hypernatraemia in children, is uncommonly recognized in debilitated elderly persons, but is rarely diagnosed in healthy, independent adults. We report a case of fatal salt poisoning in a 20-year-old lady who suffered of post-natal depression and ingested large quantities of salt as part of exorcism ritual. She presented with the highest ever documented serum sodium level of 255 mmol L(-1), associated with severe neurological impairment that was unresponsive to aggressive hypotonic fluid replacement. Post-mortem examination ruled out any other possible probable cause of death. The medical literature was reviewed, and 16 previous cases of severe hypernatraemia in adults secondary to excessive salt ingestion were retrieved. Common features of all reported cases included female gender (95% of cases) and evidence of underlying cognitive or psychiatric disorders (all reported cases). We conclude that women with documented cognitive or psychiatric disorders, in particular depression, are susceptible for psychogenic salt poisoning. Awareness should be raised to the potentially life-risking use of salty beverages as emetics or as part of 'exorcism' rituals.

A sudden death during a saline drip in a schizophrenic patient with polydipsia.

A young woman with polydipsia died suddenly while receiving a normal saline drip in a hospital for psychiatric care. Slight symptoms due to water intoxication, more specifically, nausea, vomiting, and anorexia, appeared and her serum sodium and potassium measured 106 and 1.7 mEq/l, respectively. General convulsions are thought to be the most common result of water intoxication in emergency cases, however, when she was found with circulatory collapse, no severe neurological symptoms were present. The cause of her collapse did not seem to be due to hyponatremia but to hypopotassemia. Although epinephrine is contraindicated with some psychiatric drugs, the doctor used it to raise blood pressure in treating circulatory collapse. It is possible that epinephrine induced cardiac arrest.

Salt poisoning in beef cattle.

Salt poisoning has been described under various circumstances in adult cattle. Presenting clinical signs in 6 Holstein beef cattle with such poisoning were primarily dysfunction of the central nervous system and included ataxia, opisthotonus, nystagmus, depression, muscle twitching and intermittent convulsions, as well as abdominal pain and polydipsia. Diarrhea occurred in 2, and blindness in 3/6 cattle. Hypernatremia (161.8 - 178.8 mmol/L) and hyperosmolality (331.81 - 366.18 mOsm/L) were present in all animals. To treat the affected cattle, access to fresh water was restricted, vascular volume was expanded with isotonic saline and then hypotonic fluid (5% Dextrose solution) i.v. and dexamethasone im was administered. Although biochemical parameters returned to normal reference ranges, 3/6 affected animals remained blind.

Fatal hypernatremia from saltwater used as an emetic.

An adolescent boy returned home from a party and told his parents he may have taken some pills while there. He was given saltwater to drink, in an effort to induce emesis. He vomited numerous times, then seized. Hypernatremia (195 mmol/L) was diagnosed at the community hospital, and he was transferred to a pediatric intensive care facility. He suffered numerous complications and died from cerebral herniation. This case is presented to remind physicians of the dangers of this obsolete therapy.