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ARSENIURETTED HYDROGEN POISONING
A colourless, inflammable gas, which, when liquefied, boils at about -600 C. It is formed, together with hydrogen, when acids react with metals containing arsenic as an impurity, and is readily evolved by the action of water on calcium, magnesium and sodium arsenides, or of dilute acid on other metallic arsenides. In addition, therefore, to its potential chemical warfare use as a gas in cylinder attacks, or as a non-persistent charging in shell and bombs, there is also the possibility that one of its progenitors, e.g., calcium arsenide, might be disseminated in the form of a dark-grey heavy powder, which in contact with atmospheric and soil moisture would slowly generate arseniuretted hydrogen in situ, over a period of hours or days, according to conditions.
In moderately strong concentrations arseniuretted hydrogen possesses a nauseating garlic-like odour (frequently described as reminiscent of that of acetylene or phosphorus), and gives rise to a flat metallic taste in the mouth, but when largely diluted with air, although possibly present in toxic concentrations, it may be imperceptible to the senses. It is non-irritant to the eyes, the respiratory passages and lungs, and the skin, and exerts its poisonous action only after absorption through the lungs into the body. The most characteristic feature of its action is the destruction of the red corpuscles of the blood, with the consequent appearance of haemoglobin in the urine and the development of jaundice and anaemia, but the kidney and liver are also directly affected by the absorbed arsenic. Exposure for a few minutes to a high concentration of arseniuretted hydrogen may be rapidly fatal. Even extremely low concentrations, however, can cause symptoms of poisoning, though slow in onset and mild in degree, provided that the exposure is long enough, i.e. many hours or even days.
The presence of arseniuretted hydrogen in the atmosphere can be detected by means of test-papers impregnated with mercuric chloride or bromide which develop a yellow or orange colour when exposed for some time even to very low concentrations of the gas. Such papers are liable to give a similar colour on exposure to air in industrial areas owing to reaction with the hydrogen sulphide present, and under such conditions the test for arseniuretted hydrogen should be confirmed with a differential detector in which the interfering gas is removed by passage through lead acetate granules.
In serious cases due to the inhalation of a relatively high concentration of the gas, symptoms develop rapidly-shivering, headache, pain in the epigastrium. and over the kidneys, vomiting, breathlessness, weakness and giddiness, the patient gradually becoming comatose with a steanddy deterioration of the pulse. Evidence of serious destruction of the red corpuscles in the blood is soon afforded by the passage of a deeply coloured urine, but in the most severe cases the urine may be very scanty and there may even be anuria with an intensification of the pain over the kidneys. If the case survives, intense jaundice accompanied by enlargement of the liver soon ensures.
In cases of moderate severity the symptoms are of the same general type-shivering, weakness, giddiness, nausea and vomiting, headache often associated with insomnia, renal and hepatic pain, dyspnoea on exertion, and often diarrhoea. Headache and repeated vomiting seem to be an almost constant feature. Haemoglobinuria soon makes its appearance, the colour of the urine varying from deep red (port wine colour and sometimes almost black) to reddish brown, the difference probably depending on the relative amounts of unaltered haemoglobin, methaemoglobin, bile pigments and perhaps acid haematin (in an acid urine) that are being excreted - The urine also contains albumin and casts. jaundice becomes apparent a little later on.
In mild cases anaemia may develop gradually with a progressive fall in the red cell count and the haemoglobin in the blood without the appearance of haemoglobin in the urine and with little or no jaundice, this anaemia being sufficient to account for symptoms of lassitude, headache and general malaise as well as undue breathlessness on exertion.
In the earlier stages the occurrence of tingling, or pins and needles, in the hands and feet, which has been reported by some authors, may possibly be due to the toxic effect of arsenic on the nervous system, but such a phenomenon should be distinguished from a true arsenical neuritis which occasionally occurs at a later stage in the shape of pain in the nerve trunks, particularly of the extremities, and some dulling of sensation.
Arseniuretted hydrogen is taken up chiefly by the red blood corpuscles from which it is released by haemolysis, the haemoglobin set free, some of which is converted to methaemoglobin, being partly excreted by the kidney and partly converted by the liver into bile pigments which are formed in excessive amounts and give rise to jaundice. Haemolysis may continue for several days after exposure to the gas and anaemia is therefore progressive. While haemolysis is taking place a simple estimation of the haemoglobin percentage in the whole blood will give an erroneous idea of the extent of red cell destruction since much of the haemoglobin may be in solution in the plasma and not in the corpuscles. A red cell count will make the situation clear.
In the absence of a centrifuge a simple method. may be used to identify haemolysis. Prick the finger of the patient and allow three drops of blood to fall into twelve drops of 3.8 per cent. sodium citrate solution in a watch glass or small tube. Mix well and draw up the mixture into a glass tube of length 20 cms. and internal bore 2-3 nun., the end of which has been slightly tapered, as for a pipette. Close the lower end of the tube with a short length of narrow rubber tubing that has been stoppered with a piece of glass rod or clipped. Prepare a precisely similar tube with the blood of a normal person to serve as a control. Stand both tubes vertical for half an hour or longer so that the corpuscles may sediment. If there is any haemolysis in the suspected blood it will be shown by the tint of the supernatant fluid when compared with that of the control.
Even in the early stages of poisoning there is evidence of increasing damage of the kidneys, liver and spleen, and these organs are intensely congested. This is soon followed by tubular degeneration in the kidneys, i.e. tubular nephrosis, excretion of blood casts and toxic degeneration and necrosis of the liver. If recovery occurs the excretion of blood pigments ceases though albuminuria may continue for a considerable time, the blood count reaches a minimum value which may be well below 2 million red cells per cubic millimetre, evidence of blood regeneration is afforded by poikilocytosis and anisocytosis as well as by the appearance of nucleated red corpuscles and reticulocytes and the damage to the kidney and liver is slowly repaired. If there is very severe haemoglobinuria there is some risk that actual blood clots may form in the bladder.
Death in the most severe cases may take place within 48 hours of exposure and may be preceded by complete anuria. Although it has been suggested that such anuria is caused by blockage of the capillaries of the kidney by the debris of red cells and of the tubules by cellular debris and casts, it is more probably due to the effect of acute arsenical poisoning on the kidney coupled with a failing circulation, and rapid death must be attributed as much to the poisonous effects of arsenic on the organs of the body as to the results of acute blood destruction. Deaths may continue to occur for a, number of days after exposure and are sometimes accompanied by uraemic symptoms with partial or complete cessation of the urine, and quite apart from the part played by the severe anaemia, which is so characteristic of the action of arseniuretted hydrogen, it seems evident that the toxic action of arsenic on the kidneys and other organs must be held largely responsible for the fatal result.
(1) Blood transfusion. - This is indicated in all cases in which there, is evidence of severe anaemia either by clinical observation, by percentage of haemoglobin or by the number of red cells, and definitely so if the haemoglobin falls to 60 per cent. or the red cells to 4,000,000 per c.mm. The risk of haemolysis of the transfused blood by the gas is apparently slight after an interval of two to three hours after exposure. Transfusion may need to be repeated since haemolysis may continue for several days. For a single transfusion 500 c.cm. is an advisable quantity. Owing to the general toxic effect of the gas the destruction of red cells which it causes cannot be regarded in the same light as the loss of an equal quantity of blood by a simple haemorrhage, and transfusion should, therefore, be done slowly and careful observation kept on the general circulation and the blood pressure, lest over-filling of the circulation should damage a heart already poisoned. (Editor's note: This was written in 1940 when blood transfusion was used more readily than 1918. Blood transfusion was used in 1918 but incompatibility reactions were common and transfusion was therefore only rarely used)
(2) Diuresis.- Methods to promote diuresis are beneficial. For this purpose liquids should be given freely by the mouth if they can be retained or otherwise per rectum. The quantity should be about 4 pints in 24 hours. Since arsenic is largely excreted through the kidneys a good flow of urine should; if possible, be maintained and it will, at the same time, lessen risk of blockage of the kidney tubules by cellular debris. It must, however, be remembered that in arseniuretted hydrogen poisoning there is no loss of fluid from the circulation, such as occurs in haemorrhage, and care consequently must be taken to see that the diuresis corresponds. to the amount of fluid administered lest there be retention of fluid in the body leading to the development of oedema.
Alkalis (see below) will aid diuresis, but organic mercurial diuretics should not be employed.
(3) Administration of alkalis.- Potassium or preferably sodium citrate should be administered in sufficient doses to maintain an alkaline urine. A dosage of three or four drachms in 24 hours will usually be sufficient. it is known that with haematuria the haemoglobin excreted may be converted to acid haematin in the tubules if the reaction of the urine is acid, and it has been suggested that this pigment may crystallise and thus block the tubules. Experimentally, there is little indication that such crystallization of acid haematin occurs in cases of arseniuretted hydrogen poisoning. Nevertheless the administration of alkalis may he a wise precaution for the present.
(4) Administration of glucose.- Glucose should be administered freely from the onset, either with or without insulin. It is especially indicated if there is evidence of necrosis of the liver and if necessary may then be injected intravenously. (Editor's Note: Insulin was not discovered until after the war had ended. This section only applies to 1940)
(5) Oxygen administration.- Anoxaemia only occurs in anaemia when of an advanced grade. In such cases oxygen should be administered. In arseniuretted hydrogen poisoning, the lungs are practically unaffected and there is no true cyanosis, and there may still be a considerable amount of functional haemoglobin in the blood even if much of it is in solution in the plasma. Consequently, it is unlikely that oxygen administration will result in the dramatic effect and great benefit which it affords in cases of acute pulmonary oedema due to the lung irritant gases., Anoxaemia, may, however, occur in the absence of cyanosis.
(6) Convalescence, - It must be borne in mind that arseniuretted hydrogen causes both haemolysis of red cells and necrosis of the liver and other organs. Light diet is indicated so long as the urine contains evidence of this toxic action.
The anaemia will need full doses of iron and also treatment with liver extract in view of the effect of the gas on the liver.
Cases must be kept under observation until both the blood and the urine are normal.
The diseases which may possibly be confused with arseniuretted hydrogen poisoning are Blackwater Fever and Paroxysmal Haemoglobinuria. The antecedent history of residence in the tropics and malaria and the quite recent administration of quinine, taken in conjunction with the high body temperature which is so often a feature, will eliminate the first, while the association with exposure to cold, as well as the past history of the patient, will exclude the latter. In any case instances of such diseases will only occur sporadically and are a most improbable cause of the simultaneous development of haemoglobinuria and anaemia in a number of persons such as may result from the escape of arseniuretted hydrogen into the atmosphere. There should be no great difficulty in differentiating from cases of jaundice due to other causes.
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