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Chemical cyanosis is an oxygen transport deficiency produced by exposure to aromatic nitro- or animo-compounds. Evaluation of its severity by methemoglobin determinations defines the problem incompletely and is time consuming. Twenty-nine patients were studied over a five-year period by both methemoglobin level using classical laboratory methods and oxygen saturation level, using a reflection oximeter. The two results were found to bear an inverse linear relationship. Oxygen saturation may be determined easily and rapidly by the reflection oximeter method, and may be used safely as a guide to treatment of chemical cyanosis. No changes would have been made in medical management of any of the patients if the decisions had been made on the basis of the oxygen saturation level of less than 90% rather than the methemoglobin percentage of 10% or more.

A case is presented of asymptomatic cyanosis of the hands, seen four hours after dental surgery under intravenous, local and inhalational anaesthesia. Alphaprodine hydrochloride, a synthetic opiate and one of the agents used, may produce dilatation of the venous bed with passive venous pooling. Such a mechanism is thought to have occurred in this case, manifesting as cyanosis. A weakly positive intradermal skin test to alphaprodine suggests immediate type hypersensitivity as a possible underlying cause.

In 325 cases of industrial chemical cyanosis notified to Her Majesty's Factory Inspectorate for 1961-80 the incidence of poisonings showed considerable seasonal variation with substantially greater numbers occurring in the summer months. A correlation between the number of poisonings in any one year and the hotness of that summer was also shown. The vast majority of incidents occurred during the manufacture of chemicals or dyestuffs, and two particular workplaces were responsible for 70% of the cases. Poisoning by amino compounds appear to produce early cyanosis whereas poisoning by nitro compounds tended to produce delayed cyanosis. These latter compounds were also more likely to produce anaemia. Methaemoglobin was determined in 45% of cases with results ranging from less than a few per cent to over 50%. Despite concentrations of MetHb over 50%, several workers complained only of headache and their blue appearance.

beta-Glucosidases have been isolated from Alocasia macrorrhiza plants. The enzymes are highly specific for the hydrolysis of the cyanogenic glucoside triglochinin endogenous to this plant. Upon chromatography of protein extracts on cation exchange resins and Sephadex G-200, separation into various enzymatically active bands was observed. The main fractions possess molecular weights of approximately 310000 and 105 000, as shown by preparative ultracentrifugation in a linear saccharose gradient. The beta-glucosidases are composed of subunits (molecular weight 55 000 to 60 000), as revealed by sodium dodecylsulfate gel electrophoresis. The result of alkaline disc electrophoresis and isoelectric focusing in polyacrylamide gel suggest that the beta-glucosidase fraction with molecular weight 105 000 is a dissociation product of the 310 000 molecular-weight species. The isoelectric points of the various beta-glocusidase bands, obtained by isoelectric focusing, vary between pH 4.5 and 5.0. The beta-glucosidases show a pronounced specificity for triglochinin. The Km for this substrate (3 times 10(-5) M) is 50 to 100-fold lower than for all other substrates hydrolyzed. Of the other cyanogenic glycosides, only those with an aromatic aglycone, (S)-configuration at the asymmetric carbon atom of the aglycone and glucose as sugar moiety were hydrolyzed to a measurable extent. The pH optimum of the enzyme reaction is 5.5, the temperature optimum around 50 degrees C. Cu2 ions and glucono-1,5-lactone inhibit beta-glucosidase activity approximately 50% at a concentration of 5 times 10(-4) M, while Hg2,Ag and p-chloromercuribenzoate show the same percent inhibition at 5 times 10(-7) M. Lipophilic solvents (ethanol, ethylene glycol monomethylether) activate the beta-glucosidase activity, preferentially by influencing the V values of the enzymes.

Cyanotic crises occurred in a breast-fed infant whose mother was under treatment with dipyrone for a sore throat. No abnormalities were found at physical and routine laboratory examinations. Dipyrone concentrations in mother's serum and milk and in infant's serum and urine were 3.3, 4.3 and 3.2, 3.74 micrograms/ml respectively. It is concluded that the adverse effect could be due to dipyrone ingested with mother's milk.

Rats aged from 2 to 4 mth were given phenacetin 100 mg/kg/day and 1-14 g/kg/day, orally, for up to 26 1/2 wk and 3 wk, respectively. Signs of premature ageing such as senile plagues, neurofibrillary tangles and lipofucsin pigment were not demonstrated in the brains of these animals.

A case of methemoglobinemia secondary to topical local anesthetic agents is reported. A 28-year-old, 80-kg white man was admitted to a hospital for respiratory distress two days after an accident. During intubation, Cetacaine (benzocaine, butamben, and tetracaine) spray and Americaine (benzocaine) ointment were used topically for local anesthesia. Ninety minutes later, the patient was cyanotic despite ventilation, and an arterial blood sample was chocolate-brown and contained 29 d/dl methemoglobin (normal less than 1.7 g/ dl). Methylene blue, 80 mg as a 1% solution in 5% dextrose in water, was infused over 20 minutes, and hte patient's cyanosis disappeared within the next 30 minutes. The following afternoon, the patient was reintubated, using 4% lidocaine and benzocaine as local anesthetics. He again developed cyanosis. Methylene blue again cleared the cyanosis. Abnormal hemoglobin variants and NADH-methemoglobin reductase deficiency were ruled out as sources of methemoglobinemia. A discussion of methemoglobinemia, including biochemistry, pathogenesis, symptomatology, and management, is presented. If cyanosis occurs following application of local anesthetics, methemoglobinemia secondary to these drugs should be considered in the differential diagnosis.

A voluntary intoxication by injection in the left basilic vein of 10 ml of concentrated caustic soda is reported. The main effects were, besides local necrosis, haemolysis, acute renal failure with initial anuresis, intravascular coagulation and cyanosis with a normal Pao2 due to methaemalbuminaemia. This was confirmed by using the usual spectrophotometric methods as well as electrophoretic methods.

Two cases are described and discussed in which penicillin powder applied to the theca at the end of laminectomy caused delayed convulsions.

Two twins born to a mother who had been treated with Indomethacin at the end of pregnancy presented with variable but transitory hypoxemia. Blood Indomethacin determination suggested that this disorder was iatrogenic in origin. Clinical, experimental and pharmacological data in the literature support the hypothesis that this condition was due to pulmonary arterial hypertension.

An 11 year old girl who was being treated for enuresis with imipramine developed acrocyanosis of the hands and feet. All biochemical and haematological investigations gave normal results. When imipramine was stopped the girl recovered within three days.

A case is reported of a 37 year old man who was involved in an accidental shell blast. He was admitted with black tattooing of his face, forearms, hands and legs. Repair of the severe ocular lesions and the surgical debridement of his burns required general anaesthesia. This lasted for 6 h; throughout, haemodynamic and respiratory parameters remained stable. The Pao2 was 130 mmHg. During recovery, cyanosis was noted despite a Pao2 of 65 mmHg with 92% Sao2, a normal chest X-ray and stable normal haemodynamic parameters. This paradoxical situation suggested a toxic haemoglobinopathy. Biochemical investigations revealed severe methaemoglobinaemia (40%) due to percutaneous absorption of dinitrobenzene (DNB), a constituent of the 1917 bomb. The amount of DNB absorbed had been unknowingly reduced by the surgical brushing of the burned skin. The classical treatment of methaemoglobinaemia, associated with two plasmaphereses to remove the toxic substance, were successful. Normal arterial blood gases associated with chocolate brown coloured arterial blood should make one suspect methaemoglobinaemia.

Most cases of toxic methemoglobinemia in children are caused by direct contact of the methemoglobinizing agents with the skin and mucosa and in a shorter scale, by the ingestion of such compounds. The first case we know is reported where the toxic was inhaled. The basis to establish the diagnosis of methemoglobinemia, together with the differential diagnosis with other diseases in children that show cyanosis in their course are discussed.

Nine infants with apparent life-threatening events that occurred as a result of poisoning by a caretaker are described. These episodes were characterized by apnea plus some combination of color change, choking or gagging, and abnormal muscle tone. Five of the infants responded to vigorous stimulation, and four required cardiopulmonary resuscitation. Most poisonings (seven infants) were detected by a urine drug screen. Medications detected included acetaminophen, amphetamine, benzodiazepines (two infants), cocaine, codeine, meperidine (two infants), Methadone, phenobarbital, and phenothiazines (three infants). Four infants received two or more drugs. Most perpetrators of the poisonings were mothers (seven) and five of the parents admitted administering the various agents. Reasons for the poisonings included an apparent attempt to harm an infant, the need to sedate a fussy infant, or a gross misunderstanding of the potential risk of various agents to infants. Because no history of drug administration was elicited at the time of hospital admission, six infants might have been discharged with a diagnosis of apnea of infancy had not an attempt been made to investigate the possibility of poisoning. These cases suggest that poisoning by a caretaker should be added to the differential diagnosis of any infant brought to medical attention because of an apparent life-threatening event and that urine drug screening should be considered in the evaluation.

Rats with diets containing 0.2% propylthiouracil (PTU) throughout gestation had progeny with persistent cyanosis and high neonatal mortality. Histological and histochemical studies failed to reveal lung abnormalities in these pups. Studies of the blood of PTU-fed dams demonstrated that hemoglobin, packed cell volume, and numbers of erythrocytes were significantly reduced. In their 21-day fetal young, erythrocytopenia was accompanied by an elevated mean corpuscular volume and a reduced mean corpuscular hemoglobin concentration. Imprints of marrow from dams and of liver and spleens of the young showed normoblastic erythropoiesis. A granulocytic leucocytosis was present in the blood of the PTU-fed dams, whereas their progeny had a granulocytopenic leucopenia. Tissue concentrations of copper, zinc, manganese, magnesium and iron were determined. The most striking changes observed were the significant elevations of copper in the dams' brain, liver and kidneys. No changes in the concentration of any of the trace minerals were found in the livers of the pups. Food restriction to the dam failed to significantly alter maternal or fetal hematologic or trace element concentrations as compared with controls. It is evident that PTU, when fed to pregnant rats, has demonstrable effects on erythropoiesis, granulocytopoiesis, and maternal trace element distribution. It is not presently known whether these phenomena are interrelated.

During the course of routine hospital surgical procedures, three patients lapsed into hypoxic cyanosis. Two expired immediately, another after four days of coma. Investigation of the hospital's central liquid oxygen tank revealed that it had been refilled recently and was labelled both "oxygen" and "argon." Mass spectrometric analysis of gas sampled from the questioned tank revealed a predominance of argon. A discussion of the sampling technique, method of analysis, role of the criminalist, and causes of this accident is presented.

Changes in oxygen saturation (SaO2) were studied during induction of anaesthesia in 48 healthy children receiving halothane or isoflurane for outpatient dental extractions. Substantial reductions in SaO2 occurred in more than 50% of the children given isoflurane and were associated with the irritant effects of this agent on the airway. SaO2 was largely unaltered during the use of halothane. These findings indicate that the airway complications caused by isoflurane may be associated with decreases in SaO2.

A 16-year-old laboratory technician ingested 30 g of sodium nitrite (NaNO2) in a suicidal attempt. Within a short time severe cyanosis and distressing dyspnoea developed. The conservative therapeutic approach with redox substances showed little success. However, haemodialysis resulted in rapid improvement of all signs. After three hours of dialysis the patient was symptom-free and could be discharged after two days without damage due to the intoxication. Additional experimental investigations showed NaNO2 to be easily dialysable. There is, however, no binding to active charcoal.

A unique opportunity was presented to observe the potentially toxic effects of an acute exposure to the vapors of petroleum naphtha distillate on a relatively large number of individuals. The immediate manifestation in all was dyspnea. The action on motor vehicle combustion suggested that some of this could have been due to oxygen deprivation; however, all individuals were dyspneic for several minutes after exposure. A few were cyanotic for several minutes after exposure. All were excited. Tremulousness and mild nausea followed the initial symptoms but were of brief duration. One individual manifested numerous premature ventricular contractions. Since his exposure was brief and since none of the others showed similar findings, it is unlikely that the exposure was causal. The central nervous system depression described in acute exposure cases of the intact (not distillate) petroleum naphtha fumes was not observed in any of this series. There were no delayed manifestations or complications.

A 3-week-old patient underwent cataract extraction under halothane anesthesia. After induction of anesthesia and instillation of phenylephrine hydrochloride eyedrops, the patient experienced cyanosis and cardiovascular depression. Her condition improved over the next 10 minutes. The possible contributions of halothane and phenylephrine to this response are discussed.

Sulphasalazine was first introduced for the treatment of rheumatoid arthritis in 1942. Following initial enthusiasm, interest waned until 1978 when a large open study suggested that it might have a 'second-line effect'. Since then further studies have confirmed this effect and once again rheumatologists are starting to use sulphasalazine in the treatment of rheumatoid arthritis. In this review we examine the pharmacology of sulphasalazine and its metabolites, comment upon the possible modes of action and review the recent literature pertaining to its use in rheumatoid arthritis.

Evidence of central nervous system toxicity was noted in two patients undergoing extradural analgesia for Caesarean section. There was no cardiovascular depression and both patients recovered rapidly. The patients had received total doses of bupivacaine plain solution of 357.5 mg and 356.25 mg, respectively and the relationship of these to the clinical signs of bupivacaine toxicity is discussed.

A case is reported in which a major generalised convulsive seizure followed the administration of Althesin. The patient had no clinically demonstrable predisposition to epilepsy. The fits were rapidly controlled by the intravenous injection of thiopentone.