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Three pauents of accidental gas poisoning with Freon-12 are reported. Presenting features were transient loss of consciousness, bradycardia, hypotension and anaesthesia. All patients made a rapid and uneventful recovery without any residual effects.
Freons are a group of aliphatic halogenated. hydrocarbon gases which exist in several forms (Table 1). Theyare colourlpss, odourless, and noninflammable gases which are in commercial use as refrigerants, in fire extinguishers and as propellants in nebulizers, aerosol bombs, insecticides, deodorants etc [1,2]. Given their extensive industrial applications, there are however few reports, in literature about their systemic or, long term affects in humans. We report our experience of managing three cases of accidental, exposure to Freon-12 gas.
Three patients aged 32, 24 and 23 years respectively, accidentally inhaled Freon 12 gas which had leaked from an ait conditioning system of a ship. The patients had been entrapped, in a small univentilated area for approximately 5–10 mins. They were admitted to our hospital half an hour later.
Transient loss of consciousness at onset lasted for 5 to 10 mins in two patients. On regaining consciousness, they complained of mild headache, confusion, inability to open mouth and complete loss of sensations, and had completely recovered within two hours. The third patient remained comatose for three hours (Glasgow Coma Scale score – 8), with normal sized, photorcspon-sive pupils and intact corneal reflex. He showed evidence of impending respiy depression, aid Was given 60 rag of Doxapram, administered intravenously as a trial. This resulted in dramatic recovery, ohyiating the requirement of vuritilatory assistance, which had been kept prepared.
Symptoms reported by the patients are shown in Table 2 There was no history of lacrimation, excessive salivation or irritation of eyes nostrils, throat on skin.
On clinical examination all patients were found to bave bradycardia, hypotension (systolic pressure 84 ram to 96 mm Hg), and shallow breathing. Additional findings in the third patient were Cheyne-Stokes respiration, cyanosis, and cold, clammy extremities. No arrythmias were detected in any patient. Table 3 elucidates the signs seen in our patients.
Laboratory investigations carried out included haematocrit, urine analysis, metabolic and biochemical parameters, these were all normal. Analysis of arterial blood gases was done on admission and thereafter six-hourly. The third patient had hypercapnia (pCO2 = 66 mm Hg) and acidemia (pH 7.2). Serial ECGs were taken hourly for the first twelve hours and then every three hours, for the next twelve hours. Sinus bradycardia was present in the initial ECGs, the subsequent ECGs were normal. Chest X-ray done on day 1,2,3 and 7 were all normal.
Treatment instituted in all patients included close monitoring, frequent clinical assessment, continuous inhalation of 100% oxygen and intravenous hydrocortisone. Prophylactic broadspectrum antibiotics were given initially to combat possible chemical pneumonitis (and secondary bacterial infection). All patients recovered completely within 24 hours, but were observed for delayed effects as inpatients for a week. The second patient developed bilateral pleural rub on the third day, which disappeared over the next 36 hours. Follow up of the patients a fortnight later showed them to be symptom free with no residual signs.
In the past, Freons were generally believed to be inert gases with low toxicity. Following a spate of sudden sniffing deaths in 1960, there was a renewed interest in the dangers of the sniffing fad (then prevalent amongst youngsters). This occurred due to inhalation of Freons from aerosol containers intended for frosting cocktail glasses. Over 170 cases of deaths due to Freons have so far been reported world wide [1,2].
Bass  reviewed the records of 110 sniffing deaths and inferred that sudden death was as a result of severe sudden cardiac arrhythmias. Subsequent experiments conducted on rodents suggested that the observed effects were possibly as a result of direct action on sino-atrial node and atrioventricular conduction. Taylor and Harris  demonstrated that Freons cause a reduction in sinoatrial rate, prolongation of P-R interval, fall in the T-wave amplitude and occasionally second or third degree heart blocks. They further concluded that sudden death in asthmatics was due to the cardio toxic effects of the propellant. Freons being heavier than air, lodge in the alveoli of asthmatics for a long time because of expiratory obstruction. None of our patients had bronchial asthma. Apart from slight bradycardia, no other abnormal electrocardiographic finding was evident in our patients. Sayers et al  showed that dogs and monkeys developed generalized tremors, salivation and lacrimation when exposed to concentrations above 20% volume in air. Tremors were only present in the third patient. Lester and Greenberg , demonstrated twitching and tremors at concentrations of 30–40%, and loss of reflexes at 50% in rats. At concentrations of 70–80%, corneal reflexes were abolished and the animals were in deep anaesthesia. Transient anaesthesia was a feature in all of our patients. The third patient also had absence of response to deep painful stimuli, with intact pupillary and corneal reflexes.