TREATMENT OF A CASE OF NEAR-DROWNING IN CHLORINATED FRESH WATER

TREATMENT OF A CASE OF NEAR-DROWNING IN CHLORINATED FRESH WATER

Brit. f. Anaesth. (1972), 44, 616 TREATMENT OF A CASE OF NEAR-DROWNING IN CHLORINATED FRESH WATER C. TOLAND SUMMARY One hundred and twenty-five peop...

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Brit. f. Anaesth. (1972), 44, 616

TREATMENT OF A CASE OF NEAR-DROWNING IN CHLORINATED FRESH WATER C. TOLAND SUMMARY

One hundred and twenty-five people died by aspiration. Intravascular osmotic haemolysis occurs drowning in the Republic of Ireland in 1969. The in fresh water drowning (Fuller, 1963). term "drowning" indicates that there is a threat to CASE REPORT life following immersion in water whilst if death occurs the term "drowned" is used (Miles, 1968). In At 4 p.m. a 39-year-old man, previously healthy, was about 20 per cent of those drowned, water whether noticed to be lying at the bottom of a chlorinated, heated fresh water swimming pool. The patient was apnoeic fresh, chlorinated or sea, fails to enter the lungs and showed signs of cardiac arrest when removed from but in the other 80 per cent it enters the lungs the water. Mouth-to-mouth resuscitation and closed chest massage were started immediately by two doctors (Rivers, Orr and Lee, 1970). The term secondary cardiac at the scene of the accident and continued until spondrowning is used by Rivers, Orr and Lee (1970) to taneous ventilation and a palpable radial pulse returned. denote that death following drowning may be de- Regurgitation and aspiration of stomach contents occurred at this stage. The patient was admitted to hospital in a layed from a quarter of an hour to four days after comatose state 2 hours following his removal from the the incident. It is essential to maintain a close watch water. He was deeply cyanosed and in respiratory distress. on all patients who appear to have recovered follow- The patient breathed 100% oxygen from a Boyle apparatus admission to the casualty department for approximately ing hospitalization as their respiratory status fre- on 20 min but remained deeply cyanosed. He was kept in quently deteriorates (Sladen and Zauder, 1971). the Trendelenburg position. Bloodstained frothy fluid continued to ooze from his nose and mouth. The resAlterations in biochemical values, blood volume piratory rate was 48 b.p.m. On auscultation there were and blood gases that occur before death due to rales and evidence of poor air entry over both luns fields. pulse rate was 120 beats/min and the arterial presdrowning are a consequence of asphyxia and move- The sure was 115/70 mm Hg. The pupils were widely dilated. ment of water and solutes across the alveolar mem- There was severe trismus and gross motor hyperactivity brane (Fuller, 1963). This writer also states that and a left-sided Babinski reflex. The urine was seen on "there is a rapid fall in blood oxygen and a rise in microscopy to be heavily bloodstained. carbon dioxide. Glucose is mobilized, fibrinolysins Treatment. At 6.30 p.m. atropine sulphate 0.6 mg was injected intravenously followed by suxamethonium 100 mg are released and capillary haemorrhage may occur. and the trachea was intubated via the nose using a cuffed Convulsions, hypertension, vomiting, micturition and endotracheal tube (Portex). Ventilation was controlled using 100% oxygen until spontaneous respiradefaecation occur initially and are followed by manually tion returned. Controlled ventilation using a Bird Mark depression with deep coma, vascular collapse and 8 ventilator delivering 100% oxygen was then started. the slowing of the heart action and respiration to Pancuronium was given intermittently intravenously to the gross motor hyperactivity and to permit the point of death". Water entering the alveoli acts abolish synchronization with the ventilator. The initial dose of as an irritant and causes exudation of protein into pancuronium was 7 mg and 2 mg was required hourly. the lungs (Miles, 1968). Chlorinated fresh water, being more irritant, would presumably account for C. TOLAND, M.D., B.CH., B.A.O., D.A., F.F.A.R.C.S.I., L i m e rick Regional Hospital, Dooradoyle, Limerick. greater exudation of protein into the alveoli following Present address: Barrington's Hospital Limerick, Ireland.

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This report describes the management of a case of near-drowning in chlorinated fresh water. The patient recovered fully, both physically and mentally. Complications involving the major systems of the body had developed prior to admission to hospital. Treatment included controlled ventilation via a cuffed nasotracheal tube, steroids, antibiotics and digoxin. Intravenous fluids given, and considered beneficial in influencing the prognosis, were plasma, blood, mannitol and sodium bicarbonate. The patient's condition was evaluated by frequent blood-gas analysis and appropriate adjustment of inspired oxygen concentration and ventilator settings made. High pressures were required to ventilate the patient because of the low compliance of his lungs.

CASE OF NEAR-DROWNING IN CHLORINATED FRESH WATER

FIG. 1. Portable chest X-ray at 8 p.m. showing diffuse bilateral pulmonary oedema.

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FIG. 2. A portable chest X-ray showing considerable clearing of the pulmonary oedema 24 hours after admission. aspiration of a large amount of fresh water might compromise the oxygen-carrying capacity of the blood. His arterial pressure rose to 110/70 mm Hg following the transfusion of the blood and plasma. Intravenous fluids were continued for 84 hours. Periodic hyperinflation of the lungs was started and continued intermittently to help prevent atelectatic areas developing and to re-aerate atelectatic alveoli. Dexamethasone 4 mg was injected i.m. 6-hourly and 20% mannitol 70g was infused to treat the cerebral oedema resulting from the protracted period of oxygen deprivation. Urine analysis showed albumin, red blood cells and a specific gravity of 1020; Hb was 13 g/100 ml; p.c.v. 39%; w.c.c. 9,200/cm3; s.g.o.t. exceeded 85 mU/ml (normal up to 12 mU/ml); s.g.p.t. exceeded 44.4 mU/ml (normal up to 12 mU/ml); c.p.k. exceeded 236 units mU/ml (normal up to 50 mU/ml). The raised serum enzyme levels reported at 9.30 p.m. reflect serious hypoxia of the organs and muscles. The serum electrolyte values at 10.30 p.m. were Na+ 127 m.equiv/1., K+ 5.5 m.equiv/1., Cl' 104 m.equiv/1. Blood-gas studies which were performed at 2 a.m. showed pH 7.26; Paco. 52 mm Hg; base excess —9 m.equiv/1.; buffer base 44 m.equiv/1.; standard bicarbonate 17.8 m.equiv/1.; Pao2 60 mm Hg whilst breathing 100% oxygen. The patient was a little less cyanosed at 2 a.m. The pulse rate was 100 beats/min and the arterial pressure was 120/75 mm Hg. The pupils were still widely dilated. By 6 a.m. the Paco2 had risen to 75 mm Hg. The minute volume was increased to 15 L/min (tidal volume 1 1. and respiratory frequency 15 b.p.m.) and the inflationary pressure rose from 45 to 55 cm H,O. Proxyphylline 400 mg was injected i.v. and repeated once intramuscularly after 2 hours. At 2 p.m. the Paco2 had fallen to 48 mm Hg and the Pao2 was 60 mm Hg. The tidal volume was reset at 750 ml and the respiratory

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A Ryle's tube was passed and the stomach aspirated. Large quantities of bloodstained fluid and semidigested food were aspirated from both lung fields. Sterile suction was done repeatedly. Although a variety of settings was employed using the Bird ventilator delivering 100?& oxygen the Pco2 remained at 55 mm Hg. An end-expiratory resistance was also used. A Cape ventilator was substituted continuing with a 100% oxygen. The rate was set at 15 b.p.m. and tidal volume was set at 800 ml. A chest radiograph showed marked bilateral pulmonary oedema and arterial blood-gas values at 7 p.m. showed pH 7.05, Paoo. 24.5 mm Hg, base excess —22 m.equiv/1. Sodium bicarbonate 300 m.equiv was given between 7 and 7.30 p.m. The serum electrolyte findings at 7 p.m. were Na+ 143 m.equiv/1., K+ 4 m.equiv/1., CT 105 m.equiv/1. Blood urea was 28 mg/100 ml. Hydrocortisone hemisuccinate 300 mg was given intravenously at 7.15 p.m. followed by 100 mg i.m. 4-hourly. AmpiciUin 500 mg was injected i.m. 6-hourly. The corticosteroids and antibiotics were given to help resolve the pulmonary oedema and in anticipation of pulmonary complications. An intravenous infusion of 500 ml of 5% dextrose in water was started at 7 p.m. Frusemide 60 mg was injected intravenously on admission and 20 mg was injected intramuscularly 12-hourly for 24 hours to treat the pulmonary oedema. Digoxin 0.5 mg was injected intramuscularly and 0.25 mg was continued twice daily. The electrocardiogram showed sinus rhythm with T-vector abnormalities initially. Serial tracings showed progressive improvement. By 7.30 p.m. the patient's arterial pressure had fallen to 100/70 mm Hg and his pulse rate had risen to 130 beats/min. He was still deeply cyanosed. One litre of plasma was transfused to replace the large quantities lost from the circulation in the alveoli. This transfusion was followed by 1 litre of blood starting at 8.30 p.m. it was thought that as the haemolysis resulting from the

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BRITISH JOURNAL OF ANAESTHESIA pulse rate increased to 100 beats/min. Rales were heard on ausculatation at both lung bases. Frusemide was given orally together with potassium chloride and a change was made to a different antibiotic. Four days later a chest radiograph showed complete clearing of the oedematous changes. He was discharged from hospital 16 days following admission feeling well apart from mild hoarseness and occasional bouts of coughing. DISCUSSION

rate at 15 b.p.m. A portable chest radiograph showed considerable clearing of the pulmonary oedema 24 hours after admission. Twenty-four hours after initiation of controlled ventilation attempts were made to decrease the inspired oxygen concentration from 100% because of the possibility that prolonged exposure to high concentrations of oxygen might cause pulmonary damage (Nash, Blennerhasset and Pontoppidan, 1967). Efforts were made to assess the patient's level of consciousness every few hours by asking him to open his eyes or clench his fists if he heard our questions when ventilation was being assisted or when he breathed spontaneously for 1-2 min. At 8 p.m., 26 hours following admission to hospital, the patient became semiconscious, opened his eyes on request, and moved his lips as if he was trying to form sentences. Recurring bouts of motor hyperactivity continued for 48 hours as observed when he was allowed to breathe spontaneously at intervals. Sixty-two hours following admission to hospital an inspired oxygen concentration of 50% maintained the Pao2 at 70 mm Hg. The inspired oxygen concentration was reduced further to 40% in air prior to extubation of the patient, the neuromuscular block having been reversed by neostigmine sulphate preceded by atropine sulphate 70 hours following admission to hospital. The patient was conscious and ventilation was assisted using the Bird Mark 8 ventilator set at "air mix". This regime was required because the arterial Po2 fell to 60 mm Hg when breathing air spontaneously for a few minutes following extubation, and continued to do so for 18-24 hours. Ninety-six hours following admission the patient breathed concentrations of 35% and finally 28% oxygen for a further 12 hours prior to breathing air, at which stage arterial blood values indicated satisfactory oxygenation and acid-base balance. Nine days later the patient's

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FIG. 3. A departmental film showing complete clearing of oedematous changes 13 days following admission.

Positive pressure ventilation with oxygen was essential in the treatment of this patient and difficulty was experienced in raising the arterial oxygen tension to a satisfactory level. The Cape ventilator was used following an initial short period with the Bird Mark 8. The Cape is a volume- and time-cycled flow generator and is regarded as able to deliver the same stroke volume against varying degrees of resistance. It also has a high reserve of power and was preferred in this case because high inflation pressures were required to ventilate the lungs adequately on account of the low compliance which developed following aspiration of stomach contents and gross bilateral pulmonary oedema. Because of the low compliance of the lungs, ventilation with a large tidal volume at a slow frequency has been advised (Adams et al., 1969). Large doses of methylprednisolone have been shown to reverse pulmonary oedema in near-drowning cases and a higher mortality rate has been recorded in patients who were not given methylprednisolone (Sladen and Zauder, 1971). Large doses of corticosteroids were administered to this patient. A sudden rise in the blood sugar level necessitated reduction of the doses of hydrocortisone and dexamethasone 5 days later. The patient's urine contained red blood cells and albumin for 5 days. His urinary output remained adequate. Although diuretics were given, their usefulness has not been proven in the treatment of secondary drowning (Rivers, Orr and Lee, 1970). According to Miles (1968) if the near-drowning victim can be kept alive for 24 hours, the chances are good that he will make a complete recovery even though brain damage is present as indicated by convulsions, coma or other signs. Our patient's left-sided Babinnski reflex had reverted to normal 8 days later. Subsequent clinical examinations of this patient have shown that his mental state is normal and happily he returned to bis work as an Industrial Promotions Officer three months following the accident.

CASE OF NEAR-DROWNING IN CHLORINATED FRESH WATER ACKNOWLEDGEMENTS

I thank the physicians at the Limerick Regional Hospital for their agreement to publish this case report, and the nursing and laboratory staffs for their care and co-operation. REFERENCES

inspire et le flux de ventilation. Une pression elevee etait necessaire pour ventiler le malade, en raison de la faible elasticity de ses poumons. DIE BEHANDLUNG EINES PATIENTEN, DER FAST IN CHLORIERTEM FRISCHWASSER ERTRUNKEN 1ST ZUSAMMENFASSUNG

In diesem Bericht wird die Behandlung eines Patienten beschrieben, der beinahe in chloriertem Frischwasser ertrunken ist. Der Patient erholte sich korperlich und geistig vollstandig. Komplikationen der Hauptfunktionen des Korpers waren vor der Aufnahme ins Krankenhaus aufgetreten. Die Behandlung erfolgte mit Steroiden, Antibiotika und Digoxin, ausserdem wurde kontrolliert beatmet durch einen mit Luftmanschette versehenen nasotrachealen Tubus. Es wurden intravenose Infusionen gegeben sowie Plasma, Blut, Mannitol und doppeltkohlensaures Natrium, was die Prognose bestimmt giinstig beeinflusst hat. Der Zustand des Patienten wurde kontrolliert durch haufige Blutgasanalysen, woraufhin die inspirierte Sauerstoff-Konzentration und die Ventilator-Justierung entsprechend eingestellt wurden. Zur Beatmung des Patienten war ein hoher Druck erforderlich wegen der geringen Kapazitat seiner Lungen. TRATAMIENTO DE UN CASO DE CASI ASFDCIA EN AGUA FRESCA CLORADA RESUMEN

TRAITEMENT D'UN CAS DE PRESQUE-NOYADE DANS DE L'EAU FROIDE CHLORATEE SOMMAIRE

Ce rapport decrit le traitement d'un cas de presquenoyade dans de l'eau fraiche chloratee. Le patient s'est retabli completement, physiquement aussi bien que mentalement. Des complications au niveau des systemes corporels majeurs s'itaient developpeps avant l'arriyde a l'hopital. Le traitement comprenait une ventilation controlee via un tube nasotracheal a manchon, des steroides, antibiotiques et Digoxin. Du liquide intraveineux a ete administre et on croit que le plasma, sang, mannitol et bicarbonate de soude ont favorablement influence le pronostic. L'etat du malade a ete evalue par des analyses frequentes des gaz sanguins et on modifia suivant les besoins la concentration d'oxygene

Esta communication describe el tratamiento de un caso de casi asfixia por sumersion en agua fresca clorada. El paciente se recuperd completamente, tanto fisica como mentalmente. Antes de su ingreso en el hospital se habian desarrollado complicaciones en los principales sistemas del cuerpo. El tratamiento incluyo la ventilacidn controlada a traves de un tubo nasotraqueal con manguito, esteroidesv antibioticos y digoxina. Fueron administrados liquidos in^travenosos y se considero que influyeron fayorablementesobre el pronostico el plasma, sangre, manitol y bicarbonate sodico. El estado del paciente fue evaluado mediante frecuentes analisis de los gases sanguineos y fueron efectuados ajustes apropiados de la concentraci6n: del oxigeno inspirado y funcionamiento del ventilador. Fueron necesarias presiones elevadas para ventilar ali paciente a causa de la baja adaptabilidad (complianza) de sus pulmones.

BOOK REVffiW Pharmacological Topics in Anaesthesia (International Anesthesiology Clinics) Fall, 1971 Vol. 9, No. 3. Edited by R. A. Millar, Published by Little, Brown and Co., Boston, 1971. Pp. 320; indexed; illus. This is an enjoyable and stimulating book. The 15 contributors to this volume from the International Anesthesiology Clinics series discuss in varying depth 13 specific topics. The first four chapters deal with general pharmacology of anaesthetic agents and cover the mechanisms of action and cellular effects of anaesthetics, their neuropharmacology and their effects on neurocirculatory control. Similarly the two closing chapters deal with the pharmacology of sympathetic nerve ;endings and drug receptors. The central portion of the book contains more of the applied pharmacology of anaesthetic drugs and considers nitrous oxide, the metabolism of anaesthetics,

recently introduced drugs, and pre- and postoperative medication. Respiratory depressants are considered in relation to their effects on the carbon-dioxide-ventilation response curve, and an outline is given of the design and execution of clinical trials. The great advantage of a book of this nature is that unlike a textbook it does not have to be comprehensive. The subject matter may thus be treated in as little or much depth as the authors consider necessary. This form of book is also less subject to the long delays between composition and publication which so bedevil more formal texts. Here the editor has brought together a group of authoritative contributors who have succeeded in producing a series of well balanced and up-to-date reviews of topics of present-day interest. C. M. Conway

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Adams, A. P., Morgan, M., Jones, B. C , and McCormick, P. W. (1969). A case of massive aspiration of gastric contents during obstetric anaesthesia: treatment by tracheostomy and prolonged intermittent positive pressure ventilation. Brit. J. Anaesth., 41, 176. Fuller, R. H. (1963). The clinical pathology of near drowning. Proc. roy. Soc. Med., 56, 33. Miles, S. (1968). Drowning. Brit. med. J., 3, 597. Modell, J. H., Davis, J. H.5 Giammona, S. T., Moya, F., and Mann, J. B. (1968). Blood gas and electrolyte changes in human near-drowning victims. J. Atner. med. Ass., 203, 99. Nash, G., Blennerhasset, J. B., and Pontoppidan, H. (1967). Pulmonary lesions associated with oxygen therapy artificial ventilation. New Engl. J. Med., 276, 368. Rivers, J. F., Orr, G., and Lee, H. A. (1970). Drowning: its clinical sequelae and management. Brit. med. J., 2, 157. Sladen, A., and Zauder, H. L. (1971). Methylprednisolone for pulmonary oedema after near drowning. J. Amer. med. Ass., 215, 1793.

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