Accidental Carbon Monoxide Poisoning - EBSCOhost

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Accidental Carbon Monoxide Poisoning. Emphasis on Hyperbaric Oxygen Treatment. David Gozal, MD, Avishai Ziser, MD, Avi Shupak, MD, Yehuda Melamed, ...
TOXICOLOGY

Accidental Carbon Monoxide Poisoning Emphasis on Hyperbaric Oxygen Treatment David Gozal, MD, Avishai Ziser, MD, Avi Shupak, MD, Yehuda Melamed, MD

Six cases of accidental carbon monoxide poisoning in children are presented. The importance of hyperharic oxygen therapy as the cornerstone of treatment in the prevention of either acute or delayed complications is discussed.

'ARBON MONOXIDE (CO) has an affinity for hemoglobin 240 times greater than that of oxygen.' This results, after exposure to CO, in the formation of a significant percentage of hemoglobin existing as carboxyhemoglobin (COHb). Its presence causes a left shift of the oxyhemoglobin dissociation curve'^ and a disruption of intracellular respiratory processes by combining with cytochrome a^ oxidase.'^ Tissue hypoxia ensues. The rationale for hyperbaric oxygen (HBO) treatment in CO poisoning is threefold. It improves tissue oxygenation via the increased amount of dissolved oxygen in plasma."* It increases the rate of elimination of CO, which has been shown to be 320 minutes when breathing fresh air, 80 minutes when breathing 100 percent oxygen at atmospheric pressure, and dropping to as little as 23 minutes during 100 percent oxygen breathing at 3 atmospheres absolute (ATA).-^ Finally, HBO has been shown to have a beneficial effect on cerebral edema and intracranial pressure.*^ To our knowledge, few reports have focused on the importance of HBO therapy in the management of CO intoxication in children. We report six cases From the Israeli Naval Hyperbaric Institute. Haifa. Israel. Goriespoiidence to: D. Go/al. M.D , Israeli Naval Hyperbaric Institute, P.O. Box 8040, 31 080 Haifa, Israel. Received for publication August 1984, revised October 1984, accepted November 1984.

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of accidental CO poisoning and the use of a hyperbaric chamber in their management. Methods HBO was administered in a three-compartment walk-in hyperbaric chamber constructed by Drager of West Germany. It is provided with all the necessary medical equipment and facilities required for the management of the critically ill patient. All HBO sessions are conducted with a medically qualified attendant inside the chamber. The medical staff is on call 24 hours a day year round, and the chamber can be in operation within half an hour of a phone call. In all of the patients described below, vital signs were recorded twice in the course of each HBO treatment, and included blood pessure, pulse rate, respiratory rate, and blood gases. In addition, the patients were connected to an ECG monitor and to a blood pressure manometer, making on-line surveillance possible. All patients were referred to the hyperbaric facility from nearby hospitals after telephone consultation with the resident physician on call. Before HBO treatment, the children underwent a chest x-ray to rule out the possibility of pneumothorax or other pulmonary abnormality, and a bilateral tympanocentesis in order to obviate the necessity for Valsalva Vol. 24

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maneuver in the unconscious or uncooperative patient. Case Reports

From January 1982 to February 1983, six children were diagnosed as having acute CO poisoning and were referred to our institute for HBO treatment (Table 1), Case 1 A 2-year-old boy was found unconscious in his room along with his 3-moiuh-olcl sister, who was pronounced dead at the scene. The two were exposed to smoke produced by a burning carpet in their room. The patient was admitted within 45 minutes to a local hospital, and physical examination disclosed a stuporous state reactive only to painful stimuli, A blood pressure of 90/60, a regular pulse of 112/ minute, and a respiratory rate of 32/minute were recorded. Despite oxygen administration by mask, peripheral cyanosis and diffuse rales over both lung fields were found on examination. Chest x-rays and ECG tracing were normal. Arterial blood gases on admission were as follows: PO2— 42 mmHg; PCOj—23 mmHg; pH—7,32; O2 saturation— 88%; Bic—15 mmol/1; COHb—39,2%, After an initial assessment and resuscitation, the patient was transferred to us for HBO therapy. Within 8 hours of rescue, he was given a course of 90 minutes of 100 percent oxygen at 2,8 atmospheres absolute (ATA), with full return of consciousness and clearing of respiratory symptoms and signs, COHb level at the end of the treatment was 2,4 percent. Recovery was uneventful and the patient was discharged 3 days later. Follow-up 9 months later revealed no developmental or behavioral abnormalities.

Case 2 An 11-year-old boy was admitted to a local hospital after he was found unconscious in a closed unveiuilated room, A charcoal heating system was burning inside the room. Physical examination disclosed a stuporous state with reaction only to painful stimuli, A blood pressure of 110/70, a regular pulse of 96/minute, and a respiratory rate of 2 4 / minute were recorded. Increased generalized tonus and trismus of mandible were found. Chest x-rays and ECG tracing were normal. Venous blood gases on admission were POj—19 mmHg; PCO2—36 mmHg; pH—7,14; O2 saturation—15,5%; Bic—12 mmol/1; COHb—27,2%, The patient was given oxygen by mask and slowly regained consciousness over the subsequent few minutes. Two hours after admission no further improvement in neurological findings was noted, and he was transferred to the hyperbaric chamber. He received a course of 90 minutes overall in the chamber, consisting of 60 minutes of 100 percent oxygen at 2,8 ATA and then 30 minutes at 2 ATA, COHb after the first course was 1,6 percent. Arterial blood gases in the chamber were PO2—750 mmHg; PCO2—35 mmHg; pH— 7.46; Bic—25 mmol/1. At the end of HBO therapy, the patient had regained full mental alertness, and all neurological symptoms and signs had resolved. Follow-up has been uneventful. Case 3 A 7-year-old boy was found unconscious in the same room as described in case 2, Examination revealed a deep comatose state, and no reaction to painful stimuli could be elicited, A blood pressure of 100/80 and a regular pulse of 112/minute were recorded. The patient was breathing spontaneously, and the respiratory rate was 28/minute, Cyanosis or cherry pink skin were not observed. Chest xrays and ECC were normal. Venous blood gases on admission

TAHI.K. 1, RelnmnI Clinical Data

Interval Between Rescue and Start

Blood Gas Tensions Initial COHb Level

Case

Age

Duration of Exposure to

No,

(yrs)

CO

Treatment (hours)

1

2

Few iiiimites

8

Stupor

Rales in both lung

2

It

Overnight

4

Stupor

Increased generalized tonus, trismus of mandible

3 4

7 15

Overnight 2 hours

4 VA

Deep coma Stupor, headache

5

3

Few minutes

7

Deep coma

6

5

Few minutes

7

Coma

of

Level of Consciousness

Clinical Signs

neitis



Cherry pink discoloration in cheeks, lips, and fingers Convulsions, pulmonary edema. apnea: expired Dyspnea, pulmonary edema

(%)

Oxygen (mmHg)

Carbon Dioxide (mmHg)

pH

39,2

42

23

7,32

27,2

19*

36

7,14

64

21* 79

51 37

7.18 7.45

not available

96

36

7,35

not available

70

42

7,29

24.5

* Venous determinations. CLINICAL PEDIATRICS

March 1985

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GOZAL ET AL.

were POj—21 mmHg; PCO2—51 mmHg; pH—7,18; O2 sat.—4%; Bic—18 mmol/1; COHb—64%, The patient received oxygen by mask until transferred, and the same HBO treatment as above was instituted, COHb after the HBO session was 6,8 percent, and arterial blood gases in the chamber showed PO2—800 mmHg; PCO2—42 mmHg; pH—7,43; Bic—28 mmol/1. Complete mental, physical! and neurological recovery were observed, and the patient left the hyperbaric chamber walking independently and unaided. Case 4 A 15-year-old girl was found stuporous in her room. The door and all windows were closed, and the room was being heated by a charcoal burner. From the patient's later history, an approximate 2-hour exposure time was estimated. On admission, the patient was in stupor, reacted to pain, and a cherry pink discoloration of cheeks, lips, and fingers was noted, A blood pressure of 120/80, a regular pulse of 110/minute and a respiratory rate of 36/minute were recorded. Chest x-ray and ECG were normal. Arterial blood gases on an oxygen mask were PO2—79 mmHg; PCO2— 37 mmHg; pH—7,45; O2 sat,—96%; Bic—25 mmol/1. When HBO therapy was started VA hours later, the patient was somnolent, complained of excruciating headache, and a glowing pink discoloration of face, lips, and hands was still present. At this stage, the COHb level was 24.5 percent. She received 100 percent oxygen at 2,4 ATA for 90 minutes with complete disappearance of all symptoms and signs. Arterial blood gases while breathing oxygen in the chamber were PO2—1265 mmHg; PCO2—39 mmHg; pH—7,42; Bic—25 mmol/1; COHb—0,8%, Follow-up for 1 year has been normal.

hours later, sinus bradycardia of 40 beats/minute appeared, and a brain CAT scan was performed which showed diffuse severe cerebral edema with hydrocephalus of both lateral and third ventricles. Despite aggressive supportive treatment, the patient died on the following day. Case 6 A 5-year-old boy was found in a stuporous, irritable state at time of rescue with his younger brother (case 5), On physical examination, the patient was unconscious, reacted to painful stimuli, was dyspneic but not cyanotic, and diffuse rales and wheezes were heard over both lungs, A normal blood pressure of 105/70, a regular pulse of 120/minute and a respiratory rate of 38/minute were recorded. He was intubated and given 100 percent oxygen. He became restless and sedation was given. Chest x-rays on admission were compatible with pulmonary edema, and ECG was normal. Arterial blood gases under mechanical ventilation with 100 percent oxygen showed, on admission, PO2—70 mmHg; PCO2—42 mmHg; pH—7,29; O2 sat,—89%; Bic— 21 mmol/1. Three hours later they were PO2—338 mmHg; PCO2—41 mmHg; pH—7,39; O2 sat.—99.9%; Bic—24 mmol/1. One course of HBO therapy was given under artificial ventilation as in case 5, at the end of which the patient was conscious, responded to his name, and performed voluntary movements on request. Pulmonary findings were normal. The appearance of somnolence a few hours later prompted us to administer one further course of HBO at 2,5 ATA with complete resolution of symptoms. Recovery was uneventful thereafter, and the patient was discharged 7 days after the incident. Discussion

Case 5 Two brothers were rescued from a burning building. One of the patients, a 3-year-old boy, was found unconscious and in severe respiratory distress. The child was intubated in situ by the physician of the rescue team, and given 100 percent oxygen and an intravenous bolus of prednisone. During his transfer to the hospital, he had a convulsive grand mal episode, which ceased when intravenous diazepam was given. On admission, deep coma unreactive to pain, absence of spontaneous respiration, normal blood pressure of 90/60, regular pulse of 116/minute, and diffuse rales over lung fields compatible with pulmonary edema were found. Chest x-rays showed minimal congestion, and ECG was normal. Arterial blood gases with the patient being mechanically ventilated on 100% oxygen were, on admission, PO2—96 mmHg; PCO2—36 mmHg; pH—7,35; Bic—26 mmol/1. Three hours later they were PO2—377 mmHg; PCO2—38 mmHg; pH—7.37; O2 sat,—99,8%; Bic—22 mmol/1. At this stage, the patient was transferred to the hyperbaric chamber, and HBO therapy was instituted. He received a course of 90 minutes of 100 percent oxygen at 3 ATA, during which spontaneous breathing returned and the patient became reactive to pain. Two hours later, the child's clinical condition deteriorated, as evidenced by apnea and deepening of the coma. One further course of HBO at 2.5 ATA was given, but no improvement was observed. A few

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CO poisoning is a common occurrence in the pediatric population. In 1977 alone, 338 deaths related to CO were reported in the United States in persons under the age of 20.' The lack of reliable criteria for physical diagnosis emphasizes the importance of history of exposure, which may be masked by other life-threatening situations, such as respiratory distress from smoke inhalation. The environmental concentration of CO, the duration of exposure, and the rate and depth of breathing will determine the extent of accumulation of CO and the resulting COHb level. This level, however, correlates inconsistently with clinical status.* Therapy with HBO has been shown effectively to displace CO from hemoglobin, myoglobin, and cytochrome systems.^ The clinical improvement observed in our six patients was most probably due to the liberation of CO from the tissues, the reversal of residual hypoxic damage, and possibly by reducing cerebral edema secondary to diffuse anoxia and CO poisoning. The criteria for selection of patients for HBO treatment should obviously take into account the Vol. 24

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CARBON MONOXIDE POISONING

availability of a hyperbaric facility. When a chamber is available, rhe presence of even subtle symptoms or of an COHb level greater than or equal to 25 percent are sufficienr to warranr HBO rherapy. In those cases where a hyperbaric chamber is nor readily available, immediate referral is recommended whenever rhe COHb level is grearer rhan 40 percent or when symproms are present. In rhose asympromatic parienrs with COHb levels of less rhan 40 percent, the adminisrrarion of 100 percenr oxygen by means of a righr firring mask is sufficienr. This should be conrinued unril a COHb level of less rhan 10 percenr is obrained.'" Lacey" and Binder and Roberrs'^ bave drawn arrenrion ro rhe lare neurological sequelae of CO intoxication in children, which are related ro hypoxic cenrral nervous system rissue damage. More specifically, selective necrosis and degenerarion of rhe globus pallidus were observed by Sawada et al.^^ Myers et a/.''' demonsrrared rhe beneficial effecr of HBO rherapy on rhe neurological starus ar follow-up of adulrs afrer CO poisoning. This contrasrs wirh rhe work of Smith and Brandon,'^ who found a 33 percenr incidence of personaliry dereriorarion and 43 percenr memory impairmenr in 63 parienrs nor rreated wirh HBO. We srrongly advocare rhar any child wirh a hisrory comparible wirh CO poisoning be rreared wirh HBO according ro rhe above-mentioned criteria, even if considerable delay occurs. Several rherapeutic modaliries dealing wirh rhe deprh and durarion of oxygen adminisrrarion have been recommended by different cenrers, wirh equally sadsfactory results.'*'® If rhe parienr's condirion worsens or does not rerurn ro normal rhereafrer, rhe rrearmenr should be repeated. The possible side-effects of hyperbaric oxygen administration include mainly neurologic and pulmonary manifestations.'^ Although rare and nor observed in our parienrs, rhey should be raken inro accounr even when rhe suggesred rherapeuric modaliries are followed. This is parricularly rrue in those cases where predisposing facrors, such as epilepsy or other convulsive disorders, are present. It srill remains unknown wherher hyperbaric oxygen mighr aggravare rhe associared chemical pneumoniris due ro smoke inhala^'« Conclusion Despire rhe limired number of parienrs, relarive shorr follow-up rime, and lack of conrrol parienrs, we feel rhar HBO rherapy is of benefir in all CO poisoned CLINICAL PEDIATRICS

March 1985

children, eirher in rhe acute phase or in rhe prevenrion of lare sequelae. Ir should be srressed, however, rhar rhe primary emergency care immediarely afrer rescue should always consisr of rhe administrarion, eirher by mask or mechanical ventilarion, of 100 percenr oxygen. Acknowledgments We wish to thank Mr. Richard Lincoln for his invaluable editorial assistance.

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