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CONSULTANT CONTRACT
955 ATROPINE METHONITRATE IN MANAGEMENT OF NEAR-FATAL REFLEX ANOXIC SEIZURES
SIR,-Reflex anoxic seizures from vagal-mediated cardiac standstill ("white" convulsive breath-holding attacks) are now well recognised.’ When precipitated by pain they are regarded as harmless, however horrific they may be to those who witness them. Standard management is by confident reassurance reinforced, if necessary, by demonstrating that an anoxic seizure triggered by ocular compression (OC) needs no special attention.2 Only rarely is atropine needed to block the oculocardiac reflex. 1,1,4 However, I have seen a girl whose reflex anoxic seizures were nearly fatal. The resemblance to the single published fatal case,5 and the mother’s understandable demand that there be no recurrence, made atropinisation essential and permitted study of a preparation not previously used in such cases. This girl, aged 2 years 7 months had, since infancy, a history of breath-holding without crying after all painful stimuli. She was healthy but clumsy and fell often; breath-holding attacks averaged one every 2 days. One day she bumped herself and was ignored for a moment. She took a breath; no cry came out, and she went limp and glazed and pale with eyes rolling and large pupils. She then went stiff in her mother’s arms and jerked and frothed. After this, and just as her eyes were beginning to follow again, she vomited and became limp and motionless. Her mother, a trained nurse, sucked out and then breathed into her daughter’s mouth. She thought her child had died. When the ambulance arrived an airway was put in. In the intensive-care unit the child cried and spoke to her mother, but she still looked pale and tired. 2 days later, when she was on no medication, OC supine’ induced 9.8 s asystole, general gross slowing of the EEG, and an anoxic seizure. After wakening she was pale and then slept for 4 h. The mother insisted on atropine and on OC studies to confirm protection against future attacks. Atropine methonitrate drops were started at 0-8mg 5 times daily (0-33mg/kg/day). After 3 days on this dose, OC induced asystole of 2.3 s with no after-pallor or sleepiness. No atropine side-effects were evident. 24 h later, on atropine methonitrate 8 mg/day in 5 doses, 3thafter the last dose OC still induced asystole of 2-3s, with no respiratory arrest or pallor. The heart-rate beforehand had been 102-136/min, and the patient’s mouth was dry. The day after the child had been discharged on this dose she fell off a table and held her breath but had no other vagal signs. 5 days later the mother was more confident, but the child was waking at night because of dry nostrils and her lips were cracking. Pupils were normal, heart-rate 130-140/min. The dose of atropine methonitrate was reduced to 1.6 mg three times daily. Over a month the child had three breathholding attacks, but none was followed by pallor or tiredness. She was well, her mouth was no longer dry, and she was sleeping well. Her 5 mm pupils were normally reactive; resting heart-rate was 100/min. It was decided to maintain the total daily dose but to reduce the frequency of administration. Paulson5 described a 2-year-old girl with breath-holding attacks who had a severe anoxic seizure, almost certainly the result of vagal cardiac standstill. When the child vomited, her mother attempted mouth-to-mouth respiration. Aspirate could not be cleared from the airways and vomit was probably blown into the bronchi. The child was carried erect to hospital and
irreversible anoxic cerebral cortical damage proved fatal. Paulson advised against mouth-to-mouth respiration in such circumstances. Our patient’s mother noted vomiting just as the child was regaining consciousness, when protective laryngeal reflexes were presumably returning. However, in the home, it would be difficult to persuade a mother to act differently. When total reassurance is difficult-as here in an incident resembling "near-miss sudden infant death"-atropine control may be needed, and OC testing suggests that atropine methonitrate at doses of less than 0-4 mg/kg/day will suppress the cardiac vagus. Fraser of Allander Unit and EEG Department, Royal Hospital for Sick Children, Yorkhill, Glasgow G3 8SJ
J. B. P. STEPHENSON
-
CONSULTANT CONTRACT
SIR,-Your editorial (Sept. 15, p. 567) and Dr Grant’s letter (Oct. 6, p. 746) show grave concern about the proposals for the new consultant contract which the British Medical Association negotiators seem so ready to accept. The progressive and substantial increase in full-time hospital consultant staff over the past thirty years, both in academic and district hospitals, is due largely to the increasing professional satisfaction in this role despite inadequate remuneration. It is generally recognised that the strength of the Health Service is dependent in no small measure on this segment of the consultant group. Proposals whereby full-time staff could supplement income by private practice are a very real threat to the contribution of full-time consultant staff and could well seriously hamper further recruitment. The new proposals come in the wake of increasing disparity between the earnings of part-time and fulltime staff and proposals for the full-timers have been made simply to prevent the disparity being too great. Since it seems that these proposals will be implemented we would suggest that to avoid a very serious decline in morale and recruitment in full-time staff the following arrangements should be considered: (1) Designated private beds in teaching and district hospitals should be put at the disposal of the full-time staff. This will at least eliminate the waste of travelling time and consequent unavailability for clinical teaching and research duties, an argument which has been advanced by our part-time colleagues and which we have fully supported in the past. (2) The income derived by hospital consultant staff from such private practice participation should, in line with successful geographic administrative arrangements pioneered in North America, be billed for by a self-financing hospital administrative office, and a proportion of the income so generated should be shared with other professional and ancillary groups involved in the care of patients. Northwick Park Hospital, and Clinical Research Centre, Harrow, Middlesex HA1 3UJ
N.H.S. REORGANISATION
SIR,-Professor Soothill’s letter (Sept. 1, p. 468) is the only communication I have seen in your columns which underlines the ills of the N.H.S. and suggests how they could be alleviated. The two attributes which the N.H.S. (general practice apart) lacks are individual responsibility for running the different specialties and a method of meaningful accounting. Soothill’s suggestion of a "vertical" type of organisation would at least make this possible, whereas there is little hope of improvement of services to the public by tinkering with the present "horizontal" administrative structure without a major cash in-
1.
Stephenson JBP. Reflex anoxic seizures ("white breath-holding"): nonepileptic vagal attacks. Arch Dis Child 1978; 53: 193-200. 2. Stephenson JBP. Ocular compression in reflex anoxic seizures. Arch Dis Child 1978; 53: 693. 3. Maulsy R, Kellaway P. Transient hypoxic crises in children. In: Kellaway P, Petersen, I, eds. Neurological and electroencephalographic correlative studies in infancy. New York: Grune and Stratton, 1964: 349-60. 4. Lombroso CT, Lerman P. Breath-holding spells (cyanotic and pallid infantile syncope). Pediatrics 1967; 39: 563-81. 5 Paulson G. Breath-holding spells: a fatal case. Devel Med Child Neurol 1963; 5: 246-51.
A. E. KARK H. T. DAVENPORT
crease.
SIR,-Reflex anoxic seizures from vagal-mediated cardiac standstill ("white" convulsive breath-holding attacks) are now well recognised.’ When precipitated by pain they are regarded as harmless, however horrific they may be to those who witness them. Standard management is by confident reassurance reinforced, if necessary, by demonstrating that an anoxic seizure triggered by ocular compression (OC) needs no special attention.2 Only rarely is atropine needed to block the oculocardiac reflex. 1,1,4 However, I have seen a girl whose reflex anoxic seizures were nearly fatal. The resemblance to the single published fatal case,5 and the mother’s understandable demand that there be no recurrence, made atropinisation essential and permitted study of a preparation not previously used in such cases. This girl, aged 2 years 7 months had, since infancy, a history of breath-holding without crying after all painful stimuli. She was healthy but clumsy and fell often; breath-holding attacks averaged one every 2 days. One day she bumped herself and was ignored for a moment. She took a breath; no cry came out, and she went limp and glazed and pale with eyes rolling and large pupils. She then went stiff in her mother’s arms and jerked and frothed. After this, and just as her eyes were beginning to follow again, she vomited and became limp and motionless. Her mother, a trained nurse, sucked out and then breathed into her daughter’s mouth. She thought her child had died. When the ambulance arrived an airway was put in. In the intensive-care unit the child cried and spoke to her mother, but she still looked pale and tired. 2 days later, when she was on no medication, OC supine’ induced 9.8 s asystole, general gross slowing of the EEG, and an anoxic seizure. After wakening she was pale and then slept for 4 h. The mother insisted on atropine and on OC studies to confirm protection against future attacks. Atropine methonitrate drops were started at 0-8mg 5 times daily (0-33mg/kg/day). After 3 days on this dose, OC induced asystole of 2.3 s with no after-pallor or sleepiness. No atropine side-effects were evident. 24 h later, on atropine methonitrate 8 mg/day in 5 doses, 3thafter the last dose OC still induced asystole of 2-3s, with no respiratory arrest or pallor. The heart-rate beforehand had been 102-136/min, and the patient’s mouth was dry. The day after the child had been discharged on this dose she fell off a table and held her breath but had no other vagal signs. 5 days later the mother was more confident, but the child was waking at night because of dry nostrils and her lips were cracking. Pupils were normal, heart-rate 130-140/min. The dose of atropine methonitrate was reduced to 1.6 mg three times daily. Over a month the child had three breathholding attacks, but none was followed by pallor or tiredness. She was well, her mouth was no longer dry, and she was sleeping well. Her 5 mm pupils were normally reactive; resting heart-rate was 100/min. It was decided to maintain the total daily dose but to reduce the frequency of administration. Paulson5 described a 2-year-old girl with breath-holding attacks who had a severe anoxic seizure, almost certainly the result of vagal cardiac standstill. When the child vomited, her mother attempted mouth-to-mouth respiration. Aspirate could not be cleared from the airways and vomit was probably blown into the bronchi. The child was carried erect to hospital and
irreversible anoxic cerebral cortical damage proved fatal. Paulson advised against mouth-to-mouth respiration in such circumstances. Our patient’s mother noted vomiting just as the child was regaining consciousness, when protective laryngeal reflexes were presumably returning. However, in the home, it would be difficult to persuade a mother to act differently. When total reassurance is difficult-as here in an incident resembling "near-miss sudden infant death"-atropine control may be needed, and OC testing suggests that atropine methonitrate at doses of less than 0-4 mg/kg/day will suppress the cardiac vagus. Fraser of Allander Unit and EEG Department, Royal Hospital for Sick Children, Yorkhill, Glasgow G3 8SJ
J. B. P. STEPHENSON
-
CONSULTANT CONTRACT
SIR,-Your editorial (Sept. 15, p. 567) and Dr Grant’s letter (Oct. 6, p. 746) show grave concern about the proposals for the new consultant contract which the British Medical Association negotiators seem so ready to accept. The progressive and substantial increase in full-time hospital consultant staff over the past thirty years, both in academic and district hospitals, is due largely to the increasing professional satisfaction in this role despite inadequate remuneration. It is generally recognised that the strength of the Health Service is dependent in no small measure on this segment of the consultant group. Proposals whereby full-time staff could supplement income by private practice are a very real threat to the contribution of full-time consultant staff and could well seriously hamper further recruitment. The new proposals come in the wake of increasing disparity between the earnings of part-time and fulltime staff and proposals for the full-timers have been made simply to prevent the disparity being too great. Since it seems that these proposals will be implemented we would suggest that to avoid a very serious decline in morale and recruitment in full-time staff the following arrangements should be considered: (1) Designated private beds in teaching and district hospitals should be put at the disposal of the full-time staff. This will at least eliminate the waste of travelling time and consequent unavailability for clinical teaching and research duties, an argument which has been advanced by our part-time colleagues and which we have fully supported in the past. (2) The income derived by hospital consultant staff from such private practice participation should, in line with successful geographic administrative arrangements pioneered in North America, be billed for by a self-financing hospital administrative office, and a proportion of the income so generated should be shared with other professional and ancillary groups involved in the care of patients. Northwick Park Hospital, and Clinical Research Centre, Harrow, Middlesex HA1 3UJ
N.H.S. REORGANISATION
SIR,-Professor Soothill’s letter (Sept. 1, p. 468) is the only communication I have seen in your columns which underlines the ills of the N.H.S. and suggests how they could be alleviated. The two attributes which the N.H.S. (general practice apart) lacks are individual responsibility for running the different specialties and a method of meaningful accounting. Soothill’s suggestion of a "vertical" type of organisation would at least make this possible, whereas there is little hope of improvement of services to the public by tinkering with the present "horizontal" administrative structure without a major cash in-
1.
Stephenson JBP. Reflex anoxic seizures ("white breath-holding"): nonepileptic vagal attacks. Arch Dis Child 1978; 53: 193-200. 2. Stephenson JBP. Ocular compression in reflex anoxic seizures. Arch Dis Child 1978; 53: 693. 3. Maulsy R, Kellaway P. Transient hypoxic crises in children. In: Kellaway P, Petersen, I, eds. Neurological and electroencephalographic correlative studies in infancy. New York: Grune and Stratton, 1964: 349-60. 4. Lombroso CT, Lerman P. Breath-holding spells (cyanotic and pallid infantile syncope). Pediatrics 1967; 39: 563-81. 5 Paulson G. Breath-holding spells: a fatal case. Devel Med Child Neurol 1963; 5: 246-51.
A. E. KARK H. T. DAVENPORT
crease.