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Intubation during cardiorespiratory arrest
THE LANCET
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technique improves yield in the diagnosis of tuberculosis in children. Pediatr Infect Dis J 1997; 16: 222–26. Miller FJW. Tuberculosis in children. Edinburgh: Churchill Livingstone, 1982. Galanakis E, Leveidiotu S, Siamopoulou A, Lapatsanis PD. A 3-month-old girl with fever and respiratory distress. Lancet 1995; 346: 1674. Wort SJ, Puleston JM, Hill PD, Holdstock GE. Primary tuberculosis of the oesophagus. Lancet 1997; 349: 1072.
Intubation during cardiorespiratory arrest SIR—I still do not fully understand why patients’ pillows tend to be removed during cardiorespiratory arrest situations. Yesterday I was yet again called to an arrest where a junior doctor was trying in vain to intubate a supine patient whilst his pillow sat uselessly on the floor. Junior doctors beware: it is usually difficult to visualise the vocal cords if intubation is attempted with the head and neck flat against the mattress. It is much better to take a few seconds to properly position the head and neck on the pillow in the “sniffing-themorning-air” posture. This simple manoeuvre will greatly facilitate intubation and help to avoid potentially dangerous periods of hypoxia which sometimes occur during lengthy attempts at intubation. D Steeples 16 Lancaster House, Whiston Hospital, Prescot, Merseyside L35 5DR, UK
Absence of relation between hyponatraemia and hypothyroidism SIR—In their Sept 13 commentary, Fahmy Hanna and Maurice Scanlon 1 discuss the various mechanisms that may be responsible for the hyponatraemia seen in hypothyroid patients reported in various studies. Rather than dispute the observations made in such studies with respect to the aetiology of hyponatraemia in the patients presented, we question whether there is in fact a relation
TSH range (mU/L) 0·3–1·5 1·5–3·0 3·0–4·5 4·5–10·0 10·0–15·0 15·0–20·0 20·0–40·0 40·0–80·0 >80·0
between hypothyroidism and clinically significant hyponatraemia. Studies published so far seem to report findings on small numbers of selected patients in which hypothyroidism and hyponatraemia are both present. However, as far as we are aware, no data have been published on the prevalence of hyponatraemia in a large group of unselected hypothyroid patients. We have looked at the relation between serum sodium and serum thyroid stimulating hormone (TSH) in a large group of patients (n=33 912) with archive analysis of patient results from a large city general hospital (table). The results showed that the distribution of serum sodium values was similar in biochemically euthyroid patients and hypothyroid patients (TSH >40 U/L, n=445) in whom the mean serum sodium was 138·6 mmol/L (SD 3·1). The proportion of patients with a serum sodium lying below the reference interval (135 mmol/L) showed no significant difference between the euthyroid subjects (11·4%) and hypothyroid subjects (12·8%). Hyponatraemia is a common finding in ill patients and arises in many presentations. It is found in patients with hypothyroidism, but our data indicate at no greater frequency than that which occurs in euthyroid individuals. It is perhaps not surprising therefore that no consistent mechanism explaining a relation between the two has emerged. The practical clinical message from our data is that when hyponatraemia is noted in hypothyroid patients other possible causes should be sought. *Bernard L Croal, Alison M Blake, J Johnston, Alistair C A Glen, Denis St J O’Reilly *Department of Clinical Biochemistry, Aberdeen Royal Infirmary, Aberdeen AB9 22B, UK; and Departments of Clinical and Pathological Biochemistry, Victoria and Royal Infirmary, Glasgow 1
Hanna FWF, Scanlon MF. Hyponatraemia, hypothyroidism, and role of arginine-vasopressin. Lancet 1997; 350: 755–56.
No of patients
Age (years)*
Total T4 (nmol/L)*
Sodium (mmol/L)*
Sodium <130 mmol/L (no [%])
Sodium <120 mmol/L (no [%])
14 717 12 798 2860 2120 447 206 319 377 68
58·0 (20·5) 59·7 (20·4) 63·1 (18·9) 67·0 (16·9) 69·0 (15·7) 67·9 (16·6) 67·8 (16·8) 62·9 (17·8) 58·3 (20·3)
97·1 (22·0) 94·4 (21·3) 91·8 (21·2) 86·6 (22·8) 76·2 (23·2) 68·6 (24·2) 67·7 (22·7) 33·3 (18·3) <20
139·0 (3·3) 139·0 (3·4) 138·9 (3·4) 138·7 (3·7) 138·3 (3·9) 138·1 (4·2) 138·1 (3·6) 137·8 (4·0) 138·6 (3·1)
269 (1·8) 257 (2·0) 42 (1·5) 51 (2·4) 15 (3·4) 9 (4·4) 9 (2·8) 14 (3·7) 0 (0)
19 (0·1) 16 (0·1) 0 (0) 4 (0·2) 2 (0·5) 1 (0·5) 1 (0·3) 1 (0·3) 0 (0)
The mean (SD) values for age, serum T4, and plasma sodium in 33 912 patients according to serum TSH concentration *Mean (SD).
1402
Driving and stroke S IR —P F Chinnery and colleagues (Aug 23, p 560)1 report a 34-year-old bus driver with a left homonymous hemianopia, a mild left hemiparesis, and a left hemisensory disturbance, who required a muscle biopsy to confirm the A3243G MELAS mutation. They point out that there is no specific treatment for patients with mtDNA disease, but do not comment on the specific management and advice concerning this patient’s fitness to drive. Even among patients with a first seizure, clinicians often omit to document that they have both counselled the patient about driving regulations and explained the legal requirement to inform the Driver and Vehicle Licensing Authority. 2 In a patient with symptomatic cerebrovascular disease, a group-II driving licence will be revoked until a full and complete recovery has occurred, with 5 years free of recurrence.3 A condition like MELAS, which predisposes to recurrent strokes, may mean permanent refusal of a group-II licence. However, this patient will not only have lost his job as a bus driver, but he may also not be accepted for safe driving at all if visual perimetry shows that the homonymous defect comes close to fixation.4 MOMcC is supported by a Patrick Berthoud Fellowship.
Angela M Loftus, *Mark O McCarron Department of Occupational Health, Royal Alexandra Hospital, Paisley; and *Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, UK 1
2
3
4
Chinnery PF, Turnbull DM, Walls TJ, Reading PJ. Recurrent strokes in a 34 year old man. Lancet 1997; 350: 560. Morrison AD, McAlpine CH. The management of first seizures in adults in a District General Hospital. Scot Med J 1997; 42: 73–75. Earl C, Wetherall G. Disorders of the nervous system. In: Taylor JF, ed. Medical aspects on fitness to drive: a guide for medical practitioners, 5th edn. London: Medical Commission on Accident Prevention, 1995: 99–108. Munton G. Vision. In: Taylor JF, ed. Medical aspects of fitness to drive: a guide for medical practitioners, 5th edn. London: Medical Commission on Accident Prevention, 1995: 118–32.
Authors’ reply SIR—We acknowledge the concern of Angela Loftus and Mark McCarron that physicians should counsel patients about fitness to drive after a stroke or seizure. Our patient was advised not to drive after the first stroke-like event. He still has a
Vol 350 • November 8, 1997
3 4
5
technique improves yield in the diagnosis of tuberculosis in children. Pediatr Infect Dis J 1997; 16: 222–26. Miller FJW. Tuberculosis in children. Edinburgh: Churchill Livingstone, 1982. Galanakis E, Leveidiotu S, Siamopoulou A, Lapatsanis PD. A 3-month-old girl with fever and respiratory distress. Lancet 1995; 346: 1674. Wort SJ, Puleston JM, Hill PD, Holdstock GE. Primary tuberculosis of the oesophagus. Lancet 1997; 349: 1072.
Intubation during cardiorespiratory arrest SIR—I still do not fully understand why patients’ pillows tend to be removed during cardiorespiratory arrest situations. Yesterday I was yet again called to an arrest where a junior doctor was trying in vain to intubate a supine patient whilst his pillow sat uselessly on the floor. Junior doctors beware: it is usually difficult to visualise the vocal cords if intubation is attempted with the head and neck flat against the mattress. It is much better to take a few seconds to properly position the head and neck on the pillow in the “sniffing-themorning-air” posture. This simple manoeuvre will greatly facilitate intubation and help to avoid potentially dangerous periods of hypoxia which sometimes occur during lengthy attempts at intubation. D Steeples 16 Lancaster House, Whiston Hospital, Prescot, Merseyside L35 5DR, UK
Absence of relation between hyponatraemia and hypothyroidism SIR—In their Sept 13 commentary, Fahmy Hanna and Maurice Scanlon 1 discuss the various mechanisms that may be responsible for the hyponatraemia seen in hypothyroid patients reported in various studies. Rather than dispute the observations made in such studies with respect to the aetiology of hyponatraemia in the patients presented, we question whether there is in fact a relation
TSH range (mU/L) 0·3–1·5 1·5–3·0 3·0–4·5 4·5–10·0 10·0–15·0 15·0–20·0 20·0–40·0 40·0–80·0 >80·0
between hypothyroidism and clinically significant hyponatraemia. Studies published so far seem to report findings on small numbers of selected patients in which hypothyroidism and hyponatraemia are both present. However, as far as we are aware, no data have been published on the prevalence of hyponatraemia in a large group of unselected hypothyroid patients. We have looked at the relation between serum sodium and serum thyroid stimulating hormone (TSH) in a large group of patients (n=33 912) with archive analysis of patient results from a large city general hospital (table). The results showed that the distribution of serum sodium values was similar in biochemically euthyroid patients and hypothyroid patients (TSH >40 U/L, n=445) in whom the mean serum sodium was 138·6 mmol/L (SD 3·1). The proportion of patients with a serum sodium lying below the reference interval (135 mmol/L) showed no significant difference between the euthyroid subjects (11·4%) and hypothyroid subjects (12·8%). Hyponatraemia is a common finding in ill patients and arises in many presentations. It is found in patients with hypothyroidism, but our data indicate at no greater frequency than that which occurs in euthyroid individuals. It is perhaps not surprising therefore that no consistent mechanism explaining a relation between the two has emerged. The practical clinical message from our data is that when hyponatraemia is noted in hypothyroid patients other possible causes should be sought. *Bernard L Croal, Alison M Blake, J Johnston, Alistair C A Glen, Denis St J O’Reilly *Department of Clinical Biochemistry, Aberdeen Royal Infirmary, Aberdeen AB9 22B, UK; and Departments of Clinical and Pathological Biochemistry, Victoria and Royal Infirmary, Glasgow 1
Hanna FWF, Scanlon MF. Hyponatraemia, hypothyroidism, and role of arginine-vasopressin. Lancet 1997; 350: 755–56.
No of patients
Age (years)*
Total T4 (nmol/L)*
Sodium (mmol/L)*
Sodium <130 mmol/L (no [%])
Sodium <120 mmol/L (no [%])
14 717 12 798 2860 2120 447 206 319 377 68
58·0 (20·5) 59·7 (20·4) 63·1 (18·9) 67·0 (16·9) 69·0 (15·7) 67·9 (16·6) 67·8 (16·8) 62·9 (17·8) 58·3 (20·3)
97·1 (22·0) 94·4 (21·3) 91·8 (21·2) 86·6 (22·8) 76·2 (23·2) 68·6 (24·2) 67·7 (22·7) 33·3 (18·3) <20
139·0 (3·3) 139·0 (3·4) 138·9 (3·4) 138·7 (3·7) 138·3 (3·9) 138·1 (4·2) 138·1 (3·6) 137·8 (4·0) 138·6 (3·1)
269 (1·8) 257 (2·0) 42 (1·5) 51 (2·4) 15 (3·4) 9 (4·4) 9 (2·8) 14 (3·7) 0 (0)
19 (0·1) 16 (0·1) 0 (0) 4 (0·2) 2 (0·5) 1 (0·5) 1 (0·3) 1 (0·3) 0 (0)
The mean (SD) values for age, serum T4, and plasma sodium in 33 912 patients according to serum TSH concentration *Mean (SD).
1402
Driving and stroke S IR —P F Chinnery and colleagues (Aug 23, p 560)1 report a 34-year-old bus driver with a left homonymous hemianopia, a mild left hemiparesis, and a left hemisensory disturbance, who required a muscle biopsy to confirm the A3243G MELAS mutation. They point out that there is no specific treatment for patients with mtDNA disease, but do not comment on the specific management and advice concerning this patient’s fitness to drive. Even among patients with a first seizure, clinicians often omit to document that they have both counselled the patient about driving regulations and explained the legal requirement to inform the Driver and Vehicle Licensing Authority. 2 In a patient with symptomatic cerebrovascular disease, a group-II driving licence will be revoked until a full and complete recovery has occurred, with 5 years free of recurrence.3 A condition like MELAS, which predisposes to recurrent strokes, may mean permanent refusal of a group-II licence. However, this patient will not only have lost his job as a bus driver, but he may also not be accepted for safe driving at all if visual perimetry shows that the homonymous defect comes close to fixation.4 MOMcC is supported by a Patrick Berthoud Fellowship.
Angela M Loftus, *Mark O McCarron Department of Occupational Health, Royal Alexandra Hospital, Paisley; and *Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, UK 1
2
3
4
Chinnery PF, Turnbull DM, Walls TJ, Reading PJ. Recurrent strokes in a 34 year old man. Lancet 1997; 350: 560. Morrison AD, McAlpine CH. The management of first seizures in adults in a District General Hospital. Scot Med J 1997; 42: 73–75. Earl C, Wetherall G. Disorders of the nervous system. In: Taylor JF, ed. Medical aspects on fitness to drive: a guide for medical practitioners, 5th edn. London: Medical Commission on Accident Prevention, 1995: 99–108. Munton G. Vision. In: Taylor JF, ed. Medical aspects of fitness to drive: a guide for medical practitioners, 5th edn. London: Medical Commission on Accident Prevention, 1995: 118–32.
Authors’ reply SIR—We acknowledge the concern of Angela Loftus and Mark McCarron that physicians should counsel patients about fitness to drive after a stroke or seizure. Our patient was advised not to drive after the first stroke-like event. He still has a
Vol 350 • November 8, 1997