22 THE MEDICAL JOURNAL OF AUSTRALIA

were delivered spontaneously without incident, but with-
out exact confirmation of the placental site.

The conclusion reached is that isotope placentography
offers some advantages over conventional X-ray placento-
graphy. The principal two advantages are the relatively
small dose of radiation given to mother and fetus, and
the relatively early stages of pregnancy at which it can
be used. However, the use of isotopes is feasible only
where a maternity hospital is attached to a general
hospital possessing an isotope laboratory with the
appropriate scanning equipment.

ACKNOWLEDGEMENTS

I should like to acknowledge the work done by Mr.
Kevin Bryant, who was responsible for much of the early
technical work required in initiating this project. In
particular, he prepared the radio-iodinated albumin when
1] was the isotope used. I should also like to express
my thanks to Professor L. W. Cox and Dr. R. I. Cox,
whose guidance and help have always been valuable and
readily given, and to the members of the honorary staff
of The Queen Elizabeth Hospital and the Queen Victoria
Maternity Hospital, on whose patients this study was
performed.

REFERENCES

Browne, J. C. Mch., and VEALL, N. (1952-3), “Localisation of
the Placenta by Means of a Radioactive Isotope’, Postgrad.
med. J., 28: 442.

Cerri, B., and TURCHETTI, G. (1960),
Placenta with Radioactive Isotopes”, Cent. di Med, Nucl.,
Clin. Med. Gen. Univ. di Pisa.

Ds Rezenpe, J.. Nanoum, J. C., and Penna, F. (1958),
“Location of the Placenta by. Radioactive Isotopes”, Rev.
Ginec. Obstet. (Rio de J.), 103: 469.

“Localisation of the

January 1, 1966

Gray, S. J., and Srervine, K. (1950), “The Tagging of Red
Gells ‘and Plasma Proteins with Radioactive Chromium”,

J. clin. Invest., 29: 1604.
Heacy, F. C., and Swartz, D. P. (1961), ‘“Localising the
Placenta’ with Radioactive lIodinated Human Serum

Albumin”, Radiology, 76: 936.

Hipparp, B. M. (1961), “Placental Localisation using Radio-
iodinated Serum Albumin”, , J. Obstet. Gynec. Brit. Cwlth,
68: 481.

Macares, C. H. G. (1945),
Proc. roy, Soc. Med., 39:

McGms, J., and Duron, D. (1960), “Placentography using Radio-

“Discussion on Placenta Previa’,
551.

active | Todinated Serum Albumin”, Obstet. and Gynec.,

15:

Paut, J. D., Ganres, E., ALBERT, S., TERRELL, W. D., and
Dopex, S. (1963), ‘Placental Localization Using Cr®-

tagged Erythrocytes”, Obstet. and Gynec., 21: 33.

Suoss, M., and Kratz, P. (1960), “Placental Localization with
use of Radioactive Jodinated Human Serum Albumin”,
Amer. J. Obstet. Gynec., 80: 1168.

Ten Berce, B. S. (1961), “Localisation of the Placenta by
Means of Roentgen Photography and Isotopes in (Cases
of) Suspected Placenta Previa”, Geneesk. Gids, 39: 267.

VisscHer, R. D., and Baker, W. S. (1960). “Isotope Localiza-
tion of the Placenta in Suspected Cases of Placenta
Previa’, Amer. J. Obstet. Gynec., 80: 1154.

WatpMann, T. A. (1961), “Gastrointestinal Protein Loss
Demonstrated by SGrelabelled Albumin”, Lancet, 2: 121.
WEINBERG, A., Rizzi, J.. McManus, R., and Rivera, J. (1956),
“Localisation of the Placental Site by Radioactive Sodium
Isotope (Na™)—Preliminary Report”. Obstet. and Gynec.,

: 396.

WEINBERG, A., Rizzi, J.. MCMANus, R., and Rivera, J. (1957),
“Localisation of the Placental Site by Radioactive Isotopes”,
Obstet. and Gynec., 9: 692.

WEINBERG, A. (1963), “Isotopic Placentography”,

Obstet. Gynec., 87: 203.

Youne, R. J. (1964),

Problem of Placental Localisation”,

Amer. J.

“Application of Thermography to the
Brit. med. J., 2: 978.

REPORTS OF CASES

FATAL HYPERKALAMIA IN STATUS EPILEPTICUS

J.C. WARDEN, F.F.A.R.A.C.S*
The Royal North Shore Hospital of Sydney

In status epilepticus there is a succession of convulsions
without any intervening period of consciousness. This state
is a medical emergency, since hypoxia, respiratory and
metabolic acidosis and hyperpyrexia contribute to the cir-
culatory collapse which leads to death. The convulsions
impair ventilation by impeding the action of the respira-
tory muscles and by obstructing the natural airways.
Hypoxia and carbon dioxide retention follow. At the same
time, metabolic rate, oxygen demand and carbon dioxide
production are increased by the muscular work of the con-
vulsions. Heat production increases and the metabolic rate
further rises, thus increasing the oxygen demand. Products
of anaerobic metabolism accumulate in the tissues and in
the blood, causing a state of acidosis. If an ischemic
cerebral focus is responsible for the convulsions, general
hypoxia accentuates the local oxygen deficiency and will
intensify and perpetuate the convulsive state.

The agents suggested for treatment includle pheno-
barbitone, methylphenobarbitone, paraldehyde, phenytoin,
tribromethanol, thiopentone given by the intravenous drip
method and ether or chloroform anesthesia (Adams,
1962; Yahr, 1963). All these agents (with the exception
of phenytoin) act by depressing central nervous system
activity and hence the irritability of the epileptic focus.
This will reduce muscle activity, and the metabolic demands
on respiratory exchange will he decreased. However, these
agents depress the respiratory centre, and if given in
excess will cause respiratory depression. Under-ventilation
from this cause will replace that due to muscular over-
activity, and the continuing hypoxia may still precipitate
convulsions. In any event, respiratory and metabolic

1 Senior Registrar in Anzsthetics.

acidosis of varying degree persists. The fall in pH pro-
duces a shift of intracelluiar potassium ions into the extra-
cellular fluid, and hyperkalemia occurs. This rise in the
potassium level of the extracellular fluid depresses cardiac
function and may weil make an important contribution to
a fatal outcome. The following case, in which status
epilepticus was due to thrombosis of the left internal
earotid artery, illustrates this particular sequence of
events,

Clinical Record

A man, aged 55 years, had been in good health until
18 days before his admission to hospital, when he was
found at home, aphasic, and with a right hemiplegia. He
made a partial recovery with symptomatic treatment from
his local medical practitioner, and on the day of his
admission to hospital (May 18, 1964) he presented to the
Northcott Neurological Diagnostic Centre, Sydney, for
investigation. Here he had four seizures, with involvement
first of the right side of the body and then of the left. He
was given 8 ml, of paraldehyde intramuscularly and was
transferred to The Royal North Shore Hospital of Sydney.

On his admission, the patient was noted to be a stuporose,
obese, middle-aged man. He had generalized hyperreflexia
and a bilateral Babinski response; there was no muscle
weakness. His ocular fundi were normal, his pupils were
equal and reacted to light, and both carotid pulses were
palpable. The patient had a blood pressure of 150/120 mm.
Hg, and tachycardia was present. There was no evidence
of cardiac enlargement. Urine testing showed a slight
amount of protein, glucose (2%) and a trace of acetone. At
this time a random blood sugar estimation was 363 mg.
per 100 ml., and the hemoglobin value was 14:1 grammes
per 100 ml.

After his admission to hospital he had four episodes, in
which his pupils dilated and his eyes turned to the right;
then there was a generalized tonic state for some 10
seconds, followed by a clonic phase, with more marked
January 1, 1966

twitching on the right side of the body than the left. The
patient was given a total of 20 ml. of paraldehyde intra-
muscularly, and the administration of methylphenobarbi-
tone and phenytoin was begun. It was decided at this stage
not to treat the patient with insulin, as the possible occur-
rence of hypoglycemia would cause confusion in his
management.

On the next day the patient was improved, rational and
cooperative. A random blood sugar level was 270 mg. per
100 mi.; his urine consistently showed glucose (2%), with
a trace of acetone. His urinary output was 1380 ml. in 24
hours. He became febrile, with a temperature of 100° F.
He had three convulsions on this day and was given a
total of 20 ml. of paraldehyde. The following day he had
further seizures and was given a total of 30 ml. of paral-
dehyde. He was still febrile and had persistent glycosuria
and a urinary output of 1200 ml. in 24 hours. On this
day, the serum calcium level was 9-1 mg. per 100 ml., the
serum sodium level 142 mEq/l., the serum potassium level
45 mEq/l. the serum chloride level 98 mEq/l]. and the
serum bicarbonate level 25 mEq/l. The blood urea level
was 50 mg. per 100 ml.

On May 21, fever, glycosuria and convulsions continued. A
left carotid angiogram was taken under general anesthesia
(thiopentone induction, intubation facilitated by suxo-
methonium and spontaneous respiration with oxygen and
nitrous oxide). The angiogram showed complete occlusion
of the left internal carotid artery at its origin, with faint
filling of the distal artery and its branches by collaterals.
The vessels had well marked atheromatous changes.

After the angiographic procedure status epilepticus
occurred, the patient having at one stage 22 fits at five-
minute intervais. During the day, 70 ml. of paraldehyde
and 200 mg. of soluble phenobarbitone were given intra-
muscularly, and an intravenous infusion of dextrose-saline
was commenced. At 8 p.m. the intravenous administration
of 10% mannitol solution was started in an effort to
decrease cerebral edema, and a total of 1:25 litres was
given after an initial urinary output of 3 ml. per minute
had been achieved. At midnight the patient was so coma-
tose that his airway was in jeopardy, although he was still
having convulsions intermittently, and so it was decided
to perform a tracheotomy. At this stage he had rapid,
shallow respirations and a poor airway; his blood pressure
was 8 mm. Hg systolic, and his pulse rate was 100 per
minute.

In the operating theatre the patient was pre-oxygenated,
and suxamethonium (50 mg.) was given intravenously to
facilitate intubation with a cuffed oral endotracheal tube.
Spontaneous respiration returned, and the patient was
given 2 litres of oxygen and 5 litres of nitrous oxide per
minute as fresh gas flow, by means of a Boyle anesthetic
machine with a Mark II absorber. After five minutes
the patient had a right-sided seizure; a further dose of
suxamethonium was given, and controlled ventilation with
pure oxygen was carried out. After this the patient’s blood
pressure fell progressively, and he became pulseless.
External cardiac massage was commenced at once, and
inflation of his lungs with oxygen was continued, An
electrocardiogram showed first-degree heart block, widened
QRS complex and tall T waves (Figure I), suggestive of
a high serum potassium level. Within several minutes
there were biphasic complexes present (Figure II). Cal-
cium gluconate, 40 ml. of 50% glucose solution, 60 units of
insulin and 40 mEq/l. of sodium bicarbonate were given
intravenously over 20 minutes. Within five minutes of the
completion of this therapy, sinus rhythm recommenced with
a palpable radial pulse, the electrocardiogram showing
first-degree heart block, Q@ waves, widening of the QRS
complex and T-wave inversion (Figure III). A blood sample
was taken at this stage, and a serum potassium estimation
showed the level to be 7:1 mEq/l. Despite administration of
further sodium bicarbonate and metaraminol, as well as
continued external cardiac massage, ventricular fibril-
lation occurred (Figure IV). Attempts at external defib-
rillation with a D.C. defibrillator were unsuccessful, and
the patient was pronounced dead.

At post-mortem examination, thrombosis of the left
internal carotid artery was found, and the vessel was

THE MEDICAL JOURNAL OF AUSTRALIA 23

markedly atheromatous. All the cerebral arteries were
atherosclerotic, and the left middle cerbral artery was
particularly narrowed. The brain was cdematous, and
there was softening of the left temporal lobe and in the
region of the left basal ganglia. The heart was brown
and had hemorrhagic areas on its surface, There was

Ficure I: 12.55 a.m.: Lead III, showing first-degree heart
block and high peaked T waves.

atherosclerosis of the coronary arteries with narrowing
of the major vessels. The lungs were edematous and con-
gested. The left kidney was enlarged and congested, and
the right kidney was congenitally absent.

Figure JI: 1 a.m:

Lead III,
complexes.

showing wide biphasic

Discussion

Hyperkalemia as judged by electrocardiographic findings
occurred in this case as a terminal event. Goldberger
(1962) describes the electrocardiographic changes which
occur with a high serum potassium level (Table I).

TABLE I
Serum
Potassium
Level Electrocardiographic Features
(mEq/1.)
67 Tall peaked 7 waves with a marked narrow
ase
8 P waves may disappear or wander in and out of
QRS complex
10 Wide, aberrant QRS complexes with biphasic
deflections caused by fusion of the QRS
complex, RS-T segment and T wave
12 Ventricular fibrillation and cardiac standstill

The tracing in Figure I suggests a serum potassium level
of 7 to 8 mEq/l, that in Figure II a level of about 10
mEq/l, and that in Figure III a level of 6 to 7 mEq/I.
The blood sample taken at the time when the tracing in
Figure III was recorded had a serum potassium level of
71 mEq/l. A rise in the potassium level of the extra-
cellular fluid causes hypopolarization of cardiac muscle
membrane, thus decreasing the transmission of a stimulus
24 THE MEDICAL JOURNAL OF AUSTRALIA

along the muscle fibre. Decreased myocardial contraction
results, and there is a fall in cardiac output and in pulse
pressure.

The immediate management of hyperkalemia is three-
fold: (i) administration of calcium to increase the force
of cardiac contraction by maintaining the ratio of potassium
ions to calcium ions in the blood; (ii) administration of
sodium bicarbonate to correct acidosis; (iii) administration
of insulin to cause the passage of potassium into the cells;
this must be accompanied by glucose to prevent hypo-
glycemia. This approach was temporarily successful in
the case described, as evidenced by the return of a palpable
pulse and the resumption of a more normal electrocardio-
graphic pattern (Figure III). It is interesting to note

FIGURE
first-degree heart block, Q@ waves, some QRS complex
widening and inverted T waves.

Ill: 1.33 a.m.: Lead III showing sinus rhythm,

how quickly the changes in the electrocardiographic pat-
tern progressed initially, and how quickly they reversed
after the institution of therapy. Whether the onset of
ventricular fibrillation was due to further potassium leak-
age into the extracellullar fluid to produce a serum level of
12 mEq/I1., or whether it was due to tissue hypoxia, cannot
be determined.

The most likely cause of hyperkalemia in this case was a
shift of intracellular potassium ions into the extracellular
fluid. Movement outwards of intracellular potassium could
have been due both to acidosis and to muscle tissue break-
down caused by the prolonged convulsions. In acidosis
there is a shift of hydrogen ions from the extracellular
fluid into the cells, and this results in the passage of
potassium ions in the opposite direction, thus elevating
the serum level of potassium. Foulds et alii (1958) report
significant hyperkalemia occurring in patients with respi-
ratory acidosis, Mannitol given in an attempt to reduce
cerebral oedema by intracellular dehydration may have
increased the tendency to potassium loss by the cells.
Renal failure is not considered to be a significant cause
of the high serum potassium level, since the urinary output
was between 1200 and 1400 ml. daily in hospital, and, in
the latter stages, mannitol administration produced a good
diuresis.

Acidosis in this case resulted from a number of factors.
Respiratory impairment due to convulsions and respiratory
depression from the massive doses of paraldehyde given
were certainly two causes. The untreated diabetes mellitus
and the prolonged muscular work of convulsions were
causes of metabolic acidosis. Paraldehyde itself may well
have caused metabolic acidosis, as well as the acidosis due
to its respiratory depressant effects. Beier ef alii (1963)
report a case of metabolic acidosis following paraldehyde
intoxication. Paraldehyde is presumably degraded in the
body to acetaldehyde and then oxidized to acetic acid,
which is metabolized to carbon dioxide and water in the
Krebs cycle. Acidosis may be due to accumulation of
paraidehyde metabolites or to a toxic effect on the metabo-
lism of other substances—for example, inhibition of
enzymes so that the block in the Krebs cycle may cause
a shift of the lactate-pyruvate system in favour of lactate.

Thus, in this case, in which status epilepticus was due
to internal carotid artery thrombosis, the use of large
doses of paraldehyde complicated the patient’s already
poor prognosis. Paraldehyde caused further depression of

January 1, 1966

respiration, and it exacerbated the metabolic acidosis
already present. Respiratory depression would have
increased the irritability of the ischemic focus, and the
acidosis, both respiratory and metabolic, would have aided
the development of the hyperkalemia which hastened the
fatal outcome.

In the management of cases in which convulsions are
severe and difficult to control, it would be beneficial to
avoid further increasing hypoxia and acidosis. Curarization
and intermittent positive pressure respiration provide a
way of controlling the muscular manifestations of status
epilepticus and allowing good oxygenation. The prevention
of excess muscle activity reduces oxygen demand and
earbon dioxide production. Controlled ventilation ensures
that the oxygen debt is abolished and excess carbon dioxide
is eliminated. In this way, any existing respiratory and
metabolic acidosis can be corrected. Reduction of cerebral
edema by the use of mannitol or a similarly acting sub-
stance can then be carried out. This could reduce the
irritability of an ischemic focus if one was the cause of
prolonged convulsions.

Successful management of status epilepticus by muscle
paralysis and controlled respiration has been reported by

Ficurn IV:

2 a.m.: lead III, showing ventricular fibril-
lation.

Nisbet (1959) and Robinson (1963). The latter has shown
that electroencephalographic evidence of convulsions con-
tinues despite curarization, but control of muscular activity
and efficient pulmonary ventilation help to prevent per-
petuation of the condition. Brain (1962) also mentions
the use of relaxants and controlled respiration, but does
not suggest when this technique is indicated.

It does appear that, in cases in which status epilepticus
cannot be controlled by moderate doses of agents which
depress central nervous system activity, the use of larger
doses of these drugs will only accentuate hypoxia and
acidosis and will lead to further complications such as
the one described above. In cases such as these, muscle
paralysis and controlled ventilation are indicated.

Summary

A case of fatal hyperkalemia complicating status epilep-
ticus is reported. The roles played by the large doses of
paraldehyde used and the acidosis from other causes in
this case are discussed. The place of curarization and
controlled respiration in the management of such cases
is also discussed.

Acknowledgement

I am grateful to Dr. I. R. Vanderfield, General Medical
Superintendent of The Royal North Shore Hospital of
Sydney, for permission to report this case.

References

Apams, R. D. (1962), “Status Epilepticus”, in “Principles of
Internal Medicine”, edited by Harrison, T. R., et alli, 4th
Edition, McGraw-Hill, New York: 342.

Beter, L. S., Pitts, W. H., and Gonick,
“Metabolic Acidosis Occurring during
Intoxication”, Ann, intern. Med., 58 : 155.

Brain Lord, (1962), “Diseases of the Nervous System”,
edition, Oxford Univ. Press, London: 800.

Fouups, H. P. S., MENDEL, D., and pe Mowsray, R. R. (1958),
“Changes in Serum-potassium Level and in pH of Arterial
Blood in Respiratory Acidosis”, Lancet, 1 : 405.

GovpBercer, E, (1962), “A Primer of Water, Electrolyte and

Acid-Base Syndromes”, 2nd_ edition, Henry Kimpton,
London: 231,

H.C. (1963),
Paraldehyde

6th
January 1, 1966

Goopman, L. S., and GinMAN, A. (1955), “The Pharmacological
Basis of Therapeutics”, 2nd edition, Macmillan, New York;
Nisser, H. I. A. (1959), “Status Epilepticus Treated with D-
tubocurarine and Controlled Respiration”, Brit. med. J.

Rosinson, J. S., (1963), “Therapeutic Use of the Muscle
Relaxants”, Brit. J. Anesth., 35 :570.

‘Yaur, M. D. (1968), ‘Treatment of Status Epilepticus”, in
“Cecil and Loeb, Textbook of Medicine’, edited by Beeson
P. B. and McDermott, W., 11th edition, Saunders, Phila-
delphia: 1560.

REVIEWS

Modern Treatment: Treatment of Renal Disease, edited by
E, Lovell Becker, M.D., and Treatment of Thyroid
Disease, edited by Edward A. Carr, jr. M.D. Volume 1,
Number 1; January, 1964. New York: Harper and Row
(Hoeber Medical Division), 9” x 6”, pp. 228 with illustra-
tions, Price: Subscription only, $16.00.

Tuts soft-covered publication is the first of a series
produced to cover the rapidly changing field of treatment
in medicine.

The first section on renal disease is particularly necessary,
in view of the new concepts of classification and treatment
introduced in recent years by renal biopsy and electron
microscopy. Any article on the kidney which gives refer-
ences before 1960 must be regarded as out of date, and the
chapters of this book put forward current views up to 1962
authoritatively and concisely.

The section on the psychological handling of the uremic
patient is a good example of the excellent balance of
this publication, The writers are obviously experienced
clinicians who, as well as being aware of theoretical
principles, appreciate the patient as a whole. One can
criticize, however, the high dosage corticoid schedule recom-
mended for the prolonged treatment of adult nephrotic
syndrome. The frequent investigations considered necessary
during therapy are time-consuming and expensive for the
patient, and the results quoted are not clear enough to
justify this as an accepted procedure. The chapter on the
treatment of lupus nephritis would well have been replaced
by one on the more common problem of renal disease in
pregnancy.

In the second half, thyroid disease is dealt with in a
similar fashion. The common problems of thyrotoxicosis are
discussed openly, with clear recommendations concerning
therapy. The authors do not hesitate to criticize principles
which they feel are based on incomplete studies. The use
of the acetic acid hormonal analogues in the complications
of myxcedema illustrates the necessity for keeping up with
rapidly moving fields of therapy. The warning on the
differential placental crossing of antithyroid drugs and
thyroxin is one which should be heeded by those who use
this therapy for thyrotoxicosis of pregnancy.

This book achieves its purposes very soundly, and can
be recommended for the reader who wants to update his
knowledge quickly and effectively in the particular special-
ties. Further editions should be watched for with interest.

Pterygium Throughout the World, by Malcolm E. Cameron,
M.B., B.S., D.O., M.D.; 1965. Springfield, Illinois: Charles
Si 500m 9” x 6”, pp. 206. with illustrations. Price:

THIS monograph deals with all aspects of pterygium.
The incidence of the disease in various parts of the world
is discussed and surveyed, and the author is then able to
divide the world into four zones of latitude with increasing
incidence of pterygium. The etiology is discussed, the author
favouring ultra-violet radiation as the main etiological
factor. One whole chapter is devoted to this aspect of
etiology. The marked effect of the wearing of glasses on
the reduction of the incidence of pterygium is striking, and
one wonders whether a similar sharp fall may be found in
those who constantly wear a hat outdoors. There is no
mention of the incidence of unilateral as against bilateral
pterygia.

The various surgical procedures advocated for removal of
pterygium are reviewed, and the author describes his
technique of excision, leaving a bare area to be followed by
immediate irradiation. There then follow chapters devoted
to beta radiation, differential diagnosis, macroscopic anatomy,

THE MEDICAL JOURNAL OF AUSTRALIA 25

microscopic anatomy, results of pterygium treated in
Brisbane, complications of pterygium excision and recurrence,
and the final chapter is a summary of the author's thoughts.

At the end of many of the chapters is a full list of
references. The book is well produced and contains a pro-
fusion of excellent black-and-white photographs. This book
is essential for all interested in the subject of pterygium.

Conybeare’s Textbook of Medicine, edited by W. N, Mann,
M.D. (Lond.), F.R.C.P.; fourteenth edition, 1964. Edin-
burgh, London: E. & §. Livingstone Ltd. 94” x 63”, pp.
1068, with illustrations, Price: £3 3s, (English).

THis well-known textbook of medicine was first published
in 1929, and the appearance of 14 editions in 35 years is
certainly a very good record and speaks well for the
enthusiasm in keeping the book up to date that has always
been evident. This book has always been largely written
by contributors connected with Guy’s Hospital, London.
However, this is the first edition for which Sir John
Conybeare has not been the principal editor, and his place
is admirably taken by Dr. W. N. Mann, Senior Physician
to Guy’s Hospital. He is ably assisted by 17 other contributors,
all well known in their particular fields.

This textbook of medicine aims to present the principles
of internal medicine in a reasonably short volume, and
mainly for the use of medical undergraduates. This it
achieves very well, without an enormous amount of reading.
The student can read in fairly concise form all that he is
likely to be required to know.

Because of the above-mentioned aims, the book does not
serve so readily as a reference book, and information on
particular subjects tends to the rather circumscribed. As
reference books, many British textbook suffer from a
relatively inadequate index. This book has this deficiency
to some extent, but we still think it is better than many
others.

The illustrations are quite adequate. The reproductions of
X-ray plates on art paper are extremely good, and the
originals from which they were taken are very well selected
to illustrate particular points.

As a student’s textbook of medicine, we would rate this
book as first class, covering the subjects concisely in a
thoroughly up-to-date fashion. We have virtually no criti-
eism, and hope that this book will find its way to the desks
of many undergraduates.

A Textbook of Obstetrics, by Bruce Mayes, M.V.O., M.B.,
BS. F.R.CS., BP.RACS., F.R.C.0.G.; fourth edition,
1965. Sydney, Wellington, London: Australasian Publish-
ing Company. 9” x 6”, pp. 1072, with illustrations.
Price: £9 5s,

Ir is 15 years since Professor Bruce Mayes first published
his textbook of obstetrics. That edition was so popular that
it was reprinted twice. A second edition appeared in 1959,
and now the third edition has been produced, indicating the
assured place that this textbook has among publications
within the speciality. The present edition contains 1056
pages, only 16 more than in the original edition, thus indicat-
ing that the author has resisted the temptation to add
new material while leaving the old unchanged. The original
aim is well maintained in the present edition—namely, that
it should help not only the undergraduate, but the family
doctor who practises obstetrics, and this is the more fitting
in the product of an author who was at one time himself
a family doctor.

The new sections of the book are concerned with the
medical problems associated with pregnancy—namely,
diabetes mellitus, hyperthyroidism, thalassemia and rubella,
Drugs given to the patient during her pregnancy are listed.
Recent work on the Rh factor, on feetal electrocardiography
and on localization of the placenta is discussed. Special
chapters have been contributed by Dr. E. A. Booth on obstetric
radiology, by Miss I. Nolan on the social aspects of
obstetrics, by Professor W. H. Trethowan on psychiatric
aspects and by Professor J. Loewenthal on thrombosis.

Abnormal presentations are described in a clear fashion,
although it is considered that some mention should have
been made of the well-known manipulation whereby, with
brow presentation in the presence of full dilatation of the
cervix, the over-extended posterior position of the vertex can
be easily corrected by anterior rotation of the head, the
flexion taking place at the same time.

The chapters on pre-eclampsia and eclampsia are excellent
and contain the modern methods of treatment of these