637

THE DIFFERENTIAL DIAGNOSIS OF COMABy PATRICK J. SWEENEY, M.D., M.R.C.P.I., M.R.C.P.

Latelv First Assistant, Department of Medicine, Roval Victoria and West Hants Hospital, Bournemnozuth

The difficulties in the diagnosis of the uncon-scious state are known to all. As an adequatehistory is so often lacking, physical examinationmust be exhaustive and the first essential is theaccurate assessment of the degree of unconscious-ness present. The term coma implies a state ofunconsc;ousness from which the patient cannotbe roused. Painful stimuli, e.g., firm pressureover the. supraorbital foramen, have no effect. Thecorneal and pupillary reflexes, muscle tone, andthe deep reflexes, are frequently abolished. Milderdegrees of coma exist where, although the patientis unconscious, pupillary and corneal reflexes areobtained and painful stimuli provoke a reaction.Stupor indicates a state of partial loss of conscious-ness where the response to external stimuli ismarkedly diminished and is also characterized bya tendency to resist interference and to catalepsy.It is extremely important to record carefully thedegree of unconsciousness present at the initialexamination of the patient, in order to establisha base line and follow the course of the condition.The slow development of cerebral compressionfollowing a head injury, e.g. ruptured middlemeningeal artery, illustrates the importance ofthis point. Particular attention must therefore bepaid to the pupils, fundi, muscle tone, deepreflexes, plantar responses, pulse rate and tem-perature. Other points such as the odour of thebreath, the type of breathing etc., are well knownto all, and will not be stressed here.The common causes of comatose, semi-coma-

tose and stuporose states will now be considered.

TraumaUnconsciousness following concussion is short-

lived, but prolonged coma may follow cerebralcontusion or laceration. Bleeding from the noseor ears, or subconjunctival haemorrhage, mayindicate a fractured skull and the need for radio-graphy. Lumbar puncture should be performed inall cases, as the presence of blood in the cerebro-spinal fluid is often unsuspected.

It should be remembered that an alcoholicaroma is no guarantee that a cerebral injury hasnot occurred. Coma from a slowly developingsubdural haematoma, the result of rupture ofcortical veins, is often difficult to differentiate from abrain tumour, especially as the original injury may.have been trivial and disregarded by the patient.

Case ReportA male, aged 45, admitted March 30, I948 with

a history of severe headache for a week.Examination revealed a semicomatose patient.

Pupils equal and light reactive, fundi normal,muscle tone increased and reflexes generallyincreased. No neck rigidity or fascial weakness.Bilateral extensor plantar response.

Heart and lungs normal. Blood-pressure I20/70.Pulse 62. Temperature 980.Lumbar puncture revealed a clear fluid under

a pressure of 28o mm. Slight increase of protein,and io white cells per cu. mm., mostly lympho-cytes. Two hours after the lumbar puncture, thepatient was sitting up in bed, quite rational, feelingwell, but rather euphoric and unduly talkative.

During the next three days, his conditionremained unchanged, but he complained ofoccasional headache and was subject to periods ofdrowsiness. No abnormal signs could be detectedin the nervous system.On April 5, I948, the lower limb reflexes were

found to be brisker on the left side, and the leftplantar response extensor. (The first localizingsigns.)On April 7, 1948, he again became unconscious,

with twitching and rigidity of all extremities.Both plantar responses were extensor. Blood sugarand blood calcium normal. Repeat lumbar punc-ture revealed a clear fluid under slightly increasedpressure, with a marked increase of protein, and29 white cells per cu. mm. The fundi remainednormal.He was seen by a surgical colleague who sug-

gested a diagnosis of right subdural haematoma.Ventriculography was carried out with negativeresult, and the patient died on April I0, 1948.

Post mortem examination revealed a soft vas-cular tumour in the right occipital lobe, which onsection proved to be a spongioblastoma of variedpleomorphic structure.

Periods of drowsiness, stupor or coma fromwhich recovery takes place with subsequentrelapse, and localizing pyramidal tract signs ofthe type mentioned in this case, together with aslow pulse, are considered typicaf features of asubdural haematoma. Cellular increase in thecerebro-spinal fluid is not a feature, but is more

by copyright. on July 20, 2021 by guest. P

rotectedhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.24.278.637 on 1 Decem

ber 1948. Dow

nloaded from

638 POST GRADUATE MEDICAL JOURNAL December I948

suggestive of cerebral abscess or tumour, as in thecase described

Intoxications and PoisonsDuring the past year, 40 per cent. of the coma-

tose patients admitted to the medical wards of thishospital were suffering from, in the followingfrequency, carbon monoxide, barbiturate andaspirin poisoning. An indication, perhaps', ofpresent day conditions, when coupled with thefact that alcoholic coma was not encountered.Carbon monoxide poisoning is usually obvious

from the history. It should be noted however,that the typical cherry-red colour of the face andlips is not always present, and that even a milddegree of carbon monoxide poisoning may precipi-tate cardiac failure and pulmonary oedema withresultant coma, in a patient with pulmonary orcardiac disease. A simple clinical test for carboxy-haemoglobin is to dilute-one drop of the patient'sblood in a test tube of water, and compare with acontrol from a normal person. A carmine tint willbe evident if there is much carboxyhaemoglobinpresent. A diagnosis of barbiturate or aspirinpoisoning is more difficult. Deep coma, sweatingand extensor plantar responses are common toboth. A raised temperature, cyanosis and pul-monary oedema are typical findings in barbituratepoisoning, as exemplified in the following case.

Case ReportA female aged 35 was admitted on October i9,

I947. She was found unconscious in her flat witha bottle of nembutal capsules beside her. Therewere three capsules left out of a possible originaltotal of twenty-five.

She was deeply comatose, i.e., ' corneal andpupillary reflexes absent, deep reflexes absent,limbs flaccid, no response to painful stimuli.Bilateral extensor plantar responses. Cyanosed.Moist skin. Breathing noisy and bubbly withmoist sounds throughout both lungs, obscuringthe heart sounds. Blood pressure iIo0/90. Pulsego. Temperature I00°. With large doses of cora-mine and picrotoxin intravenously, the pupillaryreflexes returned after three hours, but it wasthree days before the patient became fully con-scious and rational.

.* * *

If no history is available, barbiturates can bedetected in the urine and cerebrospinal fluid, usingMillon's reagent.

Aspirin poisoning is characterized by evidenceof vomiting, profuse sweating, and deep breathingwhich may resemble the air hunger of diabeticcoma. The ferrichloride test for salicvlates in theurine is positive. Where alcoholic coma is sus-pected, a careful physical examination is necessary

in order to exclude other medical or surgicalcauses of coma. To quote Walshe, 'alcoholiccoma is diagnosed most safely by a process ofexclusion.' Opium poisoning is seldom seennowadays. Its chief features are a cold, clammyskin, a slow respiration rate, and pin-point pupils.In all cases of suspected poisoning, gastric lavageshould be performed and the gastric contentskept for analysis. Lead poisoning is a rare causeof coma, and as a rule a preceding history of vomit-ing, abdominal colic, headache and constipationwill be obtained. If suspected, the gums shouldbe exarmined for the well known blue line, theblood for punctate basophilia and evidence ofanaemia, which may be haemolvtic in type, andthe urine analysed for lead.

Cerebral Vascular LesionsComa resulting from cerebral haemorrhage,

embolism or thrombosis is characterized by hemi-plegia in the great majority of cases. Usuallythere is conjugate deviation of the head and eyestowards the side of the lesion, the paralysed cheekflaps in and out with respiration, which is ster-torous, and a positive Babinski sign is obtained onthe hemiplegic side. Where lesser degrees ofcoma exist, a unilateral diminution or abolitionof the corneal reflex is of value in distinguishingapoplexy from other conditions. Where the pupilsare unequal, it is always well to remember thatthe larger pupil is usually on the side of thehaemorrhage. Syphilis must always be kept inmind as a cause of cerebral thrombosis. Cerebralembolism is suggested by the presence of heartdisease such as mitral stenosis and auricular fibril-lation. Pontine haemorrhage results in homo-lateral cranial nerve palsy and contralateral hemi-plegia, but all four limbs are soon paralysed as arule. A high temperature and pin-point pupilsfurther characterize this condition. In my experi-ence, subarachnoid haemorrhage, the ' apoplexyof young people,' has been the commonestindividual disorder aniongst the cerebral vascularaccidents admitted during the past year. The diag-nosis is seldom difficult. Neck rigidity is the out-standing feature as a rule, but in some deeplycomatose patients, this is absent, and the diagnosisis only apparent on lumbar puncture. Retinalhaemorrhages, usually near the disc, vitreous andsubhyaloid haemorrhages, papilloedema, and 3rdand 6th nerve palsies with resultant squint, areoccasional features of a subarachnoid haemorrhage.Frequently, bilateral extensor plantar responsesare obtained. The unne may-contain sugar andalbumin, and a rise of temperature up to ioo isa common finding.

Hypertensive encephalopathy should-be thoughtof in the comatose patient with an extremely

by copyright. on July 20, 2021 by guest. P

rotectedhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.24.278.637 on 1 Decem

ber 1948. Dow

nloaded from

December I948 SWEENEY: Differential Diagnosis of Coma 639

high blood pressure, e.g., 250/I50. There maybe slight neck rigidity, but lumbar puncturereveals a clear fluid under high pressure. Changesin the fundi depend on whether the hypertensionhas been long standing or not, and range fromslight arteriovenous kinking to papilloedema andretinal haemorrhages. Similarly, the urine maybe normal, or contain albumin and casts.

Case ReportA male aged 50 years was admitted on October

30, 1947. The history, obtained from an outsidesource, was that for two weeks the patient hadbeen complaining of headaches and had vomitedseveral times. On the day of admission, shortlybefore becoming unconscious, he had complainedof sudden blindness. Examination revealed aheavily built man, semicomatose, pale skin andslight puffiness of the eyelids. A faintly uriniferoussmell from the breath was noted. The pupilswere equal and light reactive. There was slightbilateral papilloedema and evidence of arterio-venous kinking on examination of the fundi.

Reflexes present and equal in upper and lowerlimbs. Doubtful bilateral extensor plantar res-ponses. Moderate neck rigidity. Lungs normal.heart sounds normal. Blood-pressure 240/130.Pulse 65. Temperature 980. Lumbar* puncturerevealed a clear fluid under a pressure of 300 mm.of water. The pressure was r-duced to 8o mm.,venesection was performed, and a few hours afteradmission'the patient was conscious, though com-plaining of blindness. Urine examination revealeda dense cloud of albumin, numerous red bloodcells, and moderate numbers of cellular casts.Blood urea 51 mgm. per cent. He rapidly im-proved, and in a further 48 hours his sight wasrestored. On discharge from hospital his blood-pressure was 150/I00, but his blood urea was 42mgm. per cent. and his urine contained albumin-uria and casts, indicating permanent and severerenal damage with a poor prognosis.

Diabetic and Hypoglycaemic ComaIt is surprising how often these two conditions

are misdiagnosed in practice, thd more so when itis remembered that if in doubt, an intravenousinjection of glucose will .produce a dramaticrecovery if the coma is due to hypoglycaemia, andwill do no immediate harm if it is due to hyper-glycaemia. A smell of acetone from the breath, adry skin, air hunger, soft eyeballs, flaccid muscles,depressed reflexes and flexor plantar responsescharacterize diabetic coma. The urine, obtainedby catheterization, is loaded with sugar and ace-tone. In hypoglycaemic coma, the eyeball tensionis normal, there is profuse sweating and the plantarresponses are extensor. The temperature is

always either normal. or subnormal in uncom-plicated cases of either condition. It is well toremember that although a comatose patient is aknown diabetic, the diagnosis is not always one of'hvper- or hypo-glycaemia.

Case ReportA male, aged 54, a known diabetic, was admitted

on December 5, I947, in a deep coma. He mani-fested shallow rapid respirations, sweating, normaleyeball tension and bilateral extensor plantar res-ponses. The urine contained a slight trace ofsugar, and no acetone. Blood sugar 85 mgm. percent. He had however, a temperature of ioo', anda slightly stiff neck. Lumbar puncture revealed aclear fluid with excess of cells (37 per cu. mm.-mostly polymorphs), normal sugar content, normalprotein, chloride 700 mgm. per cent. Culturesterile. A chest X-ray revealed bilateral pul-monary tuberculosis, not apparent on clinicalexamination. The patient died on December 13,I947, and at post-mortem the presence of tuber-culous meningitis was confirmed.

There are rare cases of diabetic coma wheresugar is absent from the urine, the explanationbeing that the patient was suddenly deprived ofcarbohydrate and the fat metabolism became sodisordered that coma resulted. Similarly, thereare cases where the urine may contain much sugarand albumin, but no acetone, and yet the breathmay smell strongly of acetone. In such cases thereis renal failure, casts will be found in the urineanca the blood urea is raised. Hypoglycaemic comamay be prolonged and fatal, as in a case describedby Winkler, where after an initial response to intra-venous glucose, relapse occurred and the patientdied nine days later, without having regained con-sciousness. In this case, protamine zinc insulinhad been given by the practitioner, who mistakenlydiagnosed diabetic coma. Where no history ofinsulin administration can be obtained, the pos-sibility of an islet celled tumour of th: pancreasmust be kept in mjnd.

Case ReportA female aged 39 was admitted unconscious on

March 23, 1948, with no history available. Shewas semicomatose-pupils equal and light re-active, corneal reflexes present, fundi normal,profuse sweating, bilateral extensor plantar res-ponses.

Heart and lungs normal. Blood-pressure I20/70.Lumbar puncture normal. Urine normal. Bloodsugar 43 mgm. per cent. Blood urea 30 mgm. percent.A 5 per cent. dextrose drip was commexced, and

two hours later she partially regained concious-

by copyright. on July 20, 2021 by guest. P

rotectedhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.24.278.637 on 1 Decem

ber 1948. Dow

nloaded from

640 POST GRADUATE MEDICAL JOURNAL December 1948

ness, only to relapse again and become moredeeply comatose than before. The dext.rose dripwas continued and 20 cc. of 50 per cent. glucosegiven intravenously with no effect. The bloodsugar was now ioo mgm. per cent.The patient remained unconscious for nine

davs, during which time, aneurin, riboflavin,nicotinic acid, and glucose were given in largeamounts, and her blood urea and blood sugarlevels remained within normal limits. There wereno localizing nervous signs and the fundi re-mained normal. On regaining consciousness, shewas aphasic, and did not recover the power ofspeech until April 2I, 1948. Fasting blood sugarson the I5th, 20th, 23rd and 24th of April were 43,40, 40 and 37 mgm. per cent. respectively. Anexploratory laparotomy was advised to ascertain ifan islet celled tumour of the pancreas was present,but the patient took her own discharge againstadvice.

(This patient *was readmitted to hospital onJuly 14, 1948, comatose with a blood sugar of20 mgm. per cent. At operation on July i6, 1948,a benign adenoma of the tail of the pancreas wassuccessfully removed. The patient made anuneventful recovery.)

* * *I

Cerebral damage is well known to occur follow-ing prolonged hypoglycaemia, and presumablythis is the explanation of the aphasia, which tookthree weeks to clear up.

InfectionsComa due to meningitis, encephalitis, fulminat-

ing septicaemias, malaria, pneumonia etc. and asa terminal phenomenon in the course of almostany severe infection, is not infrequently seen.

Case ReportA female aged 6o was admitted on March 22,

I948. A history obtained from the relatives statedthat the patient was well until the morning ofMarch 2I, 1948, when she complained of headacheand refused her food. She retired to bed, andbecame delirious towards evening. Examinationrevealed a pale, restless and resistive, semicoma-tose patient. Temperature IoI°. Pulse ioo.There was marked neck rigidity and a diffusepurpuric eruption on the trunk and limbs.Lumbar puncture revealed an opaque fluid,

and microscopy showed the presence of gramnegative intracellular diplococci.The patient made a good recovery with com-

bined penicillin and sulphamezathine therapy.

This. case. illustrates. the rapidity of onset. ofcoma in an acute fulminating meningococcal men-ingitis.

Somnolence and stupor are more characteristicof encephalitis than deep coma. Lumbar puncturereveals a clear fluid with excess cells, often lymph-ocytes, and in contrast with pyogenic infections,the sugar content is normal or increased. Cerebralmalaria due to the malignant tertian parasiteshould be thought of in the case of a comatosehyperpyrexial patient who is known to havereturned from an endemic area within a year.The parasites may be difficult to find in bloodfilms, but the finding of intracellular melanin pig-ment in the cells of the cerebrospinal fluid is diag-nostic. The difficulties in the diagnosis of comadue to infection are illustrated by the followingcase.

Case ReportA male aged 2I was admitted on April 21, I948.

The only history available was that the patientwas quite well at breakfast, went upstairs, andwas found unconscious 20 minutes later. Hewas restless, semicomatose, sweating profusely,with rapid bubbly respirations. Temperature 102°.Pulse 104. Pupils equal and light reactive, rightexternal rectus palsy, moderate neck rigidity, allreflexes present and equal, lower limbs ratherspastic, bilateral extensor plantar responses. Lungs-diffuse moist sounds. Heart-loud apical systo-lic murmur, and systolic and diastolic murmursheard close to the sternum. No oedema or en-gorgement of the neck veins. Lumbar puncturerevealed a cloudy fluid with 470 polymorphs percu. mm. but no organisms. The patient died a fewhours after admission.Post-mortem examination revealed mitral steno-

sis with large friable vegetations on the anteriorcusp of the valve. Infarcts present in the spleenand kidneys. The brain was congested, but showedno other naked eye abnormality.

:I * *

Multiple microscopic cerebral emboli undoubt-edly occurred in this case, with resultant coma,and excess polymorphs in the cerebro-spinal fluid.

Miscellaneous Causes of Coma(i) Uraemia. A raised blood-pressure, albumin

and casts in the urine, and retinal changes, e.g.albuminuric retinitis, suggest uraemia. A carefulexamination of the abdomen will sometimes dis-close congenital cystic kidneys, or a distendedbladder. Rectal examination to ascertain if theprostate is enlarged should never be omitted.

(2) Cerebral tumour and cerebral abscess. Diag-nosis may be extremely difficult. Cerebral abscessis usually a complication of middle ear disease orchronic pulmonary infection such as bronchiectasis;or empyema. If during the course of examination,marked bilateral papilloedema is found, caution

by copyright. on July 20, 2021 by guest. P

rotectedhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.24.278.637 on 1 Decem

ber 1948. Dow

nloaded from

December I948 SWEENEY: Differential Diagnosis of Coma 641

should be observed with regard to lumbar punc-ture.

(3) Heart disease. It is frequontly forgotten thatin congestive cardiac failure, the brain suffersfrom venous engorgement. Coma from this causeis usually obvious. In Stokes-Adams syndrome,the duration of unconsciousness is brief as a rule,*and the extremely slow or absent pulse is diag-nostic.

(4) Epilepsy. A history of 'grand mal ' isusually obtained, and the duration of the stage offlaccid coma is brief. Evidence of tongue bitingand urinary incontinence should be looked for.

(5) Hysteria. The general attitude of the patient,forced closure of the eyelids, normal pupillaryreflexes and normal deep reflexes with flexorplantar responses, usually leave the examiner inno doubt as to the correct diagnosis.

(6) Dementia praecox (schizophrenia). Thesudden onset of a stuporose state can apparentlybe the first manifestation of this disease.

Case ReportAl female aged 26 was admitted in a stuporose

condition on April 27, 1948. Her parents statedthat she had been in good health until two hoursbefore admission, when they found her uncon-scious in her bedroom. Examination revealed awell-built female, colour normal, respirationsnormnal, skin moist. There was diminished res-ponse to painful stimuli. The jaw was kept tightlyclenched. Pupils equal and light reactive. Cornealreflexes present. Fundi normal. She was generallyresistive, the arms and legs were held stiffly, andneck flexion was resented. Deep reflexes presentand equal. Plantar responses flexor. Temperature980. Pulse 6o. Heart and lungs normal. Blood-pressure I20/70. Urine examination normal.She remained in a stlIporose and resistive conditionfor 48 hours, during which time repeated physicalexaminations were made. The persistent spasm ofthe jaw was most noticeable. Lumbar puncturerevealed a clear fluid under normal pressure.Laboratory examination revealed no abnormality.Blood sugar normal.On the afternoon of April 29, I948, she became

wide awake, sat up in bed, but did not speak oranswer questions. Shortly afterwards she wasfound out of bed and refused to get back. Shenow answered questions, but gave confused replies,and appeared to think she was attending lecturesand clinical demonstrations at a medical school.She insisted on helping the ward sister to writeout her reports.

It transpired that this girl was a first-yearmedical student who had been studying very hardfor some weeks prior to admission. There was no

previous history of mental illness. A psychiatricspecialist kept her under observation for the nexttwo days, and had no hesitation in diagnosingschizophrenia of acute onset, with catatonic stupor.

Vitamin DeficiencyChronic alcoholism, carcinoma of the stomach

or oesophagus, and diarrhoeal diseases such asulcerative colitis, predispose to deficiency of thia-mine and nicotinic acid. A stuporose or semi-comatose patient with pupillary'abnormalities ornystagmus, evidence of peripheral neuritis, cog-,wheel rigidity of the extremities, and graspingand sucking reflexes, should suggest the possibilityof Wernicke's encephalopathy. Avery Jones andRobinson have described an interesting case ofthis kind, closely simulating diabetic coma, wherethe diagnosis of Wernicke's encephalopathy wasconfirmed post-mortem. They postulated injuryto the hypothalamic area by a minute haemorrhageas the cause of the hyperglycaemia.

Cerebral Emboli from Malignant DiseaseUnder the descriptive heading, coma carcino-

matosum, Purves-Stewart mentions the develop-ment of coma in patients dying from visceralcancer with secondary malignant deposits.Occasionally the meninges become infiltrated withmalignant cells, and the latter can be found in thecerebrospinal fluid.Coma must be a most unusual presenting feature

of a carcinoma of the stomach, but such was thecase in the following instance.

Case ReportA female aged 68 was admitted on December

IS, I947. Her landlady stated that for some weeksthe patient had complained of indigestion andhad only been able to eat ' sloppy' foods. Shewas found unconscious on the floor of her rooma few hours prior to admission.

Examination revealed a wasted elderly womanwith no obvious cyanosis or dyspnoea. Tempera-ture 970* Pulse 96. She was semicomatose, pupilsequal and light reactive, corneal reflexes present,arteriosclerotic changes in both fundi. Normalupper limb reflexes. Absent ankle jerks lowerlimbs. A right extensor plantar response wasobtained. Lungs, heart and abdomen normal.Blood-pressure i IO/65.

Thickened arteries palpable in both upperlimbs. Slight oedema of the ankles.Lumbar puncture revealed a clear fluid under

normal pressure, but microscopy revealed excesscells of a peculiar type (59 per cu. mm.). Theywere large and granular, with one and sometimestwo eccentric nuclei. Some showed evidence ofmitosis. Sternal puncture was performed, but

by copyright. on July 20, 2021 by guest. P

rotectedhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.24.278.637 on 1 Decem

ber 1948. Dow

nloaded from

642 POST GRADUATE MEDICAL JOURNAL December 1948

revealed no abnormality. A blood-count wasnormal except for a slight leucocytosis (i I,000white cells; polymorphs 88 per cent.).The patient remained unconscious, neck rigidity

developed, both plantar responses becameextensor, and prior to her death on December I9,1947, the cerebrospinal fluid pressure rose to 220mm. and the temperature to I03 °.

Post-mortem examination revealed a carcinomaof the stomach (papillary and trabecular on section)with secondary deposits in the adjacent lymphglands and right suprarenal. There was carcino-matous infiltra-tion of the meninges over thecerebrum and cerebellum.

Hepatic coma is usually a terminal event in thecourse of severe liver disease such as cirrhosis.

Exsanguination as a cause of coma is clinicallyobvious.

BIBLIOGRAPHY

AVERY JONES, F., and ROBINSON, V. C. (I947), Lancet, 2, 907.PURVES-STEWART, Sir James (I947), 'The Diagnosis of Nervous

Diseases.' p.153.WALSHE, F. M. R. (I947), 'Diseases of the Nervous System.' p.104.WINKLER, J. L. (I948), Lancet, I, 215.

ACKNOWLEDGMENTI wish to thank Dr. T. Robson and Dr. J. H.

Bentley for permission to publish details of thesecases.

BOOKS RECEIVEDThe Editorial Board acknowledge with thanks the receipt of thefollowing volumes. A selection from these will be madefor review.

' Progress in Clinical Medicine.' Edited byRaymond Daley, M.A., M.D., M.R.C.P., andHenry G. Miller, M.D., M.R.C.P., D.P.M.Pp. xi + 356. With 22 figures and I5 plates.J. & A. Churchill, London. 1948. 21S.

' Osteo-Arthritis of the Hip-Joint.' By H.Warren Crowe, D.M., B.Ch., M.R.C.S., L.R.C.P.Pp. Viii + 70. With 24 plates. George Pulman &Sons, Ltd. Distributed by Rolls House PublishingCo., Ltd., London. I948. 35s. 6d.'Human Embryology and Morphology.' By

Sir Arthur Keith. 6th Edition. Pp. xii + 690. With578 figures. Edward Arnold, London. 1948. 40S.

' The National Health Service Act, 1946.' ByS. R. Speller, LI.B. Pp. xc ± 497. H. K. Lewis &Co., London. 1948. 42s.

' Critical Studies in Neurology.' By F. M. R.Walshe, M.D., F.R.S. Pp. xV + 256. With i6illustrations. E. & S. Livingstone, Edinburgh.1948. I P-

' Eden and Holland's Manual of Obstetrics.' ByAlan Brews, M.D., M.S., M.R.C.P., F.R.C.S.,F.R.C.P.G. gth Edition. Pp. xii + 796. With405 illustrations and 36 plates, 12 in colour. J. & A.Churchill, London. 1948. 42S.

'Obstetrics and Gynaecology.' By Beatrice M.Willmott Dobbie, M.A., M.B., F.R.C.S., D.M.R.E.Pp. xi + 358. With 22 illustrations. H. K. Lewis,London. I948. 20S.'The Medical Annual I948 (66th Issue).' Edited

by Sir Henry Tidy, K.B.E., M.A., M.D., F.R.C.P.and A. Rendle Short, M.D., B.S., B.Sc., F.R.C.S.Pp. xii + 414. With 56 plates. John Wright &Sons, Bristol. Simpkin Marshall, London, I948.22S. 6d.

' Demonstrations of Physical Signs in ClinicalSurgery. Part III.' By Hamilton Bailey, F.R.C.S.,F.A.C.S., F.I.C.S., F.R.S.E. iith Edition. Pp.io8. With many illustrations, some in colour.John Wright & Sons, Bristol. Simpkin Marshall,London. 1948. 8s. 6d. per part.

' Clinical Endocrinology.' By Laurence Martin,M.D., F.R.C.P., and Martin Hynes, M.D.,M.R.C.P. Pp. viii + 222. With 8 plates and 22text figures. J. & A. Churchill, London. I 948. 15s.

'Recent Advances in Respiratorv Tuberculosis.'By Frederick Heaf, M.A., M.D., F.R.C.P. andN. Lloyd Rusby, M.A., D.M., F.R.C.P. 4thEdition. Pp. vii + 290. With 5 plates and 7 textfigures. J. & A. Churchill, London. 1948. 2IS.'The Natural Development of the Child.' Bv

Agatha H. Bowley, Ph.D. 3rd Edition. Pp. xvi +I90. With 84 photographic illustrations. E. & S.Livingstone, Edinburgh. 1948. 8s. 6d.

'Notes on Infant Feeding.' By G. -B. Fleming,M.D., F.R.C.P., F.R.F.P.S. and Stanley Graham,M.D., F.R.C.P.(Ed.), F.R.F.P.S. 3rd Edition.Pp. 66. E. & S. Livingstone, Edinburgh. I948.3s.

'A Surgeon's Guide to Local Anaesthesia.' ByC. E. Corlette, M.D., Ch.M., F.R.A.C.S. Pp. xi355. With 200 illustrations. John Wright & Sons,Bristol. Simpkin Marshall (I94I), London. 1948.35S.

'Viral and Rickettsial Infections of Man.'Edited by Thomas M. Rivers, M.D., Director ofthe Hospital, The Rockefeller Institute for MedicalResearch, New York. Pp. xvi + 587. With 77illustrations, 6 being colour plates. J. B. Lippincott& Co. i948. 45S.

by copyright. on July 20, 2021 by guest. P

rotectedhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.24.278.637 on 1 Decem

ber 1948. Dow

nloaded from