RESISTANT STAPHYLOCOCCI

39

Letters

to

as

RESISTANT STAPHYLOCOCCI SIR,—The article by Dr. Clarke and her colleagues (June 7) is one of several recent reports on the increasing number of drug-resistant staphylococci in hospital infections. We are apt to forget how much more heroic some branches of surgery have become under the protection of antibiotics, and it would be a tragedy if we allowed the present trend to continue. The following points regarding hospital staphylococcal ’

infection

important :

are

Staphylococci

far exceed all other pathogens as the of secondary ’infection. 2. Wards which have patients with chronic staphylococcal suppuration build up a reservoir of drug-resistant staphylococci. . 3. : The most important mode of spread is : contaminated dressings - floor - blankets - fresh wounds. It is true that many of the staff may be transient or even permanent carriers ; but masking and a no-touch technique in wound dressing wound spread, and in my opinion reduces the nose - finger droplet spread is of minor importance with respect to 1.

cause

-

staphylococci. 4. The

taken to prevent cross-infection in many appear to be concerned almost exclusively with

measures

hospitals respiratory and streptococcal infection. Adequate bedspacing, face masks, and bowls ofDettol’ have no doubt contributed to the eclipse, of the streptococcus. But when a staphylococcal infection is treated in the ward, contaminated particles’from the dressing are commonly swept from one end of the ward to the other, alighting on bed-clothes from which they are thrown up to descend on fresh wounds when these in turn are exposed. 5. This mode of spread may have little importance in acute surgical wards, but is of very great importance in orthopaedic wards. The sum of misery and frustration brought about by the ubiquitous staphylococcus is still very high. Amyloid disease still arises from unnecessarily infected tuberculous sinuses ; spinal grafts are still extruded, screws are loosened, and tendons destroyed ; chronic osteomyelitis still occurs, and is ’still one of the most distressing of all diseases. As

the staphylococcus by must consider how to stop the spread of this organism in chronic surgical wards. The measures I would suggest are : we

are

not

antibiotic therapy,

controlling

we

(a) Separation of infected from non-infected patients. Separate wards may be impossible, but there is no need to put a patient with a tuberculous abscess requiring aspiration in a bed adjacent to one with a discharging osteomyelitis. (b) Dressing-rooms for all dressings and examinations. No peeping at wounds in the open ward. (c) No dry sweeping. A vacuum-cleaner suitable for hospital wards is an urgent necessity. (d) Careful supervision of the disposal of infected plasters and dressings in the theatre as well as in the ward. (e) A patientin an orthopaedic ward, discharging staphylo,

cocci that are resistant to the antibiotics in should be isolated.

Royal National Orthopædic Orthopaedic Hospital, Stanmore, Middlesex.

common

use,

H. LACK CHARLESH. Pathologist.

PERIPHERAL FACIAL PALSY

SIR,—Mr. Terence Cawthorne’s article (June 20)

on

facial palsy and his observations on its in an earlier communieation1 provide a valuable contribution to our knowledge of this condition. Particularly interesting is the analysis of the aetiology in 129 cases in which the lesion was intratemporal, and in which the facial nerve was exposed at the upper level of the lesion. One infers that no case of Bell’s palsy was met with in which a lesion could be demonstrated in the tympanic segment or upper vertical segment (as he has named them), whereas 53 cases were found in the lower

peripheral pathology

vertical segment.

1. Lancet,

1951, ii, 593.

palsy ever involve the facial nerve as high geniculate ganglion _? Mr, Cawthorne says that between the geniculate ganglion and the level. of the chorda tympani there is no guide as to the site of the lesion except the cause. Does he consider the stapedius reflex of any value in localisation ? If the patient complains of hyperacusis as well as facial palsy and taste disturbances, would this constitute a dependable indicaDoes Bell’s

the Editor

the

tion that the level of the lesion is above the level of the nerve to the stapedius ? It would seem theoretically that the presence of hyperacusis should provide a guide for lesions suprachordal but infrageniculate (provided lacrimation is normal). I have at the moment -in general practice a schoolmaster, aged 40, who experienced a feeling of tightness’not amounting to pain in the left ear and overnight developed complete left peripheral facial palsy. In addition he complained of painfully loud hearing on the same side, particularly painful when using the telephone. There was smarting of both eyes but not He had a feeling in the left side of one more than the other. his tongue anteriorly as though it had been scalded by hot fluid. These complaints developed concurrently with the palsy. The palsy is very obvious, there being pronounced dropping of the angle of the mouth, inability to close -the eye, and loss ’

.

of forehead furrows on the affected side. Examination of the ears shows nothing abnormal. Weber test normal. Rinne’s test positive on each side, but air-conduction lasts longer ori the left than on the right side and some sounds are painful. Hearing is normal for conversation and whisper. The tympanic membrane is normal ; there are -no herpes spots. Taste tests are inconclusive, all the front of the tongue being unreliable. Blood-pressure and central nervous system normal. Wassermann reaction not yet known.-

In such a case is one entitled to conclude that the lesion of Bell’s palsy extends from the stylomastoid foramen to the geniculate ganglion, and that if decompression had to be carried out the lesion would be found’ in the tympanic part of the nerve or aboveQ All authorities agree that it is impossible to give a reliable prognosis in the first week or two after-the onset of a complete Bell’s palsy even with the help of electroHas Mr. Cawthorne, from his survey myography, &c. of 325 cases, gained any hint as to prognosis based on an assessment of the clinical features in the early days of the palsy ? Thus is there any suggestion that -a. severe case such as I have described carries a worse prognosis as regards recovery of full function than a case of complete peripheral facial palsy without evident involvement of the chorda tympani, stapedius, and lacrimal gland, or with involvement of the chorda tympani only’? It seems unsatisfactory indeed that the only indication for the operation -of decompression is the absence of clinical or electric evidence of returning function a month or more after the-onset of the palsy. One would imagine that meanwhile irreparable harm would have overtaken the nerve. E. C. ATKINSON. ATKINSON. Sheffield. * ** We have shown this letter to Mr. Cawthorne whose reply follows.—ED. L.

SIR,—The term Bell’s palsy implies a lesion of the facial nerve-trunk in the lowest part of the vertical segment just above the stylomastoid foramen. Since first the characteristic appearance recognising at of the nerve-trunk in this situation, it has been noted in all but 4 of the cases of facial palsy submitted to The swelling and discoloration of decompression. the nerve-trunk in Bell’s palsy has never been seen to extend higher than 1 cm. above the stylomastoid foramen. It remains to be seen whether in severe cases the swelling extends higher than this ; and if so whether it is the same disease. Only by looking and seeing can this be found out. That the lesion is in the lowest part of -the intratemporal part of the nerve is suggested by the effect on taste ; for in many cases taste is unaffected, although

operation