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blood. Capillary thrombi were said to be lysed and theblocked circulation restored. Using micro-cinemato-graphy, ROBB 14 observed aggregation of platelets andformation of micro-thrombi in the circulation aftervarious kinds of experimental shock, and reported thatthese were prevented or lessened by combined

fibrinolysin and heparin therapy.The position now is intriguing. Formerly regarded

as an irreversible state, long-continued haemorrhagichypotension (in animals) seems to be reversed byprophylactic or therapeutic measures as diverse as anti-adrenergic drugs, coeliac denervation or blockade,hypertonic sodium salts, heparin, and fibrinolysin, inaddition to reinfusion of the shed blood in most cases.

Obviously further work is needed to confirm, collate,and explain these results. In clinical practice some ofthese measures may prove useful for resistant shockunrelated to haemorrhage or injury, such as thatassociated with severe bacterial infection 18; but for

oligsemia following blood-loss and trauma blood-transfusion undertaken adequately and in good time islikely to remain the sheet-anchor.

"Imperforate" AnusOF the congenital abnormalities in the newborn

imperforate anus is one of the most important, becauseit is comparatively common-1 in 3000-5000 births-andbecause most general surgeons who hesitate to treat

anomalies such as oesophageal atresia and meconiumileus will operate on the "imperforate" anus. Even inexpert hands the results of treatment are mediocre, and,judging by patients referred to children’s hospitals forsecondary surgery, the diagnosis and treatment of con-genital anorectal malformations are still not widelyunderstood.

KIESEWETTER and TURNER 19 point out that the func-tional results depend on the anatomical fault and themethod of surgical correction. The descriptive term" imperforate anus " covers a heterogeneous group ofmalformations, ranging from minor anal deformities atthe one extreme to complex anorectal anomalies at theother. The .word " imperforate " is often inaccurate,because in most cases an opening of some sort is present.Moreover, it is misleading because it suggests that theoriginal treatment introduced in the 7th century byPAULUS ARGENITA, the Byzantine physician, is adequate.He simply passed a bistoury through the perineum, andlater dilated the opening with bougies 20; and even todaysome textbooks on general surgery advocate dissectioninto the perineum in the hope of finding a manageableend of the lower bowel. The success of this procedurein minor anal anomalies cannot be questioned, but inrectal deformities it is often disastrous because it destroysthe muscles of the pelvic floor without which there canbe no hope of continence. LADD and GROSS 21 describedfour types of congenital anorectal anomalies: type 1,stenosis; 2, membrane; 4, anal canal present but rectum

18. See Lancet, Dec. 14, 1963, p. 1265.19. Kiesewetter, W. B., Turner, C. R. Ann. Surg. 1963, 158, 498.20. Matas, R. Trans. Amer. surg. Ass. 1897, 15, 453.21. Ladd, W. E., Gross, R. E. Amer. J. Surg. 1934, 23, 167.

ends blindly; and 3, anus absent and rectum endingblindly at various distances above the skin. This typeincludes over 80% of the anomalies, many of themdiffering greatly in treatment and prognosis. GROSS 22recommended an abdominoperineal approach when theblind end of the rectum is more than 1-5 cm. from theanal skin, and a perineal operation when the rectum endsless than 1-5 cm. from the skin. KIESEWETTER andTURNER 19 grouped their cases according to whether theblind end of the bowel was less or more than 2 cm. abovethe anal skin, and the functional results of operationwere vastly superior in the former group. BROWNE’S 23

classification, derived from the embryological interpreta-tions of WOOD J ONES,24 and further elaborated bySTEPHENS,25-27 recognises two major groups: (1) an analgroup (referable to developmental aberrations affectingthe proctodeal pit and membrane, the perineum, andgenital folds), and (2) a rectal group (referable to failureof cloacal subdivision).Whatever the correct embryological explanation of

the various deformities, the critical factor in both treat-ment and prognosis is the relation of the terminal bowelto the pelvic floor, which STEPHENS 25-27 has shown canbe determined by means of the Wangensteen-Rice 28

principle from bony landmarks in lateral X-rays of thepelvis. In patients with rectal deformities the bowelusually ends at or proximal to the so-called pubococcy-geal line (drawn from the middle of the body of the pubisto the last piece of the sacrum), whereas in those withanal malformations it ends at or below the ischial line

(lower ossified margin of the ischium). The operationfor " high " or rectal anomalies is complex, and theresults are poor. Sacrococcygeal and urinary-tractabnormalities, inadequately developed levator muscles,and deficient nerve-supply often accompany this type ofanomaly. On the other hand, in

" low " or anal anomaliesthe operation is simple and the results are good. Nixort 2semphasised the importance of differentiating between" high " and " low " abnormalities according to whetherthe bowel ends above the levator muscle or not, becausechildren with " low " lesions should usually have normalcontinence after treatment, whereas those with " high "anomalies rarely will. But there is at least one seriousobjection to the division of deformities into high andlow-namely, that many deformities, particularly in

females, reach to intermediate levels. The boundarybetween " high " and " low " should, therefore, not bedetermined by arbitrary measurements, but rather by itsrelation t3 bony points which can be displayed on X-rays,and for this purpose STEPHENS’ pubococcygeal and ischiallines are ideal.

KIESEWETTER and TURNER 19 point out that there areat least four ways in which a surgeon may contribute to

imperfect function. First, the surgical approach may beincorrect-e.g., a

" blind " perineal approach is usually22. Gross, R. E. The Surgery of Infancy and Childhood. Philadelphia, 1953.23. Browne, D. Ann. R. Coll. Surg. Engl. 1951, 8, 173.24. Jones, F. Wood. Brit. med. J. 1904, ii, 1630.25. Stephens, F. D. Aust. N.Z.J. Surg. 1953, 22, 161.26. Stephens, F. D. ibid. 1953, 23, 9.27. Stephens, F. D. ibid. 1961, 31, 90.28. Wangensteen, O. H., Rice, C. O. Ann. Surg. 1930, 92, 77.29. Nixon, H. H. Postgrad. med. J. 1959, 35, 80.

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disastrous in cases with rectal anomalies. Secondly,fistulse may be overlooked-e.g., the minute recto-

urethral fistulse associated with rectal anomalies in males

may be missed. Thirdly, important muscles and nervesmay be destroyed-for instance, when pelvic dissectionin the abdominoperineal operation for rectal anomaliesis too wide and when the perineal dissection for analanomalies is too thorough. Finally, in rectal anomaliesthe bowel may be pulled down behind the levator muscleinstead of through the puborectalis sling. Most of thesesurgical mistakes can be avoided if the precise anatomicaldefect is recognised before operation. KIESEWETTER andTURNER believe that the sacroperineal approach ofSTEPHENS has much to commend it, especially whencombined with abdominal mobilisation of the fistula.A great deal of discussion has been devoted to the

correct designation of the abnormal opening of thebowel in these cases. In orthodox terminology, it is a" fistula "; but it has been suggested that " anus " ismore correct, because " anus " is defined as the distalorifice of the bowel. BROWNE 23 calls an orifice below thelevator an "anus", and one above the levator a" fistula "; an anus can be made to function where itlies, but a fistula cannot be made continent withouttransplantation’ and proctoplasty. When the term" anus " is retained for these abnormal openings, it isusually described as

"

ectopic ". Difficulties arise in

finding a nomenclature acceptable to academic anato-mists and practising surgeons alike, but the soonerunanimity is reached the easier it will be to standardisethe treatment and to improve results.

Annotations

BARBITURATE POISONING

TREATMENT of acute barbiturate intoxication shouldinclude measures to reduce absorption, to abate dangeroussystemic effects, and to enhance the rate at which thepoison is removed from the body. Current practice is

perhaps least satisfactory in the pursuit of the last of thesethree aims. With the long-acting barbiturates the risk ofirreversible cerebral damage and severe respiratoryinfection is especially great. At the other end of the scale,the short-acting barbiturates (cyclobarbitone, pento-barbitone, and secobarbitone) and the ultra-short actingcompounds used as anaesthetics (thiopentone and hexo-barbitone) are unlikely to produce long-continued coma.

Barbiturates are weak organic acids which are excretedin the urine by glomerular filtration and proximal tubularsecretion. In the un-ionised form they are diffusible andlipoid-soluble, and this permits back-diffusion from therenal tubular fluid into the peritubular blood, especiallyif the urine is scanty and acid. The rate at which barbi-turate is eliminated from the body is therefore enhancedby polyuria and alkalinity of the urine. Myschetzky andLassen 3 4 have recently applied this knowledge in a seriesof 57 patients. They used two solutions for infusion-a 50% urea solution in physiological saline, and anelectrolyte solution containing sodium lactate, sodium

1. Weiner, I. M., Washington, J. A. Jr., Mudge, G. H. Bull. Johns Hopk.Hosp. 1959, 105, 284.

2. Waddell, W. J., Butler, R. C. J. clin. Invest. 1957, 36, 1217.3. Myschetzky, A., Lassen, N. A. J. Amer. med. Ass. 1963, 185, 936.4. Myschetzky, A., Lassen, N. A. Danish med. Bull. 1963, 10, 104.

chloride, potassium chloride, and glucose, which wasdesigned to alkalinise the urine and to prevent electrolytedepletion from the osmotic diuresis produced by the urea.80 ml. of the urea solution and 300 ml. of the electrolytesolution are given intravenously each hour for four hours.At the end of this period there should be a brisk diuresisof at least 6 ml. per minute; then the infusion can becontinued but rather less urea and more electrolytesolution should be used. If the urine volume is less than6 ml. per minute, the volume infused per hour shouldequal the amount of urine passed in the previous hour. Acomplete failure of diuresis indicates that acute tubularnecrosis has developed, and haemodialysis 5 should bearranged immediately.The results were unusually good: only 3 of the 57

patients died, compared with 14 of a matched controlseries of 82 patients. The necessity for tracheostomy wasreduced by half, and the average duration of coma to athird that in the control patients. Complications due totreatment were infrequent. Fluid retention was neversevere, since only 1500 ml. of fluid was given in the firstfour hours and after that period fluid balance could bepreserved. Electrolyte imbalance-especially hyper-natrxmia and hypokalæmia—developed occasionally, butwas readily correctable with careful biochemical control.The efficacy of this type of therapy depends on the

magnitude of the diuresis. Myschetzky and Lassen wereable to obtain an average diuresis of 12-1 litres in 24 hours.This compares favourably with the results of Ohlsson andFristedt,6 who recorded a value of 5 litres per 24 hourswith mercurial diuretics and saline, and with those ofCirksena et al.,7 who reported 9 litres per 24 hours fromthe use of intravenous mannitol.

Balagot et at 8 have used tris-buffer (THAM) and obtaineda similar diuresis, but this was more brief and complica-tions were commoner than with urea and lactate. Suitable

preparations of urea are probably more widely availablethan intravenous mannitol and tris-buffer: urea is now

widely used by neurosurgeons in the management ofcerebral oedema.9 9

Forced diuresis may be more important than alkalini-sation, but alkalinisation is essential if the barbiturate isphenobarbitone 2 this is the only barbiturate whoseexcretion is beyond doubt greatly influenced by urinarypH. Most other medium and long-acting barbiturateshave a higher pKa; hence their excretion is unlikely to bemuch greater in alkaline urine.1O In many cases theclinician cannot obtain accurate information about the

type of barbiturate ingested. In the past, hospital bio-chemists have usually been content to report only on thebarbiturate content of plasma, using an arbitrarily chosenbarbiturate as standard. They argue that chromatographicmethods of identification take so much time that the resultis only of forensic importance, and would not be availableto the clinician on the important first day of treatment.This view has been made obsolete by the development ofthin-layer chromatography of barbiturate," 12 with which5. Kyle, L. H., Jeghers, H., Walsh, W. P., Doolan, P. D., Wishinsky, H.,

Pallotta, A. J. clin. Invest. 1953, 32, 364.6. Ohlsson, W. T. L., Fristedt, B. J. Lancet, 1962, ii, 12.7. Cirksena, W. J., Bastian, R. C., Barry, K. G. (1962). Symposium on

Clinical and Experimental use of Mannitol; p 31, Walter Reed ArmyInstitute of Research, Washington, D.C.

8. Balagot, R. C., Tsuji, H., Sadove, M. S. J. Amer. med. Ass. 1961, 178,1000.

9. Javid. M. J. Neurosurg. 1961, 18, 51.10. Milne, M. D., Scribner, B. H., Crawford, M. A. Amer. J. Med. 1958,

24, 709.11. Cochin, J., Daly, J. W. J. Pharm. exp. Therap. 1963, 139, 154.12. Sunshine, I., Rose, E., Lebeau, J. Clin. Chem. 1963, 9, 312.