4.5 the Treatment of Congenital Hydrocephalus. m.j. Joubert

8/13/2019 4.5 the Treatment of Congenital Hydrocephalus. m.j. Joubert

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23 September 1961 S A T Y D S K R I F V I R G E E E S K U DE 7957. Oliver, G. 1916): Studks in Blood Pressure. London: Lewis.. A1btl t, C. 1925): Arteriosclerosis. London: MacmilJan.9. folnar, B. 1929): Ther. d. Gegenw., 78, 191.10 Means, J. H. 1948): The Thyroid and its Diseases 2nd ed. London:Lippincott.11. IoU, C. A. In Rundle, F. F. ed. 1951): Diseases of the Thyroid 2nded. London: Heinemann.12 Fatayeva, M. . 1956): International Conference on the Peaceful Usesof Atomic Energy vo . 10, p. 215. ew York: United Nations.13. Strisower, F. H. , Gofma n, J . W ., Strisower, B. and de Lal la , O. 1958):J. Clin. Endner., 18, 721 .14 Barnes, B 0959): Fed. Prne., 18, 8.

15. MenoL P 1953): S. Aft . Med. J . 27. 41 .16. Idem 1954): Lancet, 2. 996 .17. Idem 1 956): S. Afr . Med . J. 30. 918. Marine, D. and Baumano , E. J. 1945): A mer. J. Physi o ., 144 . 69.19. Hopsu, V. K. 1960): Acta endocs. (Kbh. ). supp . 48.20. Etiinko O. 1952): Acta anat. (BaseI), s upp . 17, part 121. Green, D. M. 1946): J. Amer. Med. Assoc 131. 1260.22. Goldenbcrg, M. 1951): Amer. J. Med . 1 0. 627.23. Litcbfield. J. W. and Pearl, W. S. 1956): Lance t, 2 , 1283.24. Reuue r, F . W Zikeli. M. F. , Hamlin rn J. T. Tho rn , G . W. andFriend, D. G. 1957) : New Eng . J . Med., 257. 323.25. Goldzieber, M. A. 1939): The Endocrine Glands. New York andLondon: Appleton, Century.

THE TREATMENT OF CONGENITAL HYDROCEPHALUSM. J. JOUBERT ER.CS. En1N.), Neurosurgeon Durban

This paper deals with our experience in the treatment ofcongenital hydrocephalus by means of the ventriculoauricular-shunt operation, which was introduced into thiscountry about 3 or 4 years ago.Hitherto, the treatment of congenital hydrocephalus hasgiven urlifonnIy and universally poor results. No fewer than30 different methods of surgical approach to the problem

are known and none enjoyed popularity for any length oftime. fact i t has taunted the medical profession since thedays of Hippocrates. The multiplicity of methods of approachto this problem is an index of how difficult this neurosurgicalproblem actually is.

ANATOMICAL Al . D PHYSIOLOGICAL CONSIDERATIONSExperimentally, it has been shown that the cerebrospinalfluid CSF) is not a simple filtrate, bu t is actively secretedby the choroid plexus. The absorption of the CSF, on theother hand, is a combination of filtration and osmosis. CSFis continually secreted by the choroid plexus in the ventriclesand circulates from the lateral ventricles through the foramenof Momo into the third ventricle. From there it passes throughthe aqueduct of Sylvius into the fourth ventricle, from whereit escapes through the medially placed foramen of Magendieand the la terally p laced foramina of Luschka into thesubarachnoid space. About one-fifth of the. total quantity

for: of MONRO

Istuna hi lsmaUsOsier na Interpeduncular is

Cisle .nCl Pontisqueduct of Sylvius

For of LUS HK

Fig. 1. Diagram of the ventricular system of the brain.circulates over the spinal cord and is absorbed by the perineural lymphatics. The major portion finds i ts way into thebasal cisterns, from where i t is pumped over the surface ofthe brain and absorbed by the arachnoid villi. Fig. 1 is adiagrammatic representation of the ventricular system in thebrain.

PATHOLOGYPathologically, we recognize 2 types of hydrocephalus: Compensatory Type thi s type there is usually no enlargement of the head

and no increase in the CSF pressure. the newborn it is causedby agenesis of the brain, and its counterpart is found in theadult as cerebral a trophy. There is passive distention ofthe ventricular system and laking in the subarachnoid space. t is of very little importance clinically to us and is notanJenable to treatment.2. Hypertensive Hydrocephalus

This is caused by : a excessive formation of CSF, b obstruction to its circulation, or c defective absorption.According to Russell, the majority of cases in this groupare due to some form of obstruction. Here, there are 2sub-groups:A. The communicating type of hydrocephalus. This isreadily recognized clinically by the amount of CSF obtainedby lumbar puncture. more than 3 - 4 1nl. are obtainable,then thi s is a communicat ing type of hydrocephalus. Whenneutral phenolsulphophthalein is injected into the ventricles,it will appear in the lumbar CSF in 3 - 5 minutes. The pneumoencephalogram in this type of case shows that the ventricularsystem fills readily, and i f the subarachnoid space is filled,the level of th e obstruction can sometimes be easily demonstrated. The obstruction is usually at the incisura tentorii,the interpeduncular or chiasmatic cisterns.

B. The non communicating type of hydrocephalus. This ispractically always caused by some obstruction of the foramenof Magendie or stenosis of the aqueduct of Sylvius. Usuallyless than 3 - 4 m . of CSF is obtained at lumbar punctureand neutral phenolsulphophthalein injected into the ventricles will not readily appear in the lumbar CSF. A lumbarpneumo-encephalogram will either fill the fourth ventricleonIy, in the case of aqueduct stenosis, or will no t fill theventricular system at all, in the case of ob truction at theforamen of Magendie.

CLlNfCAL PICTUREThe diagno is of hydrocephalus is made without difficultybecause of the obvious enlargement of the head and bulging.of the anterior fontanelle. The enlargement is confirmed bymeasuring the occipito-bregmatic circumference, which willbe above the normal average. As the hydrocephalus becomesmore marked, the disproportion between the normal face andlarge cranium becomes more striking. The fontanelle and


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796 S.n. . M ED I L JO URN L 23 September 1961The method described by

Pudenz involves joining theappropriate length of theproximal and distal ends ofthe catheter by means of ametal connection in the neck.

Fig Diagram howing theventricular-venous shunt insitu

auses FailureFour of our fi rs t 8 patientshad to be re-explored atvarious times, but since weintroduced a modification ofthe Pudenz method, wherebythe junc tion of the proximal

and distal ends of the shunt2 is made immediately belowthe burr hole or eliminatedaltogether, the recurrencerate has dropped to less than25 in 20 successive cases .In 4 of the patients needing re-exploration we found:

a a kink in the tubing at the metal junction associatedin 2 cases with a crack in the tube at the bend so produced ;b blocking of the lumen of the tubing by brain tissue;c blocking or sealing off of the valve by fibrous tissuefrom the wall of the superior vena cava caused by faultyintroduction the tip of the shunt was no t introduced intothe right auricle, but was still in the super ior vena cava ig. 4). The tube can also migrate upwards towards thehead from the auricle Fig. 5).

In a few cases the shunt becomes blocked by particulatematter. A flushing device has recently been introducedwhich already shows marked improvement in the ultimateresults. consists of a f langed silicone capsule and adiaphragm valve, which is introduced into the shunt whereit comes through the bur r hole immediately under the skin.

sutures widen, the scalp veins become distended, the eyes aredisplaced downwards from pressure on the orbital plate, andthe sclera becomes visible above the iris. The patient becomesirritable and has a high-pitched cry. Feeding becomes aproblem, and there is relative weight loss of the body as thehead grows in size, even up to a point where there is frankemaciation and dehydration.Optic atrophy and mental retardation a re in inverse proportion to the rapidity of the production of the hydrocephalus,bu t we are all fami liar wi th the mild hydrocephalic with anI.Q. above the average.Some hydrocephalic enlargements become spontaneouslyarrested weeks or months after onset. Every case should beassessed on its own merits to decide when to operate. It isour pract ice to observe the baby for at least 2 weeks, whencircumstances are favourable, and if there is a s teady andregular increase in the size of the head it is unlikely thatspontaneous arrest will ensue.Al l the pat ients must be subjected to investigations, e.g.X-rays of the skull, subdural taps, and pneumo-encephalography.

SURGtCAL APPROACHFifty years ago, Payer a ttempted a ventricular-venousanastomosis. All 3 of his patients died within 4 months.Six years ago, Pudenz et al developed a ventricular-venousshunt by introducing one end of a catheter into the lateralventricle and the other end into the right auricle of the heart ig. 2). The distal tip, which is lodged in the auricle Fig. 3),has a slipcore-valve mechanism which will allow unidirectional flow of CSF. Since this method is an imitation ofnature to shunt the CSF into the venous system, it is morelikely to meet with success than other methods whereby theCSF is shunted into one or other body cavity, e.g. Eustachiantube , ext radural space, pleura l cavity, per itoneal cavity,lesser sac, ureter, duodenum or colon.

Fig. 3 X-ray showing the distal end of the tube in the right auricle note the metal connecting-piece in the neck).Fig 4 X-ray showing an obsvuction distal to the tip of the catheter at the level of the superior vena cava.

Fig 5 X-ray showing cephalic migration of the catheter the connecting-piece is again well shown).


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23 September 1961 S.A. TY SKRIF VIR G N SKUN 797When the capsule is compressed by pressure exerted on theoverlying kin, the diaphragm clo es the ventricular inletand the CSF in the capsule is forced through the ca rdiactube.The operation, as such, is technically easy to perform andhardly disturbs the baby. No baby requires transfusion, andit should be avoided for fear of over auto-transfusion from alarge reservoir in the head.Results

We had 1 postoperative death in 30cases and 36 operations.At postmortem examination, a massive intraventricularhaematoma was found, associated with anaemia and collapse

of the cerebrum. The greatest danger i intercurrent infectionand septicaemia.

SUMMARYThe horrifying condition of congenital hydrocephalus cannow be successfully treated in many cases, and the foetuswith the large head need not be destroyed by the obstetrician,no r need the hydrocephalic patient, discovered after birth,be left to die a low death.Our experience in 30 cases over a period of 3 years is mostencouraging, and should the hunt need to be replaced oradjusted as the child grows, this hould offer no difficulty toeither urgeon or patient.

SERUM TRA SAMINASE LEVELS I THE DIAGNOSIS OFMYOCARDIAL INFARCTION

H. E. ME TZ, D.Se. PRET. , A.R.Le., South frican InSTitute for Medical Research and A. L. AGRA AT, M.D.DUBL. , F.R.C.P. (EDIN.), D.T.M. Hy. RAND , Johannesburg

Glutamic oxalacetic transaminase (GOT) and glutamicpyruvic transaminase (GPT) are widely distributed in thehuman body. In comparison with the levels in the tissues,the normal serum levels of both enzymes (SGOT andSGPT) a re very low. They are liberated into the blood inincreased quantities on death of the cells in which theyoccur, and increased serum levels have been found following necrotic lesions in many different organs. Estimationsof SGOT have been used mos t oft en in investigation, ofmyocardial infarction and SGPT in liver-cell necrosis; theGPT content is greate st in liver tissue and less in heartmuscle, and the increase in SGPT is thought by some toexceed t ha t o f SGOT in hepatic disorders

t has been reported that a raised SGOT level may confirm the diagnosis of myoca rdia l infarction .3 - s The levelreaches a peak which may be 15 times higher than normalwithin 24 -48 hours, and returns to normal by the 4th-7th day. t has been suggested that with relatively small infarctsthe peak level may be within or at the upper limit ofthe accepted normal range, especially if a pat ient 's serumtransaminase in heal th is in the low range of normal; forthis reason serial determinations should be carried out .Sometimes it is difficult to distinguish on the electrocardiogram (ECG) between coronary insufficiency (ischaemia) and limited infarction. The SGOT level should be ofdiagnostic help in such cases, since it was found to remain

unaltered if ischaemia is not accompanied by necrosis.Dewar et al found that the enzyme est imation is complementary to, but not necessarily more rel iable than, theECG in showing whether necrosis has taken place.The SGOT level may also be of special value in complicated infarction. A second infarction will give a secondary peak, even though the ECG does not change 'Also, in some pat ients with previous infarct ion, the ECGcan be so distorted that on a single initial tracing aloneit may be impossible to deduce with certainty that freshinfarction has occurred. According to Keele al. anginal

pain at rest with an abnormal, but not diagnostic, EC.Gassociated with a raised SGOT concentration, carries thesame prognostic significance as does the elect rocardiographically proved infarction, while the transaminase leveldoes not t end to be raised with chest pain f rom mos t othercauses.

In this investigation we attempted to answer the following questions:I . When is the SGOT estimation of help in the diagnosis of myocardial infarction?2. What are t he minimum number of tests requiredin a single case?3. What additional information can the SGPT estimation supply?The answers to the questions are important. they areknown, the test need not be done unnecessarily, the

number of tests may be reduced to a minimum, and theinterpretation of the test may be properly assessed.Method of InvestigationTwo groups of patients were investigated on a fairlyuniform basis. Apart from 6 patient treated in the Johan-nesburg General Hospit al , all the pati ents were admitted

to a nursing home where they were under the personalcare of one of us AL.A . Electrocardiograms were doneand repeated where necessary. The SGOT and SGPTlevels were est imated daily for 1 con ecutive days andthe values were correlat ed with the clinical findings. Inorder to reduce the transaminase est imat ions to a practi cal number, the SGOT and SGPT level were assessedin most ca es for the fir t 4 days in each of the series.These values represent 4 daily con ecutive level in bloodcollected on admis ion, and as oon a ft er the episode ofcnest pain as pos ible. To prolong this investigation to6 - 1 consecutive days makes the test, in our opinion,impracticable in most instance. In fact, if a single diagnostic level should be po itive, no more estimations needbe done.

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4.5 the Treatment of Congenital Hydrocephalus. m.j. Joubert