Surgical Treatment For Brain Compartment Syndrome

ORIGINAL ARTICLES
Liver transplantation at Red Cross War Memorial Childrens

Hospital
C W N Spearman, M McCulloch, A J W Millar, H Burger, A Numanoglu, E Goddard, P Gajjar,
C Davies, E Muller, F McCurdie, D Kemm, S Cywes, H Rode, D Kahn
The liver transplant programme for infants and children at Red

Cross War Memorial Childrens Hospital is the only established
paediatric service in sub-Saharan Africa. Referrals for liver
transplant assessment come from most provinces within South
Africa as well as neighbouring countries.
Patients and methods. Since 1987, 81 children (range 6 months
- 14 years) have had 84 liver transplants with biliary atresia
being the most frequent diagnosis. The indications for
transplantation include biliary atresia (48), metabolic (7),
fulminant hepatic failure (10), redo transplants (3) and other
(16). Four combined liver/kidney transplants have been
performed. Fifty-three were reduced-size transplants with
donor/recipient weight ratios ranging from 2:1 to 11:1 and 32
children weighed less than 10 kg.
Results. Sixty patients (74%) survived 3 months - 14 years
post transplant. Overall cumulative 1- and 5-year patient
survival figures are 79% and 70% respectively. However, with
the introduction of prophylactic intravenous ganciclovir and
the exclusion of hepatitis B virus (HBV) IgG core Ab-positive
The liver transplant programme for infants and children at Red

Cross War Memorial Childrens Hospital is at present the only
established paediatric service in sub-Saharan Africa. The first
paediatric transplant was performed on 6 December 1987 for
end-stage liver disease due to alpha-1-antitrypsin deficiency.
The patient unfortunately died of complications in January
1988. The paediatric programme was then put on hold until
School of Child and Adolescent Health, University of Cape Town and Red Cross War
Memorial Childrens Hospital, Rondebosch, Cape Town
960
C W N Spearman, MB ChB, FCP (SA), MMed (Med)

M McCulloch, MB BCh, MRCPCH (UK), FCPaed (SA), DCH (SA)
A J W Millar, MB ChB, FRCS (Eng), FRACS, FCS (SA), DCH
H Burger, MB ChB, DCH
A Numanoglu, MB ChB, FCS (SA)
E Goddard, MB ChB, PhD, MMed (Paed)
P Gajjar, MB ChB, FCPaed (SA)
C Davies, MB ChB, FCPaed (SA)
E Muller, MB ChB, FCS (SA)
F McCurdie, RN, BSc (Nurs), ICU (Dip)
D Kemm, RN, MCur (SA)
S Cywes, MB ChB, OMSG, MMed (Surg) (SA), FACS (Ped), FRCS (Eng)
Edin), FRCPS (Glas), FAAP (Hon), FCS (Hon) (SA), DSc (Hon)
H Rode, MB ChB, MMed (Surg), FRCS (Edin), FCS (SA)
D Kahn, MB ChB, FCS (SA), ChM (SA)
Corresponding author: C W N Spearman (wendy@uctgsh1.uct.ac.za)
September 2006, Vol. 96, No. 9 SAMJ
donors, the 1-year patient survival is 90% and the projected

5-year paediatric survival is > 80%. Early (< 1 month) postliver-transplant mortality was low. Causes include primary
malfunction (1), inferior vena cava thrombosis (1), bleeding
oesophageal ulcer (1), sepsis (1) and cerebral oedema (1). Late
morbidity and mortality was mainly due to infections: de novo
hepatitis B (5 patients, 2 deaths), Epstein-Barr virus (EBV)related post-transplantation lymphoproliferative disease (12
patients, 7 deaths) and cytomegalovirus (CMV) disease (10
patients, 5 deaths). Tuberculosis (TB) treatment in 3 patients
was complicated by chronic rejection (1) and TB-drug-induced
subfulminant liver failure (1).
Conclusion. Despite limited resources, a successful paediatric
programme has been established with good patient and graft
survival figures and excellent quality of life. Shortage of donors
because of infection with HBV and human immunodeficiency
virus (HIV) leads to significant waiting-list mortality and
infrequent transplantation.
S Afr Med J 2006; 96: 960-963.
the adult programme had become established at Groote Schuur

Hospital and was restarted in November 1991.1 Referrals for
liver transplant assessment come from most provinces within
South Africa as well as neighbouring countries.
Patients and methods

Since 1987, 84 orthotopic liver transplants have been performed
on 81 children and all are included in this retrospective review.
The major indication for liver transplantation was biliary
atresia (57%) followed by acute liver failure (12%). There were
4 combined liver/kidney transplants for primary hyperoxaluria
(3) and congenital hepatic fibrosis associated with polycystic
kidneys (1).
Demographics. The age of the children ranged between 6
months and 14 years (mean 4.6 years) and included 38 male
and 43 female children. The racial distribution was as follows:
14 black, 33 mixed race, 4 Asian and 30 white. Their weight
ranged between 4 kg and 50 kg (mean 13 kg) and 32 children
weighed < 10 kg.
Indications for liver transplantation. The indications for
liver transplantation are listed in Table I.
Surgical techniques. The surgical techniques used for donor
retrieval and recipient liver removal and engraftment have
ORIGINAL ARTICLES
Table I. Indications for liver transplantation

Biliary atresia
Fulminant hepatic failure
Metabolic
Alpha-1-antitrypsin deficiency
Primary hyperoxaluria
48
10
7
4
3
Redo transplants
Chronic rejection
Acute rejection
2
1
Other
Autoimmune hepatitis
Cryptogenic cirrhosis
Neonatal hepatitis
Budd-Chiari syndrome
Alagille syndrome
Congenital hepatic fibrosis
Hepatoblastoma
6
2
3
1
2
1
1
16
been previously described in detail.1-3 Fifty-three reduced-size

grafts were used (31 left lateral segment, 18 left lobe, 4 right
lobe). In all the reduced-size livers and in patients with biliary
atresia, choledochojejunostomy was used for biliary drainage
without the use of stents or T-tubes. The donor: recipient
weight ratios varied between 2:1 and 11:1 (mean 3.4:1.) One
living related (mother-child) transplant was performed.
Anaesthesia. The anaesthetic time ranged from 7 to 16 hours
(mean 9 hours) and the mean blood volume transfused was 2.5
blood volumes (range 0.5 - 5.7). Blood-group crossmatch was
identical in 66, compatible in 16 and incompatible in 2 cases.
Immunosuppression. Baseline immunosuppression
consisted of triple therapy in the form of cyclosporin,
methylprednisone and azathioprine. Oral cyclosporin (5 mg/
kg) was given immediately prior to surgery and continued
postoperatively initially intravenously, but since 1997 it has
been given orally, using Neoral cyclosporin 3 times a day
aiming for a trough level of 350 - 400 ng/ml initially and a 2hour peak level greater than 1 000 ng/ml.4 Methylprednisolone
(10 mg/kg) and azathioprine (0.5 - 1 mg/kg) was given
intravenously at the time of reperfusion of the graft and the
methylprednisolone dosage was reduced in the first week
to 1 mg/kg for the first month and then further reduced to
0.2 mg/kg as maintenance. Azathioprine was continued for
approximately 6 months. Rejection episodes were managed
with 3 - 4 daily pulses of methylprednisolone, but increasingly
this has not been required with early conversion to tacrolimus
and selective use of mycophenolate mofetil. Recently antiCD25 antibodies have been used (basiliximab at 20 mg/dose
for weight > 40 kg, 10 mg/dose for weight < 20 kg; daclizumab
1 mg/kg/dose) both used as a 2-dose regimen.5 Rapamycin
has also been used in two patients with chronic rejection, high
Epstein-Barr virus (EBV) levels and associated post-transplant
lymphoproliferative disease (PTLD).
Infection prophylaxis.610 Intravenous ampicillin and
cephalosporin is given at anaesthestic induction, repeated

together with metronidazole at the time of biliary anastomosis
and continued for 3 - 5 days peri-operatively. Antifungals in
the form of oral mycostatin and amphotericin lozenges are
given, and patients with severe cholestasis and prolonged
pre-transplant inpatient treatment receive intravenous
amphotericin peri-operatively for 2 weeks. Co-trimoxazole
6 mg/kg/day in 2 divided doses is given 3 days/week for
prevention of Pneumocystis carinii infection and is continued
for 6 months. Intravenous ganciclovir 5 mg/kg twice daily
was given as viral prophylaxis against cytomegalovirus (CMV)
and EBV infections, initially for 2 weeks, but since 1996 this is
given for 3 months in children under the age of 3 and in highrisk children not previously exposed to EBV in an attempt to
prevent PTLD.11 In addition, Polygam is given intravenously
for the first 5 days post transplant and all blood products are
leucocyte filtered. TB prophylaxis is used in high-risk patients
only.
Results
Since 1987, 84 orthotopic liver transplants have been performed
on 81 children. All patients have survived the procedure and
currently 60 (74%) patients have survived 3 months to 14 years
post transplant. Fifty-one children have an excellent quality of
life.
The causes and timing of death are as follows: (i) early (b
1 month): sepsis (1), bleeding oesophageal ulcer (1), primary
non-function (1), inferior vena cava (IVC) thrombosis (1),
cerebral oedema (1); (ii) intermediate (> 1 - 6 months): rejection
and associated sepsis (1), portal vein thrombosis with variceal
bleed (1); (iii) late (> 6 months): bacterial, viral and fungal
infections (5), PTLD (7), chronic rejection (2).
Surgical complications
Hepatic artery thrombosis occurred in 2 patients and portal
vein thrombosis in 6 patients. Four patients developed early
portal vein thrombosis (< 6 months). In 2 patients, the portal
vein thrombosis was successfully repaired and the third
presented with an uncontrollable variceal bleed 6 months
post transplant. Attempts at a Meso-Rex shunt and redo
portal anastomosis failed in the fourth patient who remains
clinically stable on enoxaparin sodium (Clexane) therapy.
Two late portal vein thromboses occurred (> 1 year) resulting
in portal hypertension and recurrent GIT bleeds. They were
managed successfully with a Meso-Rex shunt. IVC thrombosis
occurred in 2 patients and this was treated with thrombolytic
therapy, which was successful in 1 patient (6 months post
transplant), but the second patient died from bleeding and
sepsis in the peri-operative period. Bile leaks occurred in 4
patients; in 2 these were successfully managed with revision of
the biliary anastomosis and in the other 2 patients, the biliary
leak was associated with a reduced-size graft and settled
961
ORIGINAL ARTICLES
spontaneously. Four patients developed postoperative GIT

bleeding. Two required relook laparotomies, with the revision
of Roux-en-Y anastomosis in 1, while the other patient was
noted to have bleeding from the cut-surface of liver, which
was cauterised. One patients postoperative GIT bleeding
settled spontaneously, and another patient presented with
uncontrollable bleeding from a postsclerotherapy oesophageal
ulcer.
Medical complications
Tuberculosis (3). Two children developed pulmonary
tuberculosis and 1 patient a pleural effusion. TB drug treatment
was complicated by chronic rejection in 1 patient and TB-druginduced subfulminant liver failure in 1 patient.
De novo hepatitis B (5). Hepatitis B virus infection is
endemic in South Africa with an HBsAg incidence of 3 - 20%
and a HB IgG core Ab incidence of 40 - 80%. Forty per cent of
the potential donors are HB IgG core Ab-positive. Prior to
1996, donors were only screened for HBsAg. Five children
(6 - 14 months post transplant) developed de novo hepatitis B.
All had been HBsAg-negative pre-transplant and the explanted
liver showed no evidence of hepatitis B infection. Three of
the children had received organs from Hep B IgG core Abpositive donors and sera was not available for testing in 2. Two
children have developed mild chronic hepatitis and 2 have
developed severe chronic hepatitis progressing to cirrhosis.
The DNA levels ranged between 1 920 and 4 800 pg/ml
(mean 3 556 pg/ml). All patients were treated initially with
famciclovir and then changed to lamivudine.12-14 Lamivudine
resistance developed in 2 patients and 2 have died as a result of
progressive chronic hepatitis B and complications of cirrhosis.
One died soon after diagnosis from TB-drug-induced liver
failure.
962
CMV infection and disease. CMV infection is endemic in

our population and 90% of donors were CMV-positive.15 CMV
infection as defined by the presence of fever together with a
positive culture or positive pp65Ag occurred in 12 patients
and was treated successfully with intravenous ganciclovir.
Ten patients developed CMV disease and the sites of disease
included the lung (4), liver (7), pancreas and GIT (1). Five of
the 10 patients with CMV disease have died. Risk factors for
CMV infection and disease include poor nutritional status,
high-dose steroids and pulsing. Since 1995, the regular use of
CMV pp65Ag monitoring has enabled earlier diagnosis and
treatment of CMV infection and consequently less disease.
At present pre-emptive intravenous ganciclovir is given to all
high-risk children and this has contributed to a decrease in the
incidence of CMV disease.
EBV and PTLD (12). EBV infection has resulted in
significant morbidity and mortality in our children. Twelve
children developed PTLD (all of them < 3 years of age) and
the mean time to development of PTLD was 9.2 months
(range 3 - 30 months post transplant). Eight had typical acute

membranous tonsillitis with associated lymphadenopathy.
Seven children were EBV nuclear antigen (EBNA)-positive at
time of transplant and all were positive at time of diagnosis
of PTLD. Sites of involvement include tonsils (8), intestine
(6), mediastinum (4) and CNS (4). On histology, there were 6
monoclonal, 2 oligoclonal and 4 polyclonal PTLD. Management
of PTLD included the reduction of immunosuppression
in all patients with complete withdrawal in 2 patients.10-11
Adenotonsillectomy was performed in 7 patients and debulking
surgery in 4. Of the 3 patients who received chemotherapy, all
died within 10 weeks of diagnosis. Two patients have received
intravenous rituximab. Seven patients died as a result of PTLD
and 1 required a retransplant for chronic ductopenic rejection.
Overall there was a 15% incidence of PTLD in our programme
with a 58% mortality, despite the use of chemotherapy,
reduction in immunosuppression and rituximab therapy.
Survival
The overall cumulative 1-year and 5-year patient survival is
70% and 79% respectively. Since 1996, with the introduction of
IVI ganciclovir for 3 months and the exclusion of HBV IgG core
Ab-positive donors, the 1-year patient survival is 90% and the
projected 5-year survival is > 80%.
Discussion
As the only established paediatric liver transplant centre within
South Africa, children are referred from all over South Africa.
In the early stages of our programme, children were referred in
a pre-morbid clinical state and frequently died while awaiting
a liver transplant. However, with increasing public awareness
and education of the medical fraternity, children are now
increasingly being referred early on in the course of their liver
disease. Successful outcomes to liver transplantation however,
are dependent on both a committed family and committed
medical support, particularly when the child returns home to a
medical centre in another province.
Endemic viral and bacterial infections, particularly TB, CMV,
EBV and hepatitis B have had a significant impact on our
programme12,13,15-17 The recent ability to monitor CMV pp65
Ag and EBV polymerase chain reaction (PCR) has enabled us
to recognise viral infections earlier, treat appropriately and
decrease immunosuppression. The de novo hepatitis B in the 5
children was probably acquired as the result of using hepatitis
B core Ab-positive donors.18 Two children have died as a
result of chronic hepatitis B and 2 have developed lamivudine
resistance. Since 1996, hepatitis B IgG core Ab-positive donors
have been excluded as potential liver donors and no further
cases of de novo hepatitis B have occurred. The hepatitis B IgG
core Ab-positive rate in the donor pool is approximately 40%
and this together with the increasing prevalence of HIV has
significantly decreased the number of potential donors.
ORIGINAL ARTICLES
With the introduction of aggressive antiviral prophylactic

regimens and the exclusion of hepatitis B core Ab-positive
donors since 1996, the predicted 5-year patient survival
figures are now greater than 80%, which is comparable with
other reported series. Despite limited resources, diminishing
manpower and a decreasing donor pool, the Red Cross
Childrens Hospital paediatric liver programme continues to
be active with survival figures comparable with large centres
elsewhere. With increasing public awareness, the number
of children requiring transplantation will increase and at
present split liver transplantation is beyond the capacity of our
restricted manpower. Other options that need to be considered
in expanding the donor pool are the increasing use of marginal
donors and embarking on an active living-related programme.
References
1. Robson SC, Spearman, CW, James MF, et al. Orthotopic liver transplantation at Groote Schuur
Hospital. S Afr Med J 1992; 82: 79-82.
2. Starzl TE, Demetris AJ, van Thiel D. Medical progress: liver transplantation Part I. N Engl J
Med 1989; 321: 1014-1022.
3. Starzl TE, Demetris AJ, van Thiel D. Medical progress: liver transplantation Part II. N Engl J
Med 1989; 321: 1092-1099.
4. Hover PF. Cyclosporin A (Neoral) in paediatric organ transplantation. Pediatr Transplant
1998: 2: 35-39.
5. Ganschon R, Broering DE, Stuerenberg I, Regiers X. First experience with basiliximab in
paediatric liver graft recipients. Pediatr Transplant 2001: 5: 357-358.
6. Whitington PF, Balistreri WF. Liver transplantation in paediatrics: indications,
contraindications and pre-transplant management. J Pediatr 1991: 118: 169-177.
7. Fishman JA, Rubin RH. Infection in organ-transplant recipients. N Engl J Med 1998: 338:
1741-1751.
8. Deen JL, Bumberg DA. Infectious disease considerations in paediatric organ transplantation.
Semin Pediatr Surg 1993: 2: 218-234.
9. Winston DJ, Wirin D, Shaked A, Busuttil W. Randomised comparison of gancyclovr and
high-dose acyclovir for long-term cytomegalovirus prophylaxis in liver-transplant recipients.
Lancet 1995: 346: 69-74.
10. Morgan G, Superina RA. Lymphoproliferative disease after paediatric liver transplantation. J
Pediatr Surg 1994: 29: 1192-1196.
11. McDiarmid SV, Jordan S, Lee GS, et al. Prevention and pre-emptive therapy of posttransplant lymphoproliferative disease in paediatric liver recipients. Transplantation 1998: 66:
1604-1611.
12. Millar AJW, Spearman W, McCulloch M, et al. Paediatric liver transplantation in a
developing country taking stock. Pediatr Transplant 2000; 4: 129.
13. Rayes N, Neuhaus R, Naumann U, et al. Treatment of hepatitis B reinfection or de novo
infection after liver transplantation with famiciclovir how effective is it. Transplant Proc
1998: 31: 481-482.
14. Grellier L, Motimer D, Ahmed M, et al. Lamivudine prophylaxis against reinfection in liver
transplantation for hepatitis B cirrhosis. Lancet 1996: 348: 1212-1215.
15. Goddard EA, Millar AJW, Spearman CWN, McCulloch MI, Kahn D. Cytomegalovirus (CMV)
infection in paediatric liver transplant recipients in a developing country. Pediatr Transplant
2000: 4: 48.
16. Spearman CWN, McCulloch M, Millar AJW, et al. Post-transplant lymphoproliferative
disease (PLTD) in paediatric liver transplant recipients in a developing country. Pediatr
Transplant 2000: 4: 53.
17. Meyers BR, Halpern M, Sheiner P, et al. Tuberculosis in liver transplant patients.
Transplantation 1994: 58: 3: 301-306.
18. Dickson RC, Everhart JE, Lake JR, et al. The National Institute of Diabetes and Digestive
and Kidney Diseases. Liver transplantation database. Transmission of Hepatitis B by
transplantation of livers from donors positive for antibody to hepatitis B core antigen.
Gastroenterology 1997: 113: 1668-1674.
Accepted 28 June 2006.
963
ORIGINAL ARTICLES
Deaths at Red Cross Childrens Hospital, Cape Town

1999 - 2003 a study of death notication forms
Wilson Grandin, Tony Westwood, Kashifa Lagerdien, Maylene Shung King
Objectives. The availability of cause-specic mortality data for

children in South Africa is limited. Hospital-based data have
the potential to contribute to understanding of the causation
of childhood death in South Africa. The objectives of the study
were to gain insights into the causes of death in a South African
childrens hospital.
Design. Prospective, descriptive study of death notication
forms.
Setting. Red Cross War Memorial Childrens Hospital, Cape
Town.
Methods. Data from 1999 to 2003 were analysed by direct and
underlying causes of death (using a modied Global Burden
of Diseases (GBD) classication) and demographic variables.
Death rates per 1 000 hospital admissions were calculated for
certain common causes of death. Seasonal correlates of mortality were examined.
Results. There were 1 978 deaths. The number of deaths per year
increased by 11.4% over the period. The death rate rose from
Knowledge of the causes of childhood death in a population

is fundamental to the promotion of the health of its children.
Research on the causes of childhood mortality in South Africa
has focussed on national or provincial data sets,1,2 individual
conditions such as diarrhoea3 or acute respiratory infections
(ARIs)4 at national level, and HIV/AIDS in hospital settings.5
Recent attempts to measure remediable health service factors in
the causation of childhood mortality are in the developmental
phases.6
The limitations of cause-specic mortality data in South
Africa have been well documented.7 Specic cause of death
has been missing on a large proportion of death certicates. A
revised death notication form was adopted in South Africa in
1998.8 This form aimed to increase the epidemiological accuracy
Childrens Institute, University of Cape Town
Wilson Grandin, Medical Student, Tufts University, Boston, USA
Kashifa Lagerdien, MSc (Occ Therapy)
Maylene Shung King, MB ChB
964
Division of Paediatric Medicine, Red Cross War Memorial Childrens Hospital and
School of Child and Adolescent Health, University of Cape Town
Tony Westwood, FCP (SA) MD
Corresponding author: Tony Westwood (westwood@ich.uct.ac.za)
15.9 to 18.4 per 1 000 admissions from 1999 to 2002, declining to

17.4/1 000 in 2003. The death rate was higher for females than
for males (18.4/1 000 versus 17.6/1 000, p = 0.007). Sixty per
cent of deaths occurred in children less than 1 year old. GBD
group I diseases (infectious, nutritional, perinatal) accounted
for the greatest proportion of deaths (58.6%), followed by noncommunicable diseases (29.1%), and injuries (7.9%). HIV/AIDS
accounted for 60% of infectious deaths (31.6% of all deaths).
Diarrhoea-related mortality was 3 times higher in summer than
in winter. Congenital conditions dominated GBD group II
(57.5%).
Conclusion. The analysis shows the value of routinely recording
data on childhood hospital deaths. The results mirror those
of the South African Medical Research Councils Burden of
Disease studies but also reect the hospitals tertiary functions.
Female children were at higher risk of death. Childhood HIVrelated deaths are a major challenge to the health system.
S Afr Med J 2006; 96: 964-968.
of death certication by allowing recording of the direct

cause of death, the sequence of causation and any associated
conditions that may have contributed to the death. Under
optimal conditions, death certicates provide a useful source
of cause-specic mortality data and there is evidence that the
new form is improving the epidemiological value of death
registration in South Africa.1,9
We studied the death notication forms for almost 2 000
children who died at an urban childrens hospital in Cape
Town. It was envisaged that this analysis would help staff
improve clinical care, enable administrators to identify the most
appropriate and cost-effective resource allocation, and provide
a foundation from which to track the changing epidemiology of
child deaths in a dened urban locality.
Methods
Information was collected on all deaths occurring under the
services of the Red Cross War Memorial Childrens Hospital
(RCCH) from 1999 to 2003. The RCCH is a 288-bed state
teaching hospital with tertiary and regional functions. It is a
referral hospital but also houses 24-hour trauma and emergency
units, both of which have overnight inpatient beds. It is the
only paediatric inpatient facility for the central health districts
of Cape Town. Its tertiary services, including an intensive care
ORIGINAL ARTICLES
unit (ICU), receive referrals from southern, central and western

parts of Cape Town, the southern half of the Western Cape,
other tertiary childrens services in the province and other
provinces and neighbouring African states. It mainly serves
children under 13 years of age, most of whom are dependent
on state services. Approximately 156 000 children attend the
outpatient and emergency services each year, of whom about
18 000 are admitted.
Death notication forms completed by physicians at the
hospital were reviewed every month by a senior physician
(TW). The following information was derived from the forms:
the hospital folder number, the childs age (stratied into
those less than 1 year of age (< 1), 1 - 5 completed years (1 - 5),
5 years and over (> 5)), the direct and underlying causes of
death (when provided) and the place of death (e.g. ICU, home).
Folder numbers were used to retrieve data from the RCCH
medical records system on the sex and postal code for each
patient who died.
The direct and underlying cause of death was classied by the
physician according to the International Classication of Diseases
version 10 (ICD-10). Following ICD-10 coding, the underlying
cause of death or the direct cause where no underlying cause
was recorded was classied according to a modied version
of the Global Burden of Disease (GBD) report10 and the South
African National Burden of Disease study.1 Under this scheme,
deaths were grouped into broad categories, with a fourth
category reserved for ill-dened deaths: (i) group I pretransitional causes, viz. communicable diseases, perinatal
conditions, and nutritional deciencies; (ii) group II noncommunicable diseases; and (iii) group III injuries.
Groups I and II were subdivided into major categories,
such as infectious diseases in the former, and neoplasms and
congenital abnormalities in the latter. Two of the larger major
categories, infectious diseases and congenital abnormalities,
were further subclassied to provide more detail on the
precise cause of death. Some of the major groups and
the subclassication of infectious diseases and congenital
abnormalities were altered from the GBD scheme to better
represent the causes of death observed at the RCCH.
Data were analysed for the whole period as well as for
individual years. Mortality rates per 1 000 hospital admissions
were calculated for the whole data set, individual years and
individual causes of death. The roles of sex and age group
were examined for certain common causes of death. Seasonal
variation was examined for two categories of death that have a
strong seasonal incidence in Cape Town, viz. diarrhoeal disease
and ARI. Deaths of patients who had been living in Cape Town
were classied according to metropolitan health districts based
on the postal code. The SPSS software package was used for all
statistical analyses.11
Permission to study the death notication forms was granted
by the RCCH Medical Superintendent.
Results
There were 1 978 deaths registered at the RCCH. The annual
number rose from 367 in 1999 to 414 in 2003, an 11.4% increase
(Table I). One hundred and thirty-nine deaths occurred outside
the hospital (at home, dead upon arrival at the hospital, or
died at a primary care facility but registration took place at
RCCH). In addition, 172 deaths occurred in the emergency
room, leaving a total of 1 667 inpatient deaths. The absolute
number of inpatient deaths as well as the rate of death per
1 000 admissions increased from 303 deaths (15.9 per 1 000
admissions) in 1999 to 357 deaths (18.4 per 1 000 admissions) in
2002. The odds ratio of the death rate in 2002 compared with
1999 was 1.16 (95% condence interval (CI): 1.0 - 1.4, p = 0.052).
The rate dropped to 17.4 per 1 000 admissioins in 2003.
Female inpatients died at a greater rate than males (18.4
versus 17.6 deaths per 1 000 admissions, p = 0.007). Over
the 5 years, a female patient admitted to the hospital was
approximately 14% more likely to die than a male patient.
The absolute number of deaths declined as age rose (Table I).
More than half of all the deaths occurred in children who
came from three very low-income health districts in Cape Town,
viz. Khayelitsha (26.5%), Nyanga (20.1%) and Langa (11%).
The most common locations for deaths within the hospital
were the ICU (37%) and the medical wards (36%). The vast
majority (96.4%) of the deaths outside hospital occurred at
home.
GBD group I diseases accounted for the greatest proportion
of deaths (58.6%), followed by non-communicable diseases
(29.1%), and injuries (7.9%). Ill-dened deaths made up 4.3% of
the deaths (86 cases). Included in this category were 7 cases of
sudden infant death syndrome.
Overall the mortality prole was similar for males and
females. The prole of death for each of the age groups was
distinct (Fig. 1).
The group I causes of death were predominantly infectious
diseases (89.5%), with perinatal conditions contributing
5.7% and malnutrition 4.8%. Of the deaths attributed to
malnutrition, 60.7% were due to kwashiorkor.
Table I. Number and proportion of deaths by year and age

group (N (%))
Age group (yrs)
Year
<1
1-5
>5
Total
1999
2000
2001
2002
2003
Total
215 (58.6)
242 (61.7)
237 (60.0)
247 (60.2)
242 (58.6)
1 183 (59.8)
83 (22.6)
94 (24.0)
97 (24.6)
95 (23.2)
98 (23.7)
467 (23.6)
69 (18.8)
56 (14.3)
61 (15.4)
68 (16.6)
73 (17.7)
327 (16.5)
367
392
395
409
413*
1 977*
*Age unknown for 1 patient.
965
ORIGINAL ARTICLES
Fig. 2 shows the infectious causes of death. HIV/AIDS

caused over 60% of the 1 038 deaths and, causing 31.6% of all
deaths, was by far the most prevalent specic cause of death.
There were 95 deaths attributable to the disease in 1999, the
number rising each year to peak at 148 deaths in 2002 and
dropping to 135 deaths in 2003. The mortality rate for HIV/
AIDS per 1 000 hospital admissions peaked at 6.5 in 2002,
dropping to 5.8 in 2003. The proportion of total hospital deaths
attributed to HIV/AIDS increased from 26.2% in 1999 to 36.1%
in 2002 before falling to 32.6% in 2003. Of the 626 HIV-related
deaths, 72% occurred in children < 1, 22% in the 1 - 5 group, and
6% in the > 5 group. The age-related mortality burden from HIV
infection decreased with increasing age: 451 (38.1%) of deaths
in children < 1, 138 (29.6%) of deaths in the 1 - 5 group, and 37
(11.3%) of deaths in the > 5 group. The proportion of deaths
due to HIV infection increased in all age groups over the study
period. This was particularly evident in the 1 - 5 group; 19.3%
of the deaths were associated with HIV in 1999 compared with
36.7% in 2003.
Fig. 3 provides a subclassication of the 576 deaths due to
non-communicable disorders, based largely on organ systems.
Cerebral palsy constituted more than 75% of the nervous

system disorders, and cardiomyopathy accounted for a similar
proportion of the cardiovascular mortality. Neoplastic deaths
were most commonly caused by cancers of the nervous system
and of the blood or immune systems.
Fig. 4 provides a breakdown of the 331 congenital causes of
death. Congenital abnormalities contributed signicantly to the
overall mortality, with other congenital conditions comprising
nearly 10% of all deaths and congenital heart disease (CHD)
making up nearly 7% of all deaths. Given the frequent comorbidity of Downs syndrome and CHD (16 of the 26 Downs
syndrome patients had some form of CHD), any patient whose
cause of death was attributed to both of these conditions was
classied as Downs syndrome for the purposes of this analysis.
Females had a greater number of CHD deaths than males (p =
0.003). Mortality rate for CHD per 1 000 hospital admissions
was 65% higher for female children (OR 1.65, 95% CI: 1.18
- 2.32) than that for male children.
There were 156 deaths (7.9% of all deaths) attributed to
injuries. There was insufcient information on the nature of
100
N = 1 183
N = 467
Neoplasms
12.2%
N = 327
Cardiovascular diseases
6.8%
Proportion of total deaths for age groups
90
Digestive system disorders

5.7%
80
Nervous system disorders

13.4%
70
Respiratory diseases
2.1%
60
Genito-urinary diseases
1.4%
I l-defined
Group III
Group II
Group I
50
Endocrine/metabo ic disorders
1.0%
30
20
10
<1
1-5
>5
Age groups (yrs)
Fig. 1. Proportion of deaths within each age group in relation to the 4

Global Burden of Disease categories of causes.
Septicaemia
6.2%
Diarrhoeal diseases
8.2%
Congenital abnorma ities

57.5%
Fig. 3. Non-communicable causes of death at Red Cross Childrens

Hospital from 1999 to 2003 (N = 576)
Meningitis/meningococcaemia
5.4%
Tuberculosis
4.0%
Myocarditis
2.6%
Acute respiratory infections

10.9%
Hepatitis
1.3%
abnormalities 3.0
Respiratory abnorma
Other infection s
1.2%
n
s
966
HIV/AIDS
60.3%
Fig. 2. Infectious causes of death at the Red Cross Childrens Hospital from
1999 to 2003 (N = 1 038).
Fig. 4. Congenital causes of death at Red Cross Childrens Hospital from

1999 to 2003 (N = 331).
ORIGINAL ARTICLES
the trauma to further subclassify these deaths. From the data

available, it appeared that motor vehicle accidents were the
most common form of fatal trauma.
Analysis of the specic causes of death by age group
revealed some clear differences in the mortality proles. HIV
infection was the leading cause of death for children <1 and
1 - 5. In children > 5, it was the third most common cause of
death following injuries and disorders of the nervous system
(largely cerebral palsy). Infectious diseases accounted for
over 60% of deaths in children < 1, 50% in children 1 - 5, but
24% in children > 5. In children < 1, 5 of the top 10 causes of
death were infectious diseases, with HIV infection, ARI and
diarrhoeal disease accounting for just over half of the deaths.
Non-communicable conditions such as neoplasms, nervous
system disorders, and cardiovascular diseases became more
prominent in the older age groups. Injuries did not appear in
the top 10 causes of death for children < 1 yet were the second
most common cause in children 1 - 5 and the leading cause of
death in children > 5.
Admissions to the hospital were particularly high in the
summer and early autumn and lowest in the winter. However,
there was no seasonal pattern in total deaths or the rate of
inpatient death (data not shown). Seasonal uctuation was
observed in two specic categories of death, viz. diarrhoeal
disease and ARI. Deaths due to diarrhoeal disease consistently
peaked in mid-summer to early autumn, with nearly 60% of
these deaths over the 5 years occurring between February
and May. The death rate from diarrhoea per 1 000 hospital
admissions was 3 times as high during these months as in the
other 8 months (3.0 v. 1.0).
Deaths due to ARI exhibited a different pattern, tending to
peak in early winter (May - June), with the lowest incidence
in the late spring and summer (November - January). There
appeared to be a second peak in mortality rates per 1 000
hospital admissions for all respiratory deaths occurring in the
late winter and early spring (August - October) (Fig. 5). This
9.00
Total Infectious Respiratory Deaths

Infectious Respiratory Deaths per 1000 Admissions
8.00
Infectious respiratory deaths

without an underlying cause
7.00
6.00
5.00
.00
3.00
2.00
1.00
r
be
be
em
em
ec
D
ob
N
ov
ct
O
em
er
r
be
st
gu
Se
pt
Au
Ju
ly
ne
Ju
M
ay
ril
Ap
ry
br
ua
ar
Fe
nu
Ja
M
ar
ch
0.00
Month
Fig. 5. Seasonal variation in mortality rate per 1 000 hospital admissions

infectious respiratory diseases.
disappeared when patients at increased risk of respiratory

infection (underlying HIV/AIDS, malnutrition, disorders of the
blood or immune system, cerebral palsy, CHD) were excluded
from the analysis (Fig. 5).
Discussion
This study has shown the value of keeping routine data on
deaths in a hospital. The data were systematically recorded
over 5 years, allowing an analysis that can inform managers,
planners and clinicians. For example, the demonstration that
there is a tripling of in-hospital mortality from diarrhoea in the
summer months requires investigation. The magnitude of the
effect of HIV/AIDS on childhood in-hospital death demands
a response in terms of health resource provision. However,
although this study used both direct and underlying cause of
death, which allowed more detail than the Burden of Disease
studies for South Africa1 and for Cape Town,12 this method is
still limited by the lack of detail on other factors (e.g. health
service factors) that contributed to the deaths. Nevertheless
if simple data such as those collected here were routinely
recorded, valuable information on trends and patterns of
hospital-related deaths would be available. Indeed it is notable
that ill-dened causes of death were considerably fewer than
in other South African death certication studies,7,13 reecting
the potential value of hospital-related mortality data. Simple
guidelines on lling in the second page of the death notication
form have been supplied to most new medical staff at the
RCCH since the late 1990s. These have been reinforced by the
clerical staff responsible for collating the forms.
While the RCCHs large referral base complicates the drawing
of conclusions on the relevance of these data to child mortality
in general, comparison of these gures with a study of
mortality in Cape Town in 200112 shows that 1 in 6 of the 1 845
deaths under the age of 14 years in metropolitan Cape Town in
2001 were registered at the RCCH. Similarly the preponderance
of deaths from the metropolitan areas that refer children with
primary- and secondary-level health problems to the RCCH
enables conclusions to be drawn regarding common causes of
death in childhood in these largely low-income communities.
The leading causes of death in this study are congruent with
the South African and Cape Town Burden of Disease studies,12,14
supporting the potential utility of the RCCH data in drawing
conclusions on mortality in the surrounding population. The
differing rates of perinatal (lower) and congenital (higher)
causes of death reect the RCCHs position in the health care
system.
Causing at least 1 in 3 deaths, HIV/AIDS stands out as by
far the most common cause of death. This gure is likely to
be an underestimate of HIVs role in causing death as to some
extent doctors remained reluctant to certify it as the cause of
death.9,15 The predominance of HIV parallels the ndings of
the Burden of Disease studies of the South African Medical
967
ORIGINAL ARTICLES
Research Council in which HIV accounted for 40% of under-5

deaths.14 This method of collecting data cannot prove that the
children certied as dying of HIV/AIDS and its complications
were indeed infected by the virus since infection was not
conrmed with laboratory assays for the virus, but it is likely
that disease severe enough to kill the children reected true
infection in most cases. Its dominance is a challenge to the
health system to prevent mother-to-child transmission of HIV
and to provide antiretroviral therapy to infected children. In
this way, a considerable impact could be made on infant and
under-5 mortality rates. An increasing proportion of older
children died from HIV/AIDS, a sign of a maturing childhood
epidemic in Cape Town. It is possible that the decrease in
HIV-related mortality in 2003 is indicative of the efcacy of
moves to control this epidemic in the Western Cape. Another
potential explanation for this phenomenon that more patients
were being sent home to die is not supported as there was no
increase in out-of-hospital HIV-related deaths in 2003.
The contribution of malnutrition to mortality will have been
underestimated using this methodology. Only the most severe
forms of malnutrition are likely to have been recorded as causes
of death, and even then only where other severe conditions
were not present. An unpublished study of HIV/AIDS deaths
at the RCCH showed that over half of the children were
severely malnourished (T Westwood and L Henley personal
communication, 2002).
The higher death rate in female children was an unexpected
nding. This phenomenon in HIV/AIDS and CHD, both of
which accounted for a large number of deaths, may simply
reect an inability to demonstrate a similar difference for
less common conditions. The higher mortality among
female children undergoing cardiac surgery for CHD has
been described in California, USA16 but an equivalent risk in
HIV/AIDS has not been described before. This phenomenon
requires investigation.
The demonstration of a distinct seasonal prole for death
rates attributable to diarrhoea and ARI is further proof of the
value of routinely analysing child deaths. The higher death rate
in certain seasons might reect higher acuity or, alternatively,
the inability of the health system to cope with increased
numbers of sick children. The two possibilities would have
different solutions. Further research will be necessary. These
ndings have led to a concerted drive to prevent summer
diarrhoea in children in Cape Town and to improve its
management.
968
Deaths due to injury require further analysis. Injuries

represented a signicant cause of childhood mortality in this
population, especially in the older age groups. The current
system of data collection around injury-related deaths provides
insufcient detail to allow for meaningful clinical or public
health intervention. However, many of the trauma-related
deaths at RCCH have forensic postmortem examinations, so a
system to marry the forensic details with the current mortality
database would allow a more complete assessment of injuryrelated deaths.

Childhood deaths are largely preventable. It is therefore
important to have as much detail as possible on their causes
in order to implement appropriate and timely responses.
Current and sufciently detailed information is therefore
critical. Many approaches are being employed to improve child
mortality information systems in South Africa. The Morbidity
and Mortality approach recommended by the Western Cape
Department of Health is now being implemented at the RCCH.
This is staff-intensive and is not carried out consistently in
all departments. The large number of deaths each month
complicates complete data capture, but the system could be
useful in providing a forum for preventable causes of mortality
to be identied and remedial actions to be taken. A more
extensive approach involving detailed classication of factors
that lead to the death of children who present to hospitals has
been explored in the North West province.6 Further renements
of the methodology are taking place. Its practicality and value
for routine collection in a large urban environment such as
Cape Town have yet to be demonstrated. This study has clearly
demonstrated that, with clinical supervision, the collection and
analysis of simple routine hospital data on childhood deaths
can lead to useful outputs.
We thank Dr Michael Hendricks for reviewing the manuscript
and the Medical Superintendent of the Red Cross War Memorial
Childrens Hospital for permission to publish. A full report on this
study is available from the Childrens Institute of the University of
Cape Town.
References
1. Bradshaw D, Groenewald P, Laubscher R, et al. Initial Burden of Disease Estimates for South
Africa, 2000. Cape Town: South African Medical Research Council, 2003.
2. Bradshaw D, Nannan N, Groenewald P, et al. Provincial mortality in South Africa, 2000
priority-setting for now and a benchmark for the future. S Afr Med J 2005; 95: 496-503.
3. Yach D, Strebel PM, Joubert G. The impact of diarrhoeal disease on childhood deaths in the
RSA, 1968 - 1985. S Afr Med J 1989; 76: 472-475.
4. von Schirnding YE, Yach D, Klein M. Acute respiratory infections as an important cause of
childhood deaths in South Africa. S Afr Med J 1991; 80: 79-82.
5. Zwi K, Pettifor J, Soderlund N, Meyers T. HIV infection and in-hospital mortality at an
academic hospital in South Africa. Arch Dis Child 2000; 83: 227-230.
6. Krug A, Pattinson RC, Power DJ. Saving children an audit system to assess under-5 health
care. S Afr Med J 2004; 94: 198-202.
7. Van der Merwe S, Yach D, Metcalf CA. Peering into the black hole the quality of black
mortality data in Port Elizabeth and the rest of South Africa. S Afr Med J 1991; 79: 419-422.
8. Bradshaw D, Kielkowski D, Sitas F. New birth and death registration forms a foundation
for the future, a challenge for health workers? S Afr Med J 1998; 88: 971-974.
9. Westwood ATR. Childhood deaths due to HIV the role of the new death certificate. S Afr
Med J 2000; 90: 877-878.
10. Murray CJ, Lopez AD. The Global Burden of Disease: A Comprehensive Assessment of Mortality
and Disability from Diseases, Injuries and Risk Factors in 1990 and Projected to 2020. Vol. 1. Global
Burden of Disease and Injury series. Boston: Harvard School of Public Health, 1996.
11. SPSS Version 11.5 Software. Chicago, Illinois: SPSS Inc., 2002.
12. Groenewald P, Bradshaw D, Nojilana, et al. Cape Town Mortality 2001. Cape Town: City of
Cape Town, South African Medical Research Council, University of Cape Town, 2003.
13. Meel BL. Certification of deaths at Umtata General Hospital, South Africa. J Clin Forensic Med
2003; 10: 13-15.
14. Bradshaw D, Bourne D, Nannan N. What Are the Leading Causes of Death Among South African
Children. Medical Research Council. Policy Brief No. 3, December 2003. Cape Town: South
African Medical Research Council, 2003.
15. Bah S. A note on confidentiality of death notification forms. S Afr Med J 2003; 93: 238.
16. Chang RK, Chen AY, Klitzner TS. Female sex as a risk factor for in-hospital mortality among
children undergoing cardiac surgery. Circulation 2002; 106: 1514-1522.
Accepted 10 May 2006.
ORIGINAL ARTICLES
Surgical treatment for brain compartment syndrome in

children with severe head injury
A A Figaji, A G Fieggen, A Argent, J C Peter
Objectives. Traumatic brain injury accounts for a high
percentage of deaths in children. Raised intracranial pressure
(ICP) due to brain swelling within the closed compartment of
the skull leads to death or severe neurological disability if not
effectively treated. We report our experience with 12 children
who presented with cerebral herniation due to traumatic brain
swelling in whom decompressive craniectomy was used as an
emergency.
Outcome measures. Computed tomography (CT) scanning, ICP

control, clinical outcome.
Results. Despite the very poor clinical condition of these
children preoperatively, aggressive management of the raised
pressure resulted in unexpectedly good outcomes.
Design. Prospective, observational.
Conclusion. Aggressive surgical measures to decrease ICP in

the emergency situation can be of considerable benefit; the
key concepts are selection of appropriate patients and early
intervention.
Setting. Red Cross Childrens Hospital.
S Afr Med J 2006; 96: 969-975.
Subjects. Children with severe traumatic brain injury and

cerebral swelling.
Compartment syndrome of the limbs or the abdomen is
a well-known entity in general surgical and orthopaedic
practice, characterised by an increase of pressure within
a musculofascial compartment leading to progressive
neurovascular dysfunction. Although it has not been described
as such, raised pressure within the intracranial compartment is
arguably the most dramatic example of the same pathological
principle, given the rigidity of the cranium and the importance
of its contents. When increasing intracranial volume exceeds
the compensatory capacity of the brain, the ensuing rise of
intracranial pressure (ICP) leads to brain herniation and
cerebral ischaemia. If no intervention is forthcoming, severe
neurological injury or death is inevitable as a consequence of
what is, in essence, a brain compartment syndrome.
sustained at the moment of impact, it is now recognised that

avoidance or early treatment of secondary insults can make a
dramatic difference to outcome in individual patients.2 Of these
secondary insults, raised ICP is the most widely recognised.
In South Africa, traumatic brain injury (TBI) is common

and probably represents an under-appreciated reality in our
society. Traumatic injury accounts for most deaths in children
in the 5 - 15-year-old age group.1 Motor vehicle accidents,
falls and assaults are common causes of injury in children
and it is usually the severity of the head injury sustained that
determines the eventual outcome. Of those who survive severe
TBI, many are left neurologically disabled, placing a significant
burden on the immediate family and State resources. Although
there is little one can do once the primary injury has been
Decompressive craniectomy has been used in various

forms, and for various indications, to manage the problem of
increased pressure within the intracranial compartment. The
rationale for the operation is intuitive the removal of a section
of the cranium enlarges the available space for brain swelling
and reduces the contained pressure therein, thereby preventing
cerebral herniation and allowing blood flow to return to the
brain. Yet despite the apparent simplicity of the principle, it has
remained controversial primarily because of concern regarding
its effectiveness. However, careful analysis of the reported data
reveals likely reasons for the lack of demonstrable benefit in
the earlier literature on the subject.
Divisions of Paediatric Neurourgery and Paediatric Critical Care, School of Child

and Adolescent Health, University of Cape Town, and Red Cross War Memorial
Childrens Hospital, Rondebosch, Cape Town
A A Figaji, MB ChB, Dip Obstet, FCS (Neurosurgery), MMed
A G Fieggen, BSc, MB ChB, MSc, FCS (Neurosurgery)
A Argent, MB BCh, OCH, MMed, FCP
J C Peter, MB ChB, FRCS (Neurosurgery)
Corresponding author: A Figaji (agaji@ich.uct.ac.za)
Space-occupying traumatic haematomas causing raised

ICP are readily removed via emergency craniotomy, thereby
relieving pressure on the brain. However, when the aetiology
of raised ICP is swelling of the brain itself, the management
becomes much more challenging. Medical treatment remains
suboptimal and despite the promise of pharmacological
research to interrupt the biochemical cascades that occur in
severe brain trauma, nothing has been developed as yet that
prevents the development of traumatic brain swelling in
humans.
In our experience with severe traumatic brain injury (TBI)

in children, the use of decompressive craniectomy in carefully
selected patients with brain swelling has produced dramatic
ICP control in patients thought to be herniating. Given the
severity of the clinical problem, the outcome in this series is
surprisingly favourable. In this study we update our early
969
ORIGINAL ARTICLES
results3 with a larger number of patients and long-term

follow-up. Based on our experience and increasing numbers
of favourable reports from other centres, we believe that the
key to the optimal use of the procedure is the identification of
suitable patients, early intervention and the adequate technical
performance of the operation.
Methods and materials

Patients were identified from a prospectively collected
database of decompressive craniectomy operations performed
for traumatic brain swelling (without haematomas) from
September 1999 to September 2005. Collected data included
(among others): mechanism of injury, initial clinical assessment,
radiological findings, ICP readings, neurological deterioration,
extracranial injury, timing of the operation, technical details
of the operation, change in postoperative ICP readings and
radiological findings, and clinical outcome. Outcome was
reported based on clinical assessment at the last neurosurgical
clinic visit and school reports. Craniectomy usually entailed
removing a large part of the hemicranium ipsilateral to the
side of most severe swelling, although in three cases bifrontal
craniectomy was done where both hemispheres were equally
swollen. Expansion of the dura was achieved by the insertion
of a dural graft.
Results
970
Twelve patients had decompressive craniectomy performed for

post-traumatic brain swelling. All had radiological evidence
of brain swelling with obliteration of the basal cisterns on
preoperative computed tomography (CT) imaging. In 11
patients there had been a documented secondary deterioration
in neurological status or refractory rise in ICP that prompted
the decision to operate (Table I). The combination of the
radiological appearance of obliterated perimesencephalic
cisternal spaces, the clinical signs and acute secondary
deterioration was consistent with cerebral herniation. One
patient had previously had an extradural haematoma taken
out via craniotomy, after which he recovered but went on
to develop secondary deterioration with brain swelling. All
of these patients underwent surgery within 12 hours of this
deterioration. In the one exception, there was no secondary
deterioration the decision to operate was made on the
grounds of the poor clinical condition at the outset, swollen
brain on CT, and elevated ICP. This was the only patient who
failed to improve despite surgery. Although ICP control was
achieved, he died on day 3 post trauma. Control of ICP and
clinical improvement was seen in all of the other patients.
Postoperative CT imaging confirmed the reappearance of the
previously obliterated basal cisterns (Fig. 1). Increased brain
oedema beneath the bone flap was not seen on postoperative
imaging in any of the cases. The mean sustained ICP reduction
achieved by craniectomy was 53.5% (range 39 - 61%) in
patients who had both pre- and postoperative ICP monitoring.

This was calculated from the difference between the mean
preoperative ICP readings averaged over 5 hours and the mean
postoperative ICP over 10 hours. The first 6 hours of readings
in the postoperative period were excluded from analysis to
avoid the potential confounding effect of general anaesthesia
in lowering ICP. A longer period for analysis of postoperative
readings was chosen to take into account possible later rises in
ICP.
Outcome
Follow-up for survivors was conducted prospectively at the
neurosurgical clinic with a minimum follow-up period of 1
year; the median duration of follow-up was 35 months (range
1 - 6 years). All survivors had a favourable outcome: 6 patients
had a Glasgow Outcome Score (1 to 5) of 4, and 5 patients
had a score of 5. One patient developed bone flap sepsis after
the bone had been replaced, which required removal of the
flap. Another demonstrated slight subsidence of the flap at
follow-up. Asymptomatic subdural hygromas were observed
in 2 patients. Long-term behavioural disturbances and mild
cognitive deficits were relatively common (Table I).
Discussion
The use of decompressive craniectomy for the relief of
intracranial hypertension was originally described by Kocher
in 1905. Since then, its use in trauma has been surrounded
by controversy. The debate is largely centred on the issue of
whether it is of clinical benefit in TBI, and therefore, whether
its use justifies the additional effort and risk that the operation
may entail. There are also concerns about potential adverse
consequences of cranial decompression, such as the possibility
of increasing cerebral oedema beneath the bone flap, which
may further exacerbate the problem of raised ICP and
compromise tissue perfusion.
Exacerbation of cerebral oedema

In theory, brain tissue that is compressed may develop
increased oedema when the transmural hydrostatic pressure
gradient is reduced by craniectomy, thereby favouring
enhanced vasogenic oedema.4 Of the experimental data
reported, the results from Hatashita et al.5 are of particular
interest. These investigators studied 4 groups of cats 1
control group and 3 treatment groups which were subjected
to: craniectomy alone, induced hypertension alone, and
craniectomy plus induced hypertension. In their experiments,
cerebral oedema after craniectomy occurred only when the
mean arterial pressure was elevated. Enhanced oedema was
not seen in the animals that underwent craniectomy without
induced hypertension. In another experiment, evaluation of
brain water content in 16 cats that underwent craniectomy
compared with 16 controls also showed no increase
ORIGINAL ARTICLES
Table I. Patient data

No.
Age
Initial presentation
Initial imaging
Fall from height.

Initial GCS 5T/15
MVA pedestrian,
GCS 8/15
11
Blunt assault,
GCS 14/15
Cisterns compressed, 2T/15, unilateral unreactive

midline shift 1 cm
pupil, Cushings reflex,
hemiparesis
Small temporal
GCS 5/ 15, unilateral fixed
contusion, cisterns
pupil, hemiparesis
open
Parietal contusion,
GCS 8/15
cisterns open
12
Fall from train,

GCS 10/15
Crush injury (gate),

GCS 5T/15
11
MVA pedestrian,
GCS 5T/15
Fall from height, GCS
8/15, left pupil fixed
11
10
6.5
11
12
MVA pedestrian,
shocked, hypoxic,
GCS 6T/15
Deterioration
Right frontal
contusion, cisterns
open
Temporal contusion,
cisterns compressed
GCS 8/15, bradycardic
Swelling, cisterns
effaced
EDH
ICP uncontrolled
Cisterns open
Gunshot wound,
GCS 13/15
Repeat CT scan
Outcome
Nil
Good outcome.
Behavioural problems.
Slightly sunken flap
Cisterns obliterated Bone flap sepsis, mild
cognitive deficits,
special schooling
Increased swelling, Good outcome
compressed
obliterated
Increased swelling, Good outcome,
cisterns obliterated behavioural change
GCS 4T/15, unilateral fixed Nil

pupil
GCS 5T/15
Mild hemiparesis but

independent, CN III
palsy
Iincreased swelling, Good outcome. Mild
cisterns obliterated cognitive deficits
Cisterns obliterated, Good outcome. Mild
PCA infarct (from hemiparesis and VF
herniation)
defect but independent
GCS 3T/15, pupils fixed

1 cm midline shift,
bilaterally, ICP uncontrolled cisterns obliterated
(50 mmHg), bradycardic
GCS 8/15, pupils bilaterally Nil
unreactive, hemiplegia
Gunshot tract high

parietal, cisterns
compressed
MVA pedestrian (bus), Grossly swollen brain, Nil
Nil
GCS 3T/15, pupils
DAI, depressed skull
bilaterally fixed,
fracture, loss of greyhaemopneumothorax, white interface
extensive facial injuries,
ICP elevated
MVA pedestrian,
Contusions, cisterns GCS 5T/15, brain herniation Nil
GCS 6T/15, unilateral effaced
decompressing through basal
pupil fixed, hypotensive
skull fracture (nose and ears),
ICP uncontrolled
MVA, polytrauma,
Cisterns effaced
GCS 2T/15, pupil unreactive Cisterns obliterated
GCS 10T/15, left
hemiparesis
Good outcome. CN VI
palsy unchanged
Good outcome, no
motor deficits
Died day 3 post-injury
Good outcome but

behavioural
disinhibition
Good outcome.
Mild cognitive deficits
MVA = motor vehicle accident; GCS = Glasgow Coma Score; CN = cranial nerve; EDH = extradural haematoma; PCA = posterior cerebral artery; VF = visual field; DAI = diffuse
axonal injury.
after craniectomy.6 Neither was there any increased fluid

extravasation detected by Evans blue histological staining
in 4 rabbits after craniectomy compared with 3 controls in an
experiment by Rinaldi et al.7
In this current clinical series increased oedema was not
visible radiologically in any of the patients in the postoperative
period. There was also no late increase in ICP that would have
been consistent with increased oedema.
Brain entrapment
Another concern about the operation is the potential for
brain entrapment, which may occur when the oedematous
brain is compressed against the sharp edges of the

durotomy or bone defect, causing venous congestion by
impaired venous drainage. To address this concern, Yoo and
colleagues8 demonstrated no increase in epidural pressure
after craniectomy using a novel air-pouch system, Whitfield9
performed angiography that demonstrated no venous
obstruction, and Jaeger et al.10 and Stiefel et al.11 showed
improved oxygenation of the involved brain segment after
craniectomy. However, we still prefer to employ a large
craniectomy, primarily to maximise the ICP reduction achieved,
but also to dissipate the pressure over a larger surface area so
as to diminish any possibility of brain entrapment. Not only
971
ORIGINAL ARTICLES
972
Fig. 1. A: Initial axial CT scan of patient 6 demonstrating a patent quadrageminal cistern and no signicant brain swelling. B: CT scan of the same patient
after clinical deterioration showing worsening brain swelling with cisternal obliteration; ICP baseline was 40 mmHg with spikes to 90 mmHg despite medical therapy. C: Axial CT scan after bifrontal craniectomy showing re-appearance of the basal cisterns. D: Lateral CT surview demonstrating the extent of the
craniectomy.
ORIGINAL ARTICLES
are small craniectomies ineffective in ICP reduction, they may

well lead to a focus of high pressure against a small defect in
the bone and dura, promoting herniation through that defect
if the pressure remains uncontrolled. In our experience with
adults and children, this is not seen when the decompression is
of adequate size, unless there is unsalvageable refractory brain
swelling.
ICP reduction
The mechanical benefit of decompressive craniectomy is well
documented in the experimental and clinical literature. Because
the cranium represents a non-compliant system and cerebral
perfusion pressure is adversely affected by rising ICP, the
removal of a large bone flap expands the available volume
for brain swelling, increases the compliance of the system
and compensatory capacity of the cerebrospinal fluid axis,
and improves cerebral perfusion.6,12,13 It is also worth noting
the additional benefit obtained by expanding the rigid dura
mater. Yoo et al.8 demonstrated this graphically with an 85%
immediate reduction in ICP after craniectomy: 50% occurred
when the bone flap was removed and a further 35% when
the dura mater was opened and expanded. Other clinical
reports have also confirmed the 2-step reduction in ICP, almost
doubling the benefit with the dural augmentation.10
The mechanical benefits of craniectomy may be even greater
in children, as it has been demonstrated that children have
a lower pressure-volume index than adults, i.e. ICP is more
sensitive to changes of intracranial volume.14
Medical therapy
Although medical therapy is often effective, particularly in
patients who have a less aggressive course of elevated ICP,
the treating physician must be aware of the limitations of the
available options. External ventricular drainage is effective in
reducing ICP by releasing CSF from the ventricular system.
However, in patients with swollen brains the ventricles are
usually effaced and accurate placement of a catheter is often
impossible, the amount of CSF that can be drained is limited,
and the risk of infection with prolonged drainage must be
considered. Mannitol may also be effective in ICP reduction,
but usually for a limited period of time only. Repeated doses
may be associated with extravasation into the brain with
reversal of its effect15 and renal injury has been documented
even without elevated serum osmolarity.16 Hypertonic saline
may be safer than mannitol but fewer data are available on
its use. Barbiturates reduce ICP by decreasing metabolism,
but prolonged weaning from ventilation after discontinuation
and hypotension are common with its use, particularly with
the high doses required to achieve burst suppression on the
EEG.17 Ward et al.18 reported hypotensive episodes in more than
50% of subjects on barbiturates compared with 7% of controls.
This is of particular concern given the strong association of

hypotension with poor outcome.2
Clinical benefit of decompressive

craniectomy
Early studies reported poor results from decompressive
craniectomy in trauma, leading to the initial pessimism
surrounding the operation. However, it was originally
performed only as a salvage operation most of these studies
were limited by the poor clinical grade of patients and the
prolonged period of refractory hypertension that patients were
exposed to prior to surgery. Of 2 patients treated by Clark
et al.,19 one had decerebrate posturing and the other had no
response to painful stimulus; both had bilaterally fixed pupils.
Kerr and colleagues20 also reported 2 patients, both of whom
were decerebrate, one with a unilaterally fixed pupil and
the other with bilaterally fixed pupils. Eighty-nine per cent
of the 73 adults reported by Kjellberg and Prieto21 displayed
decerebrate posturing, with unilateral or bilaterally fixed
pupils, while 11 of 13 patients reported by Venes and Collins22
had evidence of brainstem dysfunction at the time of surgery.
All of the 50 head-injured adults reported by Cooper et al.23 had
acute subdural haematomas and all but 2 were in a premorbid
state, demonstrating decerebrate posturing and/or pupillary
abnormalities in fact, 23 had bilaterally fixed pupils and 27
had absent corneal reflexes. It is probably true that most of the
patients in these series suffered severe primary brain injury, for
which any radical therapy would probably fail to show benefit.
By contrast, favourable outcome has been reported in more
recent clinical reports.24-26
Complications and outcome

The complication rate in this series is low. One case of bone
flap sepsis required removal of the flap. Another showed
slight subsidence of the flap at follow-up. Behavioural
disturbances were common at follow-up and preoperative
signs such as hemiparesis and oculomotor palsy were not
completely reversed by surgery in all cases. However, given
the overall outcome and considering that avoidance of death
and severe neurological morbidity was probably a benefit of
this aggressive approach, these are considered relatively minor
problems.
Clinical outcome
Although TBI is a heterogenous condition, a number of factors
can be used to predict clinical outcome. The Glasgow Coma
Score is perhaps the most common of these. Marshall et al. 27
analysed the outcome of 746 patients with severe TBI from
the Traumatic Coma Data Bank (TCDB), including all patients
with an initial GCS of 8 or less, or who had deteriorated to
this level within 24 hours. Overall mortality was 36%. They
973
ORIGINAL ARTICLES
further analysed outcome according to a novel classification

of diffuse injury by CT criteria (Table II). For patients with
grade III swelling the mortality was 34%, while 23% remained
vegetative and 27% had a severe disability. Only 16% had a
favourable outcome. Of those with grade IV injury, 56% of the
patients died, 18% were vegetative, 18% were left with a severe
disability, and only 6% had a favourable outcome.
Table II. Classification of diffuse injury from the
Traumatic Coma Data Bank (TCDB)27
Grade
CT features
I
II
No visible intracranial pathology

Cisterns present with midline shift of
0 - 5 mm and/or no high- or mixeddensity lesion greater than 25 cc
Cisterns compressed or absent with
midline shift of 0 - 5 mm
Midline shift greater than 5 mm
Any lesion surgically evacuated
High- or mixed-density lesion greater
than 25 cc, not surgically evacuated
III
IV
Evacuated mass lesion
Non-evacuated mass
lesion
Loss of pupillary reactivity is also a strong indicator of

outcome. From the TCDB data, 47% of patients who had a
unilateral unreactive pupil and 82% of those with bilaterally
unreactive pupils died or were in a vegetative state at
discharge. Pupillary abnormalities also appear to be associated
with compression of the basal cisterns, which is unsurprising
given the significance of the perimesencephalic cisterns as a
feature of transtentorial herniation.28 Complete obliteration of
the cisterns has been shown to be associated with unilateral
or bilateral pupillary abnormalities in 75% of cases.29 These
authors also found that outcome in 96% of their cases could be
predicted by a combination of CT findings (brain parenchymal
lesions and state of mesencephalic cisterns) and clinical
findings (motor score and pupil abnormalities).
Finally, the association of raised ICP and poor outcome has
been well documented. Outcome is worse in patients with
persistently raised ICP as well as those who suffer secondary
neurological deterioration with raised ICP.
974
Taking these various factors into consideration, the

favourable outcome in this cohort of patients is unexpected.
All patients fulfilled the TCDB criteria for analysis. All met
the criteria for grade III or grade IV swelling. Six patients
had one unreactive pupil, 3 had bilaterally unreactive pupils,
and 5 patients had a GCS of 4 or less prior to surgery. With
the exception of one patient, each demonstrated a secondary
deterioration in clinical condition or ICP control that prompted
the decision to operate. The mean sustained ICP reduction
achieved by craniectomy was 53.5% in patients who had both
pre- and postoperative monitoring. There were no late rises
in ICP or CT evidence of increasing oedema after surgery.
Postoperative CT scans of all the patients demonstrated
patency of the previously obliterated basal cisterns. The
absence of severely impaired survivors argues against the

potential criticism that aggressive therapy leads to poor quality
survival.
Outcome in children compared with

adults
Although it is often thought that outcome after TBI in children
is better than in adults, reported data are not consistent on this
issue. Important potential confounding factors are the inclusion
of elderly patients in the adult group (a cohort of patients
in which the mortality is known to be significantly higher)
mechanism of injury (e.g. cerebral gunshot wounds in adults),
and evaluation of outcome. The data from the largest published
series in children reflects a surprisingly high mortality figure
for children. Johnson and Krishnamurthy30 reported the results
of a survey of 5 level 1 trauma centres in the US and compared
outcome after severe TBI of 4 041 children with that of 14 789
adults. The overall mortality rate for children in the study
was 36.5%; no hospital reported a mortality rate less than
30% and for patients who were referred indirectly, i.e. via a
local hospital, the mortality was as high as 50%. The authors
contend that mortality rates between adults and children are
similar if selection bias and confounding factors are excluded.
In their comparison of childhood and adult mortality after TBI
sustained in motor vehicle accidents, there was no significant
difference.
Another feature of childhood head injury often quoted is
the predominance of cerebral hyperaemia as a cause of brain
swelling. On this basis it has been claimed that raised ICP
in children responds better to medical therapy. Although
earlier reports seem to suggest this, more recent data have
not upheld this contention.31 Finally, although brain plasticity
is often considered a mechanism by which children may
recover better than adults, this is potentially countered by
the early vulnerability of the developing brain. The extent to
which either of these factors is more significant in a particular
individual may be impossible to determine.32
Interpretation of results
Although the outcome was favourable in this series of patients,
these results cannot necessarily be extrapolated across the
spectrum of head injury in children. With the exception of the
one patient who died, all patients in this series were selected
because the primary injury was thought to be salvageable,
but had been compounded by the secondary contribution of
raised ICP. This is key to understanding the effectiveness of
the operation despite the poor preoperative condition. In these
patients, uncontrolled raised ICP rather than the primary injury
was considered to be the prime determinant of mortality. This
situation should be clearly distinguished from patients who
present with a devastating primary brain injury that is unlikely
to be consistent with meaningful outcome. These patients
often present with posturing and pupillary abnormalities at
ORIGINAL ARTICLES
the outset, CT signs of severe brain injury and initial elevated

ICP. Depending on the circumstances it may be inappropriate
to pursue aggressive strategies in this group. In the one patient
who died, the severity of the primary injury was probably
not consistent with meaningful survival, given the fact that
the Glasgow Coma Score was 3T/15, both pupils were fixed
and the brain was grossly swollen at the outset. In retrospect
perhaps this patient should not have been treated aggressively.
Equally, there is a population of head-injured patients with a
less aggressive course of raised ICP in whom medical therapy
is effective and who therefore do not require surgery. The
decision regarding optimal treatment should take all of these
factors into account.
There are a few limitations to this study that should be
considered. First, because surgical treatment of raised ICP was
not specifically compared with continued medical treatment
it is impossible to categorically claim that decompressive
craniectomy is superior to medical treatment, even in these
highly selected patients. Unfortunately, randomisation of
patients in this context is extremely difficult, where the
difference in outcome may well be survival or death. Only
one randomised trial of decompressive craniectomy has been
done.26 The authors of this study made a valiant attempt to
randomise patients between surgical and medical therapy,
but the study was limited by slow patient recruitment, small
numbers and a very conservative operative strategy. Still, the
authors reported reduced ICP in the surgically treated group
and improved outcome. There is now strong support, even in
the Brain Trauma Foundation Guidelines, for the feasibility
of performing trials of decompressive operations in the first
instance, as opposed to second- or third-tier therapy for posttraumatic intracranial hypertension.33
Another limitation of this study is the lack of preoperative
ICP monitoring in all of the patients undergoing craniectomy.
Although it can be questioned whether one can confidently
diagnose raised ICP from clinical status and CT imaging, the
diagnosis is upheld in this setting where all patients who
had not been monitored had neurological deterioration with
cisternal obliteration on CT prior to surgery which improved
after craniectomy. The decision to operate on these patients
as an emergency was made on the basis of the clinical and
CT findings of cerebral herniation with the rationale that
delay in effective ICP reduction would lead to death or severe
neurological impairment.
In conclusion, we believe that aggressive treatment of
secondary insults after brain trauma can have a dramatic
impact on outcome. The control of ICP is critical and treatment
must be individualised according to the clinical circumstances.
In the appropriate setting, decompressive craniectomy can
achieve dramatic control of ICP and result in surprisingly good
outcomes, sometimes even in dire circumstances. A multicentred randomised trial of decompressive craniectomy in
adults is now under way, initiated by Cambridge University
(www.rescueICP.com). Given the favourable pressure-volume

index and the relatively higher incidence of diffuse injury in
severe TBI, we would recommend a similar trial in children.
References
1. Bradshaw D, Bourne D, Nannan N. What are the leading causes of death among South
African children? MRC policy brief No. 3, Dec 2003.
2. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in
determining outcome from severe head injury. J Trauma 1993; 34: 216-222.
3. Figaji, AA, Fieggen AG, Peter JC. Early decompressive craniotomy in children with severe
traumatic brain injury. Childs Nerv Syst 2003; 19: 666-673.
4. Cooper PR, Hagler H, Clark WK, Barnett P. Enhancement of experimental cerebral edema
after decompressive craniectomy: implications for the management of severe head injuries.
Neurosurgery 1979; 4: 296-300.
5. Hatashita S, Koike J, Sonokawa T, Ishi S. Cerebral edema associated with craniectomy and
arterial hypertension. Stroke 1985; 16: 661-668.
6. Hatashita S, Hoff JT. The effects of craniectomy on the biomechanics of normal brain. J
Neurosurg 1987; 67: 573-578.
7. Rinaldi A, Mangiola A, Anile C, Maira G, Amante P, Ferraresi A. Hemodynamic effects of
decompressive craniectomy in cold-induced brain edema. Acta Neurochir Suppl 1990; 51: 394396.
8. Yoo D, Kim D, Cho K, Huh P, Park C, Kang J. Ventricular pressure monitoring during
bilateral decompression with dural expansion. J Neurosurg 1999; 91: 953-959.
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management of posttraumatic intracranial hypertension. Br J Neurosurg 2001; 15: 500-507.
10. Jaeger M, Soehle M, Meixensberger J. Effects of decompressive craniectomy on brain tissue
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hemicraniectomy for the treatment of refractory intracranial hypertension. J Neurosurg 2004;
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12. Hase U, Reulen H.-J, Meing G, Schurman K. The influence of the decompressive operation
on the intracranial pressure and the pressure-volume relation in patients with severe head
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13. Shapiro K, Fried A, Takei F, Kohn I. Effect of the skull and dura on neural axis pressurevolume relationships and CSF hydrodynamics. J Neurosurg 1985; 63: 76-81.
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15. Kaufman AM, Cardoso ER . Aggravation of vasogenic cerebral edema by multiple-dose
mannitol. J Neurosurg 1992; 77: 584-589.
16. Gondim F de A, Aiyagari V, Shackleford A, Diringer MN. Osmolality not predictive of
mannitol-induced acute renal insufficiency. J Neurosurg 2005; 103: 444-447.
17. Roberts I. Barbiturates for acute traumatic brain injury. Cochrane Database Syst Rev 2000; 2:
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18. Ward JD, Becker DP, Miller JD, et al. The failure of prophylactic barbiturate coma in the
treatment of severe head injury. J Neurosurg 1985; 62: 383-388.
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craniectomy in children with traumatic brain injury and sustained intracranial hypertension.
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Accepted 4 July 2006.
975

Surgical Treatment For Brain Compartment Syndrome

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ORIGINAL ARTICLES

Liver transplantation at Red Cross War Memorial Childrens

The liver transplant programme for infants and children at Red

The liver transplant programme for infants and children at Red

C W N Spearman, MB ChB, FCP (SA), MMed (Med)

Corresponding author: C W N Spearman (wendy@uctgsh1.uct.ac.za)

September 2006, Vol. 96, No. 9 SAMJ

donors, the 1-year patient survival is 90% and the projected

the adult programme had become established at Groote Schuur

Patients and methods

Table I. Indications for liver transplantation

been previously described in detail.1-3 Fifty-three reduced-size

September 2006, Vol. 96, No. 9 SAMJ

cephalosporin is given at anaesthestic induction, repeated

spontaneously. Four patients developed postoperative GIT

CMV infection and disease. CMV infection is endemic in

September 2006, Vol. 96, No. 9 SAMJ

(range 3 - 30 months post transplant). Eight had typical acute

With the introduction of aggressive antiviral prophylactic

Accepted 28 June 2006.

September 2006, Vol. 96, No. 9 SAMJ

Deaths at Red Cross Childrens Hospital, Cape Town

Objectives. The availability of cause-specic mortality data for

Knowledge of the causes of childhood death in a population

Corresponding author: Tony Westwood (westwood@ich.uct.ac.za)

September 2006, Vol. 96, No. 9 SAMJ

15.9 to 18.4 per 1 000 admissions from 1999 to 2002, declining to

of death certication by allowing recording of the direct

unit (ICU), receive referrals from southern, central and western

September 2006, Vol. 96, No. 9 SAMJ

Table I. Number and proportion of deaths by year and age

*Age unknown for 1 patient.

Fig. 2 shows the infectious causes of death. HIV/AIDS

Cerebral palsy constituted more than 75% of the nervous

Proportion of total deaths for age groups

Digestive system disorders

Nervous system disorders

Age groups (yrs)

Fig. 1. Proportion of deaths within each age group in relation to the 4

Congenital abnorma ities

Fig. 3. Non-communicable causes of death at Red Cross Childrens

Acute respiratory infections

Fig. 4. Congenital causes of death at Red Cross Childrens Hospital from

the trauma to further subclassify these deaths. From the data

Total Infectious Respiratory Deaths

Infectious respiratory deaths

Fig. 5. Seasonal variation in mortality rate per 1 000 hospital admissions

September 2006, Vol. 96, No. 9 SAMJ

disappeared when patients at increased risk of respiratory

Research Council in which HIV accounted for 40% of under-5

Deaths due to injury require further analysis. Injuries

September 2006, Vol. 96, No. 9 SAMJ

database would allow a more complete assessment of injuryrelated deaths.

Accepted 10 May 2006.

Surgical treatment for brain compartment syndrome in

Outcome measures. Computed tomography (CT) scanning, ICP

Design. Prospective, observational.

Conclusion. Aggressive surgical measures to decrease ICP in

Setting. Red Cross Childrens Hospital.

S Afr Med J 2006; 96: 969-975.

Subjects. Children with severe traumatic brain injury and

sustained at the moment of impact, it is now recognised that

In South Africa, traumatic brain injury (TBI) is common