Background and purpose

Stroke is a leading cause of death and neurological disability in adults, and imposes a heavy emotional and financial burden on the family and society. We carried out this study to describe the epidemiological pattern of stroke at the Obafemi Awolowo University Teaching Hospitals Complex, Ile-Ife and also to describe the risk factors, the computerized tomography (CT) scan findings and the outcome of stroke in our practice setting.


We prospectively studied one hundred and thirty five consecutive patients presenting to the neurology unit of the Obafemi Awolowo University Teaching Hospitals Complex, Ile-Ife over a six year period (2000- 2005). The socio-demographic and clinical data as well as the CT scan findings were collected. Statistical analysis was done using SPSS version 11.0.


The 135 patients comprised 76 male and 59 female with a mean age of 62+ 12years. The major risk factors were hypertension and diabetes mellitus. Cerebral infarction was the most common subtype of stroke seen. The case fatality rate was 15.6% and among the survivors the outcome was poor as only 3% made full recovery.


Stroke is still a major problem and the major predisposing factor remains uncontrolled hypertension. The case fatality was very high and there is a risk of moderate to severe neurological disability among the survivors. The utilization of CT scan is sub-optimal even when it is available because of financial constraints. CT scan is recommended for all cases of stroke for definitive diagnosis and timely as well as accurate management.

Key words: Stroke, Clinical profile, computerized tomography scan, Nigerians.



Les accidents vasculaires cérébraux (AVC) causent une mortalité et un handicap importants dans la population adulte entraînant également une forte charge émotionnelle au sein des familles et de la population.


Nous avons mené une épidémiologique sur la configuration des AVC à l’université Obafemi Awolowo Teaching Hospitals Complex, Ile-Ife


Nous avons étudié cent trente-cinq patients de manière consécutive à l’université Obafemi Awolowo Teaching Hospitals Complex, Ile-Ife, sur une période de six ans (2000-2005). Les données socio-démographiques ainsi que celles du CT-scan ont été recueillies. L’analyse statistique a été réalisée à l’aide du SPSS version 11.0


Parmi les 135 patients, 76 étaient de sexe masculin et 59 de sexe féminin avec une moyenne d’âge de 62+12 ans.Les facteurs de risque prédominant étaient l’hypertension artérielle (HTA) et le diabète. L’infarcissement cérébral était observé le plus fréquemment. Le taux de mortalité était de 15.6% et parmi les survivants seuls 3% avaient eu une récupération complète.


Les AVC restent un problème majeur de santé en rapport avec un mauvais contrôle de l’HTA. Le taux de mortalité est très élevé et la morbidité variable. Le CT-scan est sous utilisé compte tenu des contraintes financières. Son utilisation devrait être la règle.

Mots Cles : Accident vasculaire cérébral, Afrique, Epidémiologie, Hypertension artérielle, Nigéria, Scanner


Stroke, defined by the World Health Organization as “rapidly developing signs of focal or global disturbance of cerebral or intracranial neuronal function with symptoms lasting for more than 24 hours or leading to the death of the patient with no apparent cause other than that of vascular origin”17 is a major cause of death worldwide, second only to ischaemic heart disease8. Stroke is the leading cause of neurological disability in adults5, 18. Stroke is also a leading cause of morbidity and mortality in adults in the productive ages that contribute the work force of the society6.

The hospital frequency of stroke at the University College Hospital Ibadan in 1969 was between 0.9 and 46% of all hospital admissions and 41% of all neurological admissions10. There appears to be an increase in the hospital frequency of stroke as a recent review at the University College Hospital Ibadan, 30 years later showed that stroke is now the leading cause of adult neurological admissions16. Stroke is increasingly becoming a major cause of morbidity and mortality in Nigeria and other developing countries19. Stroke has thus become a major public health problem in Nigeria.

Stroke patients suffer from post stroke depression, a complication which occurs in 30% of cases19 and is associated with increase in morbidity and reduced survival14, 3. Apart from the burden of stroke on the survivors, those who care for them are also prone to emotional distress and a reduced quality of life. In a recent study at out center, the primary care givers of stroke patients were observed with higher rates of anxiety and depression and a lower quality of life when compared with matched controls2.

With the increasing availability of computerized tomography scanners (CT scan) in most facilities including ours, the stroke sub-type can now be more accurately determined. The need to do CT scan was further highlighted in a study by Ogun et al7 in which the accuracy of clinical assessment was about 70% even in tertiary centers with many neurologists.

The major risk factors for stroke in Nigerians are hypertension, diabetes, and hyperlipidaemia10. Cerebral infarction is the most common type of stroke seen occurring in 48% of patients while intracerebral haemorrhage occurs in 15.7% of patients and subarachnoid haemorrhage in 11.3% of patients11, 1.

The mortality and severity of stroke is on the decline in developed countries because of life style modification, increased use of preventive measures such as adequate blood pressure control, increased use of anti- lipid drugs and aspirin15. This is in contrast to the increasing hospital frequency noted in our environment thus having a great burden on the health facilities in Nigerian hospitals.
This study aims to find out the clinical profile of stroke in Ile-Ife, Nigeria where no previous study of such has been carried out. We also want to determine the subtype of stroke, activity at onset, risk factors and outcome of stroke patients in our hospital.


The study was a prospective hospital based study conducted at our centre which is a referral centre for about six out of the thirty-six states in the country. All the patients with diagnosis of stroke presenting to the Neurology unit of the Obafemi Awolowo University Teaching Hospitals Complex, Ile- Ife over a six year period (2000 to 2005) were consecutively recruited. Stroke was diagnosed using both clinical criteria and brain CT scan findings.
Clinical and demographic information were recorded using a structured questionnaire. CT scan of the brain was carried out using the Siemens Somaton A.R.T. Scanner (3rd generation) machine. All the patients with non-stroke pathology on CT scan were excluded from the study.
Statistical analysis was done using the SPSS 11.0 Software package. The profile of the patients, stroke sub- type and activity at onset were reported in percentages.


One hundred and thirty five stroke patients were managed during the 6-year study period. Stroke was responsible for 2.9% (135/4583) of all medical admissions and 22% (135/615) of all neurological admissions in our centre.
There were 76 male and 59 female patients studied, with a male to female ratio of 1.3:1. The ages ranged between 35 and 90 years with a mean of 62+ 12years. Over half of the patients affected were between 51 and 70years. A third of the patients were businessmen and civil servants while another third were retirees (Table 1).

The major predisposing factors noted were hypertension, diabetes mellitus and heart disease (atrial fibrillation) accounting for 73%, 16% and 2% respectively. Over half of the hypertensive patients (53.6%) were non-compliant with their drugs prior to the episode while 7% were previously unaware of their hypertensive status.

The duration of symptoms before presentation ranged between 1 and 336 hours with a mean duration of 23 hours (SD 39). The duration of hospital admission ranged between one and 63 days with a mean of 10 days (SD 13).
In about a third of the cases (25.6%), stroke occurred on waking up from sleep while 16.3% occurred while the patients were sitting down. The other activities at onset which were peculiar to intracerebral haemorrhage were driving, while preaching, during an argument, coming back from night vigil, during sexual intercourse and while defecating. The other activities and stroke type is shown in table 2. Two thirds (66.7%) of the patients were conscious at presentation. The GCS at presentation were < 8 in 21 cases (15.6%); 9-12 in 19 patients (14.1%); 13-14 in 20 cases (14.8%). The rest had GCS of 15. The speech was normal in 58 cases (43%). Aphasia occurred in fifty-five cases (41%) with majority of these (96%) having motor aphasia. One case each had sensory and global aphasia. In 22 cases the speech could not be assessed because the patients were unconscious at presentation. An upper motor neuron involvement of the 7th nerve (82%) was the most common cranial nerve involvement. This is followed by combined 7th and 12th nerve involvement in 4% of the cases. The 3rd cranial nerve was involved in 3% of the cases. Fifteen (12%) of the cases had no cranial nerve involvement. The majority of the cases were right handed 134 (99%), thus dominant hemisphere involvement presenting with right hemiplegia occurred in 66% of the cases, while left hemiplegia was present in 32%. Upper limb monoplegia was present in 4 cases (3.0%), while 7 cases (0.05%) had quadriparesis. Hemianaesthesia was demonstrated in only 7 cases (5%) while the sensation was normal in 71 cases (53%). In 57 cases (42%) sensory involvement could not be demonstrated because of altered level of consciousness and aphasia. The most common type of stroke by clinical diagnoses was cerebral infarction 94 (70%). 49 patients (35.3%) had CT scan done of which cerebral infarction was the most common finding (53.1%). The other findings were intracerebral haemorrhage (34.7%) and others such as atrophy and hydrocephalus in 12.2% figure1. The 30 day outcome using the Glasgow outcome score is as shown in Table 3. Only 4 cases (3%) made full recovery without any neurological deficit. Two cases ended up in persistent vegetative state due to the use of a combination of antihypertensive drugs (nifedipine, alpha-methyldopa and hydralazine) given at onset of stroke from the referral center. DISCUSSION

Stroke is undoubtedly an important disease worldwide and emerging as a public health problem in many nations. In our environment, the incidence of stroke in the community and the country is largely unknown since most studies in the country are hospital based. Even then a trend is seen as the hospital data shows progressive rise in the cases of stroke. Most authors believed that the hospital data is just a tip of the iceberg when compared to what may be seen in the community. Studies to determine the epidemiology of stroke in the community including the rural areas are therefore necessary to plan the prevention of stroke as well as manage the scarce resources in the treatment of the disease8. In this study, stroke accounted for about a quarter of the patients managed in the neurology unit of our centre during the six year period. In total, 135 patients that fulfilled the criteria were managed. The mean age was 62years (SD12) with a peak in the 5th and 6th decades of life (Table 1). This is in keeping with the findings of previous workers6, 11 where majority of the patients with stroke are in their fifth and sixth decades of life. We also noted a slight male preponderance (M:F = 1.3:1), also supporting findings in other studies and from community based studies16. Many studies showed that the male patient appear to have enhanced risk, especially for thrombotic strokes4. The higher prevalence of stroke in males might be due to the higher presence of cardiovascular risk factors in them. Also many of the males are in the upper social class and business men constantly exposed to stress and more likely to adopt a western type diet with consumption of refined, high cholesterol foods in combination with a sedentary lifestyle resulting in increased prevalence of cardiovascular risk factors such as hypertension, diabetes and hyperlipidaemia19.

Our study like others in the country shows that thrombotic strokes were the most common11, 1. It is important to note that despite the availability of CT scan in our centre; only a third of the patients could afford the test. This clearly shows that cost is a major hindrance to the utilization of CT scan among stroke patients in Nigeria. This is a major problem that needs to be addressed as surgically treatable lesions such as glioma, meningioma, brain abscess and sub-dural haematoma could be mis-diagnosed as stroke in 8.6 to 13.5% of the cases3. At our centre, about twenty patients were excluded from the study as the CT scan showed surgically treatable lesions. This underscores the need for the attending physician to take a very good history of the events at onset of the stroke; however this may not be enough as it is sometimes difficult to differentiate medical from surgical conditions based on the clinical features alone without the aid of imaging modalities. The case of a 46year old long distance driver who slumped while taking his bath and hit his head aptly illustrates this point. He was being managed by the neurosurgical unit for head trauma and was to be taken for exploratory burr hole, when the relations were able to do a CT brain scan which showed massive intracerebral haemorrhage with intraventricular involvement Figure 2.

All our patients save one were right handed, two-thirds of them had dominant hemispheric lesion with right hemiparesis. In a recent review of 450 cases in 20years by Onwuekwe et al9, their findings were similar to ours. The male to female ratio was 1.27:1 ant the mean age of their patients was 53.5yrs. They however found that their patients had almost equal distribution of right and left hemiparesis. They also found no significant difference between handedness and the sex of their patients.
Many studies have shown that hypertension is a major risk factor for stroke. Hypertension predisposes to various types of strokes especially the haemorrhagic type. Hypertension is a dominant risk factor in our study. All the patients with haemorrhagic stroke and presenting with coma were hypertensive and in more than half of these patients, the hypertension was not well controlled. Also 7% of the cases were unaware of their hypertensive status. The fact that some of our patients did not know their blood pressure status and many of those who knew did not have good blood pressure control implies that a lot needs to be done in increasing the awareness of the populace on regular blood pressure control and particularly to ensure drug compliance. Other predisposing factors identified were diabetes mellitus, hyperlipidaemia and heart disease (atrial fibrillation). Factors such as sickle cell disease, younger age, obesity, anaemia, dehydration, malnutrition, infections and congestive heart failure which were noted by Osuntokun were not documented or diagnosed in many of our patients13. The case fatality of 15.6% is low when compared with that from Ibadan and Lagos11, 1. It is also low when compared with a case fatality of 17% from the Oxfordshire community stroke study in the UK15. Our study is hospital based and patients with severe stroke might have died at home or on the way to the hospital. However, when outcome from our own study is compared with that from Oxfordshire, it is poorer as majority of our cases had disabling stroke (Table 3). In Oxfordshire, the incidence of major disability stroke has reduced over 20yrs because of increased use of preventive treatment such as aspirin, antilipids, antihypertensive and reduction in alcohol consumption and cigarette smoking15. At our centre, we manage these patients in the intensive care unit. The unit is ill equipped with very limited facilities especially for monitoring the patients. Management in stroke units is ideal and should be goal of every centre involved in the management of stroke patients.

There were two cases of persistent vegetable state following cerebral infarction. One, a 48year-old woman (Figure 3a & 3b) with multiple infarcts had rapid reduction of her blood pressure at the secondary care center where she subsequently lapsed into coma prior to referral to our centre. This is a common practice by general practitioners with limited knowledge of the pathophysiology and treatment of stroke. Since majority of the patients will be attended to initially by this group of doctors, they need regular updates on the emergency care of stroke so as to improve the outcome of patients. Better still, they should be more actively involved in preventive programmes to detect risk factors and increase awareness generally.

In conclusion, stroke is still a major problem in our environment and the major risk factor remains uncontrolled hypertension. The case fatality remains very high with a risk of moderate to severe neurological disability among the survivors. There is sub-optimal utilization of CT scan even when it is available because of financial constraints. We recommend that community based intervention measures such as health education of the community with emphasis on control of the predisposing factors, and education of general practitioners who are usually the first to handle stroke patients be put in place to address the burden of the problem and the inadequate control of blood pressure among hypertensive patients. The primary health workers should also be educated and trained to pass across information to the populace at every available opportunity the advantages of exercise, maintaining a healthy weight, avoid or quit smoking and monitoring of blood pressure and glucose levels regularly. There is also the need for pubic enlightenment campaigns to educate the populace about the need to check their blood pressures regularly and if hypertensive to comply with their medications. Efforts to make radiological imaging test available and affordable should be pursued both by the government and public institutions as well as by non governmental organisations.

Table 1: Socio-demographic profile of stroke patients in Ile-Ife (N=135).

Age Range Male n=79 (%) Female n=59(%) Total N=135
31-40 3(75.0%) 1(25.0%) 4
41-50 11(52.3%) 10(47.6%) 21
51-60 26(63.4%) 15(36.6%) 41
61-70 22(51.2%) 21(48.8%) 43
71-80 9(47.4%) 10(52.6%) 19
81-90 5(71.4%) 2(28.6%) 7
Retiree 18(50.0%) 18(50.0%) 36
Civil servants 24(72.7%) 9(27.3%) 33
Petty traders 5(16.7%) 25(83.3%) 30
Farmers 8(61.5%) 5(38.5%) 13
Artisans 13(100.0%) 0(0%) 13
Businessmen 8(88.9%) 1(11.1%) 9
Housewives 0(0%) 1(100.0%) 1

Table 2: Activity at onset of stroke patients in Ile-Ife (N= 135)

Activity Infarction N (%) Haemorrhage N (%)
Waking up from sleep(n=48) 44(8.3%) 4(8.3%)
At work (n=24) 13(51.1%) 11(45.8)
Sitting down (n=33) 18(81.8) 4(18.1%)
Coming from the bathroom (n =13) 8(61.5%) 5(38.5%)

Others: During an argument (1), coming from night vigil (1), during defecation (1), during sexual intercourse (1), while preaching (2), while fetching water (1), while driving (2), and unknown (6).

Table 3: Stroke outcome in Ile-Ife.

Glasgow Outcome Score N (%)
Good outcome 8(5.9%)
Moderate disability 74(54.8%)
Severe disability 27(21.0%)
Persistent vegetative state 2(1.5%)
Died 21(15.6%)
Total 132*

* 3 cases discharged against medical advice

Figure 1

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Neurological Development in french speaking African Countries


Connus des neurochirurgiens depuis très longtemps comme une complication du traumatisme crânien, les hématomes intra-cérébraux post-traumatiques (HICT) sont rares. Facilement diagnostiqués au scanner ou à l’IRM, ils sont trop souvent considérés comme banaux, alors que la littérature fait encore état de nombreux points flous tant sur le plan diagnostique, que sur le plan physio-pathologique ou encore sur celui des traitements à adopter (traitement médical, chirurgical ou mixte).


1 – C’est une définition anatomo-pathologique :

Un hématome intra-cérébral post traumatique (HICT) est une collection de sang à l’intérieur d’un foyer lésionnel remplissant plus des 2/3 de ce foyer, le reste étant constitué de tissu cérébral lésé et de zones d’hémorragies microscopiques [3, 4, 13]. C’est ce qui le distingue des contusions parenchymateuses dans lesquelles la quantité de sang reste bien moindre par rapport à la fraction tissulaire et où du tissu nécrotique est centré sur une hémorragie péri-vasculaire [3].

Le scanner a modifié les idées sur l’hématome intra-cérébral : longtemps considéré comme une lésion tardive (48 heures), on sait maintenant que l’HICT se constitue en réalité de façon précoce : dès la 6eme heure pour Ruiz-Sandovall, le plus souvent dans un délai compris entre 8 heures à treize jours voire plus avec une moyenne de deux jours [13, 23].


1 – Physiopathologie des hématomes intra-cérébraux post-traumatiques

Deux mécanismes traumatiques peuvent être à l’origine d’un hématome intra-cérébral :

– un choc très violent avec rupture de vaisseaux profonds en regard d’une contusion corticale extensive quelle que soit la région cérébrale touchée . Cela d’autant que l’impact s’est produit sur une petite surface crânienne, dans le cas entre autres des plaies tangentielles par arme à feu ou par arme blanche et des fractures de la voûte crânienne avec enfoncement dans le parenchyme (les plaies crânio-cérébrales sont exclues de cette étude).
– le «contre-coup» classique par choc direct entre cerveau et structures vulnérantes de la boîte crânienne (sphénoïde, clivus, os frontal, ptérion, faux du cerveau et tente du cervelet), sachant cependant qu’au niveau du tronc cérébral, l’hémorragie post traumatique reste exceptionnelle. C’est ainsi que les hématomes se développent préférentiellement au niveau des zones polaires (pôle frontal, base du lobe frontal, pôle et face externe du lobe temporal).

Si ces mécanismes expliquent la présence des hématomes intra-cérébraux post-traumatiques sur le scanner effectué immédiatement après le traumatisme, il ne peuvent par contre pas rendre compte des hématomes d’apparition secondaire (24 à 72 h) qui pour Ninchoji et col. [20] présentent des aspects particuliers :

– les mécanismes sont souvent dynamiques (tête en mouvement),
– la plaie si elle existe n’est pas forcement grave,
– les signes cliniques sont d’apparition lente et insidieuse,
– la majorité des patients ont une fracture de la base du crâne ou de la voûte crânienne associée,
– l’apparition de l’hématome intra-cérébral survient dans les 72h dans la plupart des cas,
– le pronostic est souvent défavorable,
– la présence d’une contusion cérébrale initiale est le facteur majeur contribuant à l’apparition des hématomes intra-cérébraux tardifs.

Différents facteurs étiologiques ont donc été évoqués, la plupart expliquant la constitution secondaire d’une plaie vasculaire :

– l’hypoxie, souvent présente dans le traumatisme crânien, peut provoquer une accumulation locale CO2 dont le pH acide engendre une hémorragie péri-vasculaire par vasoplégie suivie d’une vasodilatation secondaire avec diapédèse.
– la perte de l’auto-régulation avec augmentation de la pression intra-vasculaire.
– l’existence d’une coagulopathie post-traumatique peut également contribuer à
l’apparition de ce genre de lésions.
– la transformation de foyers de contusions iso-denses passées inaperçues au scanner initial en foyers hémorragiques secondaires (Tsukokawa)

– la stase veineuse avec œdème vasogénique secondaire (Czernickiz), comme dans le cas des hématomes survenant après chirurgie décompressive (évacuation d’un hématome extra-dural, hématome sous-dural ou suite à un volet décompressif).

Par contre, l’hypothermie longtemps discutée comme facteur favorisant des HICT , n’est en rien responsable, comme l’a démontré Resnick [21].

Au plan évolutif l’hématome intra-cérébral se développe souvent en deux phases :

Une phase initiale brève d’hypertension intra-crânienne proportionnelle au volume et à la rapidité de constitution de l’hématome, suivie au bout d’une semaine environ d’une deuxième phase dite «impansive», correspondant à la mise en jeu des mécanismes tampon de la pression intra-crânienne (compression des structures veineuses et augmentation du débit veineux jugulaire, mise en jeu des villosités arachnoïdiennes de la queue de cheval) au cours de laquelle la pression baisse rapidement.

Si donc l’hématome n’est pas massif et n’implique pas un risque vital ou si un traitement palliatif (drainage ventriculaire externe ou traitement médical) a été rapidement mis en route et se révèle efficace sur les chiffres de pression intra-crânienne, le patient franchira la période aiguë et pourra donc éviter une intervention. C’est sans doute ce mécanisme qui rend compte du petit nombre d’opérations nécessaires.

Le tableau 1 résume les différents mécanismes physiopathologiques (isolés ou associés) décrits dans la genèse des HICT [14].

Tableau 1 – Mécanismes physiopathologiques

Phénomènes « mécaniques » – Décompression chirurgicale par une autre lésion
– augmentation du volume disponible
– suppression d`un effet « tampon  »
– variation rapide de la pression et du volume intracrânien provoquant des lésions des petits vaisseaux, une mobilisation des caillots, une modification du calibre des vaisseaux et donc une hémorragie .
– Sérum hypertoniques. Leur prescription par voie veineuse peut entraîner les mêmes conséquences que la décompression chirurgicale
– Congestion veineuse. L`hyper pression dans les veines(ventilation mécanique, broncho-pneumopathie) peut entraîner des suffusions perivasculaire autour des petits veines encéphaliques
– Rupture secondaire d`un anévrysme traumatique.
Phénomènes nécrotiques, enzymatiques et biochimiques – Nécrose tissulaire du foyer lésionnel y compris les parois artérielles
– Destruction ou ouverture des parois vasculaires par libération de radicaux libres et accumulation de peroxydases, fragilisation des parois et hémorragies
– Augmentation de la perméabilité et hémorragies perivasculaires par accumulation de CO2(pH acide) ou hypoxie
Phénomènes « réflexes » pariétaux – Perte de l`autorégulation des parois avec hémorragies autour des vaisseaux et accumulation de sang(soit spasme, soit dilatation des vaisseaux)
– Traitement anticoagulant
– Coagulation intravasculaire disséminée
– Antécédents de troubles de la coagulation

2 – Prévalence des hématomes intra-cérébraux post-traumatiques

La survenue d’un hématome intra-cérébral dans les suites d’un traumatisme crânien est relativement rare. Sa manifestation peut être aiguë mais le plus souvent c’est dans les jours qui suivent l’accident que l’on constate l’apparition de l’hématome. La répétition des examens tomodensitométriques est donc capitale.
Pour Soloniuk et col. [24], 20 % seulement des hématomes intra-cérébraux post-traumatiques sont présents sur les scanners post-traumatiques initiaux : 35 % sont détectés dans les 24 premières heures et 80 % dans les 72 heures.
Beaucoup de cas ne justifient pas d’un traitement chirurgical. Avant l’apparition du scanner le nombre d’HICT opérés était de 3% des patients hospitalisés pour traumatisme crânien [5, 6], alors qu’il n’est plus que de 0,55% [7, 8] depuis l’utilisation systématique de cet examen.


1 – les aspects évolutifs habituels des HICT

Les hématomes intra-cérébraux se distinguent par la diversité des symptômes observés dépendant à la fois de la taille de l’hématome, de sa localisation et de la rapidité de sa formation. Parmi les manifestations cliniques fréquentes on retrouve notamment :

– la dégradation progressive de l’état de conscience souvent au dessus de 8 dans la phase initiale exprimée selon le score de Glasgow.
– l’apparition ou l’aggravation de troubles moteurs
– l’existence de crises comitiales assez souvent focalisées.

Même s’il est classique d’affirmer qu’il peut s’aggraver brutalement par engagement, cette évolution est une éventualité plus rare (3%) que dans les suites d’hématomes extra-duraux ou sous-duraux aigus (82%) selon Andrews et col. [1] et survient surtout dans les localisations temporo-pariétales qui peuvent se compliquer de compression du tronc cérébral.

Dans certains cas, la constitution de l’hématome est tardive, au bout de plusieurs semaines et se caractérise alors par l’apparition brutale d’un déficit neurologique, selon le tableau de « Splät apoplexy » décrit par Bollinger [4] en 1891.

Quoiqu’il en soit, précoce ou tardif, le diagnostic d’HICT repose sur le scanner et sa répétition selon le protocole actuellement mis en place dans les services de neurochirurgie.

2 – Les aspects particuliers

a – étiologiques

Toutes les variétés de traumatisme peuvent être à l’origine d’hématomes intra-cérébraux. Les accidents de la circulation avec impact crânien direct prédominent chez les sujets jeunes, alors que les chutes ou les accidents domestiques atteignent plutôt
les sujets âgés.

L’âge est un facteur classique, l’hématome intra-cérébral étant une conséquence des traumatismes crâniens survenant après 50 ans. Il existe d’ailleurs à ce propos une relation inversement proportionnelle entre l’importance de l’impact crânien et l’âge du patient.

Certaines pathologies peuvent modifier l’aspect clinique et surtout l’évolution spontanée
des hématomes intra-cérébraux. Dans la plupart des cas, il s’agit de pathologie préexistantes de la crase sanguine : coagulopathies en rapport ou non avec un éthylisme chronique, thrombopénies d’origines diverses ou thrombopathies de consommation tels que l’on peut en voir chez des patients polytraumatisés multi-transfusés.

Enfin, le sida peut par son retentissement sur la coagulation avoir une incidence aggravante dans les cas d’HICT.

b – topographiques

Comme nous l’avons déjà signalé, l’hématome intra-cérébral est généralement situé dan
entre le cerveau et les structures osseuses (face interne du sinus frontal, ptérion, petite aile du sphénoïde, clivus).

On peut cependant l’observer également dans les régions profondes de la substance blanche de l’encéphale au contact des noyaux gris centraux et dans cette localisation il se rapproche des hémorragies spontanées de l’adulte.

Les hémorragies intraventriculaires que l’on pensait rares et systématiquement mortelles avant le scanner sont en réalité présentes dans une proportion de 3 à 10% des traumatismes crâniens mais gardent souvent le pronostic péjoratif qu’on leur prêtait auparavant. Elles surviennent dans les cas de traumatismes crâniens très violents (accidents de moto) et sont souvent associées à d’autres lésions corporelles. Elles sont en général responsables de troubles d’emblée graves de la conscience (score de Glasgow < 8), en rapport avec une hypertension intra-crânienne aiguë par gêne à l'écoulement du liquide céphalorachidien imposant en urgence un monitoring de la PIC et un drainage ventriculaire externe du LCR réalisés en un seul temps opératoire. Si l'HIC est la règle dans 50% des cas, l'hydrocéphalie est par contre peu fréquente, l'HIC étant de trop brève durée pour dilater les cavités ventriculaires. La fosse postérieure est une localisation rare qui se caractérise par une somnolence, des troubles d'idéation, suivis rapidement par des troubles de la conscience qui peuvent s'aggraver brutalement par engagement des amygdales cérébelleuses au niveau du trou occipital. Cette dernière complication impose plus que dans toute autre localisation un monitorage combiné de la PIC et de la PIV.avec drainage ventriculaire externe. c – évolutifs

La répétition des examens TDM dans les suites des traumatismes crâniens a permis de vérifier que les H.I.C.T. peuvent exister aux différents moments de l’évolution. Ils peuvent s’observer sur le scanner initial ou au contraire apparaître de façon plus ou moins tardive alors que le premier examen TDM était normal ou ne montrait que des images de contusion. Dans cette deuxième hypothèse le scanner a pu permettre de vérifier que l’H.I.C.T. pouvait se former secondairement par confluence de plusieurs pétéchies, puis évoluer progressivement soit vers la stabilisation, soit vers l’augmentation de volume, généralement sans œdème associé.

Il semble donc illusoire sur un plan théorique de classer les H.I.C.T. en hématomes immédiats et hématomes retardés selon la classification anglo-saxonne, puisque en réalité, ils peuvent survenir à n’importe quel moment de l’évolution d’un traumatisme crânien (dans les 10 à 12 premiers jours).

Fukamachi [14] a cependant proposé une classification qui tient compte de ces problèmes et a séparé les HICT en 4 types basés sur son expérience tomodensitométrique dans 84 cas :

– Type I : hématome toujours présent sur le scanner initial (moins de 6 heures) : 39%,
– Type II : hématome petit et augmentant de volume sur les scanners successifs :11%,
– Type III : hématome dans lequel, le scanner à l’admission ne montre aucune image pouvant faire soupçonner la constitution ultérieure de la lésion ( 24%),
– Type IV : hématome dans lequel le scanner initial trouve une image « poivre et sel » ou une petite flaque de haute densité à l’endroit où siégera la lésion (26%),

Seuls les types III et IV, représentant 50% des cas peuvent être qualifiés d’hématomes tardifs.


Figure 1 – contusion hémorragique temporale gauche au J1 posttraumatique

Figure 2 – transformation de la contusion en HICT au J2, discret effet de masse,

Figure 3 – important œdème perilesionnel au J6 du traumatisme – intervention chirurgicale a cause de l’aggravation clinique

Figure 4 – J2 postopératoire, évolution favorable de l’imagerie et de la clinique


Au scanner, les hématomes intra-cérébraux se distinguent de l’attrition par leur topographie en général plus profonde, leur hyperdensité plus nette et mieux limitée, l’absence ou la discrétion initiale de l’œdème périphérique. Ils prennent la forme de flaques plus ou moins arrondies, aux bords quelquefois « en carte de géographie » quand l’hématome a pris naissance au sein d’une contusion cérébrale.
Le moment d’apparition n’influence pas l’aspect de ces lésions, mais peut conduire à rechercher l’existence d’une malformation vasculaire (IRM, artériographie) lorsque la constitution est tardive par rapport à l’accident.

Dans leur localisation profonde, au contact des noyaux gris, l’aspect est celui de taches hyperdenses à bords nets et précis sans œdème périphérique traduisant le « cisaillement » des artères perforantes qui en est la cause.

Les hémorragies intraventriculaires ont une densité variable selon la quantité de sang présente dans le LCR et donnent donc des aspects variant de l’hyperdensité modérée à des formations très hyperdenses traduisant la présence de caillots qui déforment la structure ventriculaire tendant à prendre un aspect « soufflé » et arrondi.

Au plan évolutif, du fait de la lyse progressive des caillots, ces images varient autant
en forme qu’en densité au cours des examens TDM répétés. S’associent ainsi dans
le temps des images d’hypodensité traduisant l’aspect séquellaire, cicatriciel de ces lésions. Cet aspect est également vrai pour les hémorragies ventriculaires dans lesquelles le LCR participe au « lavage » des caillots (réalité physiologique puisque le LCR diminue la coagulabilité sanguine), faisant ainsi apparaître des images modifiées d’un examen sur l’autre, quelquefois associées, chez les patients non décédés, à une hydrocéphalie conséquence des perturbations de l’hydraulique du LCR.

L’IRM n’est pas couramment pratiquée à la période aiguë des traumatismes crâniens.
Elle apporterait cependant selon certains auteurs un élément prédictif précoce de la transformation des contusions en hématomes secondaires lorsqu’elle permet d’objectiver en T2 des zones hyper-intenses au sein même du foyer contus.

Les autres examens n’apportent aucun élément intéressant dans le diagnostic d’HICT, hormis l’EEG qui doit toujours être pratiqué pour rechercher des crises focales ou un état de mal épileptique, difficilement décelables chez les patients hospitalisés en réanimation.


1 – Les éléments à prendre en compte

Il n’existe toujours pas de consensus sur les critères conduisant au traitement chirurgical, en effet de nombreux éléments doivent être pris en compte dans cette décision tels que la profondeur et la localisation de la lésion, l’état clinique initial, l’évolution clinique et radio-scannographique, l’âge du patient, ses pathologies pré-existantes, etc…

Il faut cependant souligner que les recommandations chirurgicales fixent une indication opératoire formelle aux hématomes responsables d’un déplacement de la ligne médiane ≥ à 5mm ainsi qu’à ceux entraînant une HIC menaçante pour la vie du patient.

2 – Les méthodes médicales

Compte tenu des critères que nous venons de décrire, Il est évident que tous les HICT ne méritent pas une évacuation. Il faut d’ailleurs remarquer à ce propos que l’intervention s’impose beaucoup plus rarement en cas d’hématome intra-cérébral (4 à 5% environ selon les séries) que dans les autres variétés d’hématome intra-crânien traumatiques.
Le traitement médical n’est pas spécifique de ce type de lésion ayant pour objectif la lutte contre l’HIC, le dysfonctionnement du tronc cérébral et les crises comitiales.

Il doit être réalisé sous monitoring de la PIC, des pressions artérielle et veineuse centrale et de la pression de perfusion cérébrale (PPC). Il associe généralement :

– Le drainage ventriculaire externe de liquide céphalo-rachidien .
– l’hyperventilation
– les osmotiques (le mannitol ou mieux le sérum salé en prêtant attention à l’effet rebond)
– les anticomitiaux (en utilisant de préférence les médicaments associant l’effet cérébro-protecteur et anticomitial tels les hydantoïnes)
– la neurosédation et les barbituriques (Thiopental, GammaOH ®, Midazolam, Fentanyl)
– Une mention particulière doit être réservée à la corticothérapie qui bien qu’ayant prouvé son inefficacité à travers de nombreuses études [22, 9, 18], continue malheureusement à être largement prescrite).

3 – Les méthodes chirurgicales

La mesure de la PIC avec drainage externe réalisée au bloc opératoire et par opérateur entraîné à cette pratique constitue un moyen de surveillance inégalable des traumatismes crâniens graves.

La ponction stéréotaxique ou par voie endoscopique a été décrite par certains pour évacuer ces lésions mais la craniotomie ouverte reste actuellement la meilleure technique en usage [2, 19].

Un petit volet de craniotomie ou à défaut un trou de tréphine réalisés généralement sous magnification optique et avec l’aide d’écarteurs malléables, en prenant soin de traverser le minimum de substance cérébrale, seront le plus souvent suffisants pour diminuer le volume de l’hématome et son effet de masse. Signalons, à ce propos, la découverte exceptionnelle de malformations artério-veineuses responsables du saignement dans les parois de la cavité opératoire.

La décompression sous temporale pour traiter l’HIC, après avoir été abandonnée
connaît à nouveau un regain d’intérêt à la suite du travail de Gower [15] pour lequel la mortalité par HIC réfractaire passerait de 82% à 40% grâce à l’utilisation de cette méthode.


Chaque patient victime d’un traumatisme crânien grave avec présence d’un hématome intra-cérébral post-traumatique sur le scanner, doit être hospitalisé dans une unité de réanimation.

Le monitoring de la pression intra-crânien doit être systématique dès que le score de Glasgow < ou = 8. L‘indication d'évacuation d'un hématome intra-cérébral post-traumatique dépend des critères suivants :
1 – aggravation de l’examen clinique,

2 – évolutivité des images TDM

3 – augmentation de la pression intra-crânienne,

4 – absence de réponse au traitement médical,

5 – engagement sur le scanner cérébral ≥ 1 cm,

6 – dans le cas des hématomes intra-cérébraux temporaux un volume ≥ 30 CC et/ou un diamètre ≥ 3 cm, sont des indications de chirurgie urgente du fait du risque important d’engagement,

7 – selon les recommandations pour la pratique clinique, un hématome intracérébral ou une contusion hémorragique d’un volume supérieur à 15ml avec déplacement de la ligne médiane supérieur à 5mm et oblitération des citernes de la base devrait être évacué le plus rapidement possible

8 – l’apparition tardive d’un hématome intra-cérébral avec aggravation clinique doit également être considérée comme une urgence chirurgicale, surtout s’il est temporal, eut égard aux risques de décompensation plus importants vers un engagement dans cette localisation

9 – l’évacuation de l’hématome s’il est situé dans une zone silencieuse doit s’accompagner de l’ablation complémentaire du parenchyme cérébral manifestement contus adjacent.

Par contre doivent bénéficier d’un traitement médical sous monitoring de la PIC et
de la PPC avec examen clinique et TDM répétitifs :

1 – les patients présentant des hématomes intra-cérébraux post-traumatiques envahissant les noyaux gris centraux et le thalamus,

2 – les malades présentant des petits hématomes intra-cérébraux post-traumatiques dont l’examen clinique initial est normal et qui ne relèvent pas d’une indication chirurgicale dans les premières heures.

3 – les patients présentant des hématomes intra-cérébraux multiples, sauf si une des lésions est manifestement responsable des phénomènes de compression.

La lobectomie peut être préférable dans certains cas à l’évacuation d’un hématome ou d’une contusion (à la condition qu’elle intéresse la région traumatisée, siége de l’hémorragie).

La crâniectomie décompressive semble être utile à la phase aiguë du traumatisé crânien grave dans des situations extrêmes d’hypertension intracrânienne non contrôlée « refractaire ».


L’évolution et le pronostic des patients victimes d’un hématome intra-cérébral post-traumatique dépendent de plusieurs facteurs et en particulier de :

– la taille, la localisation de l’hématome et sa date d’apparition
– la présence ou l’absence d’autres lésions cérébrales,
– la gravité de l’état neurologique initial,
– la prise en charge du patient (unité de réanimation),
– l’âge du patient et ses antécédents personnels.

La morbidité est importante de l’ordre de 33 à 35% des cas.

Le taux de mortalité moyen est de 25 et 30 % des cas, mais peut atteindre 50 % chez les patients victimes d’un traumatisme crânien sévère et qui développent un hématome intra-cérébral secondaire (Crooks, Hirsch) [11, 17].

Compte tenu de l’absence d’études réellement validées, l’avis des différents auteurs diverge à propos des résultats de la chirurgie comparés à ceux du traitement médical, puisque certains estiment que le recours à une intervention améliore la morbi-mortalité alors que d’autres pensent que les résultats sont identiques [6, 7].

Le tableau 2 résume les différentes études réalisées et leurs principaux résultats.

Ninchoji et col – 1984

Etude de 25 cas d`hématomes
– représentent 32% des traumatismes crâniens
– 50% de décès – 76% de mauvais résultats
Cet auteurs ont étudié une série d`hématomes « retardés » et insistent sur la localisation des secondaires basée sur les signes hématomes au sein des contusion, avec pronostic clinique et TDM péjoratif
Soloniuc et col – 1986

Etude de 35 cas de H.I.C.T. repartie selon leur date d`apparition en 4 catégories. Posent le problème critères opératoires
– 20% d`hématomes immédiats(0-3 h)
– 6% d`hématomes intermédiaires(3-6 h)
– 29%d`H tardifs(6-24h)
– 49% d`H très tardifs(>24h)
– 49% de décès au cours de la 1-ere année

Mortalité par H.temporal(57%) > H.frontal(37%)
L’étude montre que le délai d`apparition des hématomes est tes variable, que le scanner est un mauvais facteur prédictif de la survenue des hématomes.
Le pronostic est péjoratif.
Bullock et Col – 1992

Etude de 43 patients porteurs d`hémorragies intra-ventriculaire
– Mauvais resultats 33%
– Bons et myoens resultats : 67%
– Identiques chez les patients operée ou non operée
– PIC>30mmHg chez 46% des patients
– Pas de raport direct entre taille/localisation de l`H. et etat neurologique
– Le critere pronostic le + meilleur est la PIC
L’étude prouve que la PIC est un des meilleurs facteurs pronostic. Pour cet auteur les résultats globaux sont identiques avec ou sans intervention.
Leroux et col – 1992

Etude de 42 patients porteurs d`hémorragies intra ventriculaires
2.8% des traumatismes crâniens age de 7 à 83 ans

40% de décès ou mauvais résultats
L’étude prouve que ces hémorragies sont rares, que leur pronostic est péjoratif mais moins mauvais que décrit au paravent. L`évolution hydrocephalique est rare.


Au total l’hématome intra-cérébral post-traumatique est une lésion qui demeure rare dans les suites de traumatisme crânien, dont le pronostic est toujours sévère, avec une morbidité de l’ordre de 33 à 35% des cas, une mortalité moyenne de 25 et 30 %, pouvant cependant atteindre les 50% et dont les critères de surveillance sont la réalisation répétée de l’examen clinique, des examens TDM (volume de l’hématome, état des citernes de la base) et le monitoring de la PIC et de la PPC.

Une minorité (# 5%) de ces hématomes nécessite une intervention chirurgicale, mais le consensus n’existe pas sur les critères opératoires, d’autant que certains auteurs estiment qu’elle n’améliore pas le pronostic global.



A 45 year-old man with periodic muscular weakness is presented. He had 4 similar transient generalized weakness epizodes since the age of 38. His initial evaluation showed mild proximal weakness with no clinical or electrical myotonia. The serum potassium level was 2.7 mEq/lt. He showed dysmorphic features with short stature, a hypoplastic mandible, hypertelorism, low set ears, micrognathia, bilaterally short index fingers, broad forehead. His three children had almost the same dysmorphic features
His cardiological examinations including echocardiography, holter monitoring and electrocardiograpy were normal. Hypokalemic challenge test with intravenous glucose (2gm/kg) followed 30 minutes later by insulin (0.1 unit/kg intravenously) resulted in no change in muscle strength despite a drop in serum potassium from 4.3 to 3.7 mEq/lt. Potassium challenge was not performed, because of danger of fatal cardiac complications.
With these clinical, radiological and laboratory findings, the patient was diagnosed as Andersen Syndrome.

Key words : Potassium, dysmorphic features, weakness, Andersen syndrome


In 1971, Andersen et al [1] described an 8-year-old boy with a distinct syndrome marked by clinical triad of PP, cardiac dysrhythmia and developmental anomalies named as Andersen syndrome (AS).
AS includes severe cardiac involvement and skeletal anomalies, such as short stature, low-set ears, hypoplastic mandible, clinodactyly, scoliosis, hypertelorism, micrognathia, short index fingers, broad forehead, prognathism, cleft palate, high arched palate [8]. The importance of recognizing the syndrome lies in the frequent occurence of cardiac involvement. This varies from a prolongation of the QT interval through ventricular tachycardia to fatal cardiac arrest [9].

The attacks are often superimposed on a background of generalized weakness. The inheritance pattern appears to be autosomal dominant with significant phenotypic heterogeneity. The mutations affect a potassium channel, called Kir 2.1-a member of a large family of potassium channels that help regulate the flow of potassium out of muscle cells [5].


A 45-year-old man with periodic, sudden onset, generalized weakness is presented. From his detailed history, it was learned that he had 4 similar transient generalized weakness epizodes since the age of 38. The epizodes were of variable duration from 1 to 3 days and were either spontaneous or induced by prolonged inactivity or following meals and rest after exercise. There was no family history of systemic or neurological illness except his fathers’ death of hearth failure at age 38.

Physical examination of the patient revealed prominent dysmorphic features such as hypoplastic mandible, hypertelorism, low-set ears, micrognathia, broad forehead [figure1], bilateral short index fingers [figure 2] and short stature. Also similar dysmorphic features were recognized from his father’s photograph [figure 3]. He had 3 children and their physical examination also revealed almost the same but milder dysmorphic changes [figure 4,5,6]. The patient’s blood pressure and pulse rate were normal. On neurological examination cranial nerves were intact. Generalized proximal muscle weakness with more prominent in lower extremities was found. Tendon reflexes were decreased, sensation was normal. There was no clinical myotonia.

Full blood counts and biochemical examinations were performed and no abnormality was seen except the potassium level. His initial potassium level was 2.7 mEq/lt. After infusion of 1000 cc Isolyte M solution (includes 0.15 g potassium) to the patient in 24 hours’ time, potassium level increased to 4.5 mEq/lt. And then his neurological examinations became to normal state. Cardiac examinations including electrocardiography (ECG), echocardiography and Holter monitoring were unremarkable. Brain and spinal cord magnetic resonance imaging were normal. Electromyography (EMG) of limb muscles showed no evidence of myotonia. Muscle biopsy from deltoid muscle, showed mild myopathic findings with chronic denervation.

Hypokalemic challenge with intravenous glucose (2 gm/kg) followed 30 minutes later by insulin (0.1 unit/kg intravenously) resulted in no change in muscle strength despite a decrease in serum potassium from 4.3 to 3.7 mEq/lt. Potassium challenge was not performed, because of danger of fatal cardiac complications.
The physical, neurological, clinical and laboratory findings of the patient was thought to be compatible with the diagnosis of Andersen Syndrome and Acetazolamide treatment was given to the patient.


Andersen’s syndrome is characterized by periodic muscle paralysis, cardiac arrhythmia and abnormal growth that includes short stature, and deformations of the spine, fingers, toes and face [6]. Weakness occurs episodic, lasting one hour to days, attacks may be rare though some patients may have persistant generalized background weakness, onset from early childhood to anytime in adulthood. The beginning of the attacks in our patient was at the age of 38. It was slightly a long time for the occurence of the symptoms.

Hypokalemia, potassium administration, exercise are the precipitants for attacks or it may be idiopathic. In AS, potassium shifts during attacks of weakness are inconsistent.
Clinical recognition of this syndrome is vital given the predisposition for cardiac dysrhythmia and sudden death. Cardiac evaluations using serial ECG’s with measurements of the QTc interval are essential and should be performed early on all patients undergoing work up for periodic paralysis (PP) [9]. As alteration in serum potassium may aggravate cardiac arrhytmias in AS, provocative testing for hypo or hyperkalemic PP in AS patients must be applied if they do not have a contraindication [4].

Recognition of the characteristic face in AS permits an early diagnosis and the detection of the severe systemic manifestations associated with the syndrome. Severity of the facial involvement does not correlate with the the severity of heart or muscle involvement [2].

The patient’s electrophysiological examination included nerve conduction study and electromyography (EMG) exclude the presence of myotonia and muscle biopsy showed mild myopathic findings with chronic denervation. In periodic paralysis muscle biopsy may show a wide range of abnormalities, vacuoles being more specifically linked to the disease. Frequency or severity of attacks did not correlate with the presence of vacuoles but those were more easily found in patients with long term disease [10]. Vacuoles and tubular aggregates are frequent changes in PP and therefore helpful for the diagnosis. Important myopathic findings in the muscle biopsy suggest a permanent myopathy which probably developes after severe crises or long term disease [7].
AS is relatively rare and there have been no standard protocols for the treatment. The carbonic anhydrase inhibitors cause only mild hypokalemia and may therefore be preferable to the thiazide diüretics for the control of periodic weakness. The arrhythmias are more difficult to treat because of their lack of the response to antiarrhytmic agents [3].
Patients who have experienced a cardiac arrest or who continue to have syncope in spite of medication are candidates for an implantable defibrillator or pacemaker [4]. Our patient did not have cardiac symptoms and we preferred Acetazolamide for this clinical entity. During one-year follow up period, no PP attacks were seen and his general condition remained good.


The clinical diagnosis of AS is not always apparent and physicians should be aware of the possible physical, clinical manifestations and laboratory findings; because early diagnosis and treatment may reduce the risk of potentially lethal cardiac dysrrhytmias.

Figure 1

Figure 1

Figure 2

Figure 2

Figure 3

Figure 3

Figure 4

Figure 4




For a century since the first cerebrospinal fluid (CSF) shunt surgery was performed, ventriculoperitoneal (VP) shunts insertion for the treatment of hydrocephalus has been routinely done. Complete migration of the entire VP shunt is extremely rare in clinical practice but do occur and this case is to illustrate one of such.


Case report


VP shunt procedures have come to stay and will remain with us despite recent advances such as the endoscopic third ventriculostomy. A lot of common and rare complications following this procedure have been reported in 24-47% of the cases. Care should be taken to prevent all complications whether common or rare by paying particular attention to patient selection, shunt selection, and surgical details.

Keywords: Ventriculoperitoneal shunt, Hydrocephalus, Endoscopic third ventriculostomy, Shunt catheter.

Mots cles: Complication, Hydrocéphalie, Intraventiculaire, Shunt ventriculo-péritonéal


Cerebrospinal fluid (CSF) shunt operation was first realized in 1908 by Kausch [7] and since then ventriculoperitoneal (VP) shunts have remained the main method of treating hydrocephalus even with the recent increased interest in endoscopic third ventriculostomy. Although VP shunt procedures are easy to perform they are not without complications, adequate management of which may require further surgical procedures. These complications are many ranging from the very minor ones to major complications. Most often, despite appropriate surgical techniques, careful attention to operative details, strict compliance with asepsis and the use of prophylactic antibiotics to prevent or reduce the common complications that may follow VP shunt insertion, some complications still occur, some very unusual and rare [6]. One of these rare complications is complete proximal migration of the entire VP shunt system.

Migration of the shunt or its parts have been reported but usually it is the distal or the peritoneal catheter that migrates after breakage or disconnection into many locations such as the scalp, heart, anus/rectum, urethral, knee, umbilicus, chest, pleural cavity, inguinal canal and scrotum [3].

Complete or total migration of the shunt as a whole is very rare and few cases are described in the literature. Distal migration rather than proximal shunt migration is more common and presumed to be due to intestinal peristalsis which may pull down the shunt. We aimed to present in this brief communication an unusual and a rare complication of Ventriculoperitoneal shunt placement which is total upward migration of the entire VP shunt system into the ventricular system of a child. The mechanism, management, and possible preventive methods are discussed.


AO is a 4year-old boy who first presented to our neurosurgical service at the age of five months with progressive hydrocephalus. VP shunt was advised but the parents refused until the child was 3years old due to poor milestone development and gross head enlargement. A right occipital VP shunt was inserted with satisfactory result. A year after, he presented with recurrent symptoms of active hydrocephalus and raised intracranial pressure associated with visual impairment. Examination revealed that the part of the VP shunt proximal to the shunt valve could not be palpated. This was confirmed by the shunt series, shuntogram, and computerized tomography (CT) brain scan which shows shunt disconnection proximal to the shunt valve with the ventricular catheter lying in the right lateral ventricle. There were no clinical features of sepsis and CSF culture did not yield any organism. A new shunt system was inserted with the aid of artery forceps leaving the detached ventricular catheter in situ. During the second shunt surgery, attention was placed on technical details so as to prevent recurrence of the complications, however the patient came back four weeks later with fever, vomiting, gross malnutrition and obtundation. This time no part of the VP shunt could be palpated along its entire length. A repeat shunt series shows the entire VP shunt system in the right lateral ventricle (Figure 1). CT scan was not done due to financial constraints. Sepsis screen did not yield any organisms but the patient was placed on, ceftriaxone. He later had limited craniectomy to retrieve the VP shunt system and the previously detached ventricular catheter. An external ventricular drainage was left in place to monitor and prevent excessive rise in the intracranial pressure until a new shunt could be placed. There was no improvement in his clinical and neurological status until three weeks later when his parent requested for discharge against medical advice. He presented once to the surgical out-patient clinic but had since been lost to follow-up.


Complete proximal migration of the entire VP shunt system is a well known complication though very rare in occurrence as few cases had been reported in the literature [10, 5]. This upward migration involves patient motion that creates a “windlass” effect with no resistance to the movement of the tubing and also requires a potential space such as the subgaleal or the ventricular spaces for the shunt to migrate to. Why this occurs in some patients is not known. A lot of factors had been attributed for the possible mechanism underlying this rare complication. These include the negative sucking intraventricular pressure, the positive pushing intraabdominal pressure and the tortuous subcutaneous track as well as neck movements. Other factors are related to the patient, the surgical technicalities and to the shunt itself.

The patient related factors includes the age of the patient, severe and gross hydrocephalus with very thin cortical mantle, malnutrition, anaemia, sepsis, and repeated head movements and rotation (Bobble-head syndrome). Many of these predisposing factors were present in our patient who had a gross head enlargement with very thin cortical mantle. The patient presented also was malnourished and anaemic. The supine position in which the infants are nursed as well as the shorter distance between the ventricular and the peritoneal ends in these children facilitate proximal migration of the shunt. In all the cases reported in the literature all were infants and young children except Eljamel [5] that reported a case in an adult. This may not be unusual as majority of VP shunt are carried out in this age groups. In addition to the predisposing factors in this patient, we found out that the parents were constantly tampering with the shunt system at the region of the shunt valve, and thus likely to dislodge the shunt from the underlying tissues.
The shunt related factors that have been found to contribute to this complication are a unisystem type of shunt in particular a valveless type and without an intervening reservoir. In our environment, the Chhabra shunt systems are used due to availability and low cost. These shunt systems have a valve with an incorporated reservoir but the valve is cylindrical with a diameter just larger than the shunt tubing itself. Warf [8] in his paper compare the outcomes between the Chhabra and the Codman-Hakim micro precision shunt systems and found no significant difference in the outcomes or complications. This is also corroborated by Adeloye [1] who devised and used the Malawi shunt for treating hydrocephalus in Malawi children. In their series they noted only two cases of shunt disconnection though the operations were routinely performed by the consultant and assisted by the residents.
Surgical technique related factors includes repeat surgery, previous surgery with or without complications, use of forceps instead of shunt passer which result in extensive subcutaneous dissection, inadequate fixation of the shunt especially to the pericranium, and the use of straight in the place of angulated connector. Majority of the cases in the literature as well as our patient had this complication after a repeat surgery and usually about a month to three months after. In some cases the upward migration may be due to peritoneal scarring and cyst formation because of poor CSF absorption, the resultant pressure in the cyst tends to eject the catheter into the fibrous tract that surrounds it. The migrated shunt system can be extracted from the ventricle through a small craniectomy [10]; however this can also be carried out with minimal morbidity via the endoscopes. Whitfield et al [9] reported the safe removal of retained ventricular catheters using intraluminal choroids plexus coagulation, a technique which was successfully used in 12 patients with 13 blocked and adherent ventricular catheters. This approach also minimizes the risk of life-threatening intraventricular haemorrhage.

This complication can be prevented by careful attention to surgical details particularly if performed by an experienced surgeon [1], careful patient selection, use of shunt with bulbous shunt valves and/or reservoirs, use of burr hole cover [4] to prevent the upward migration through the burr hole defect especially when large burr hole is made, and use of frontal burr hole site [3] with a small but preferably a cruciate rather than a linear dural incision to access the ventricle rather than other sites. The parents and/or the guardian of such children should also be educated on the care and handling to avoid undue tampering and dislodgement of the shunt system. The use of endoscopic third ventriculostomy (ETV) should be explored and encouraged for future treatment of hydrocephalus in selected and fit patients as an alternative to shunting procedures in selected patients [2].
VP shunting for hydrocephalus has come to stay and almost always will be accompanied by some complications, both common and uncommon. Care should, however, be taken to minimize these complications by careful patient selection, choice of shunt and paying close attention to surgical details.

Figure 1a

Figure 1a

Figure 1b

Figure 1b

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