Original Paper Pediatr Neurosurg 2013;49:287–291 DOI: 10.1159/000363701
Received: November 27, 2013 Accepted after revision: May 14, 2014 Published online: September 2, 2014
Hydrocephalus after Decompressive Craniotomy: A Case Series Abrar A. Wani Altaf U. Ramzan Humam Tanki Nayil K. Malik Bashir A. Dar Department of Neurosurgery, Sher-i-Kashmir Institute of Medical Sciences (SKIMS), Srinagar, India
Abstract Background: Post-craniectomy hydrocephalus in patients with intracranial hypertension is becoming a major concern for neurosurgeons because of the increasing number of hospital admissions for head trauma, stroke and other lesions which may lead to severe brain oedema requiring decompressive craniectomy. Methods: We collected records of all the paediatric patients who developed hydrocephalus following decompressive craniotomy from October 2011 to October 2013 and analysed their clinical profiles. Results: We had 3 patients in this group, ranging in age from 6 to 18 years; 1 patient died and the other 2 patients continue to remain in follow-up. Conclusion: Post-traumatic hydrocephalus is one of the rare complications of decompressive craniotomy; CSF diversion remains the only option for improvement in neurological status. © 2014 S. Karger AG, Basel
Introduction
Decompressive craniectomy, carried out either alone or in conjunction with the evacuation of any mass lesion, is one of the common procedures done in neurosurgical practice [1, 2]. Many studies have been conducted to date to gauge the effectiveness of wide decompressive craniectomy in decreasing intracranial pressure and improving © 2014 S. Karger AG, Basel 1016–2291/14/0495–0287$39.50/0 E-Mail [email protected] www.karger.com/pne
the outcome of such patients [3–6]. There is substantial evidence suggesting an improvement in long-term functional outcome and quality of life compared to standard medical therapies [7, 8]. However, such an extensive procedure is often associated with complications such as increased hospital stay, a cosmetically unacceptable cranial defect and the vulnerability of the underlying brain to injury and sometimes the development of hydrocephalus. The incidence of post-traumatic hydrocephalus has been found to range from 0.7 to 86% [9–12]. Various factors such as age, long duration of coma, associated subarachnoid haemorrhage and craniotomy have been reported to increase the risk of developing hydrocephalus.
Subjects and Methods Case 1 A 14-year-old boy presented with severe head injury with a Glasgow Coma Scale score of 6 and was found to have acute subdural hematoma with midline shift (fig. 1). He was operated on by right fronto-temporo-parietal decompressive craniotomy and evacuation of hematoma with duraplasty. Post-operatively, the patient improved gradually by a score of 2 but he started deteriorating after 10 days. A CT scan was done which showed hydrocephalus (fig. 2). A ventriculo-peritoneal (VP) shunt was carried out, after which the patient improved and is now on follow-up. Case 2 A young boy had a fall from a 2-storey house and was found to have acute subdural hematoma (fig. 3) in the right front temporal area. He was in a comatose condition and was operated on by fronto-temporo-parietal decompressive craniotomy and evacuation of hematoma with duraplasty. The patient improved from a coma
Dr. Abrar Ahad Wani Department of Neurosurgery Sher-i-Kashmir Institute of Medical Sciences Soura, 190001 Srinagar, Jammu and Kashmir (India) E-Mail abrarwani @ rediffmail.com
Downloaded by: UCSF Library & CKM 169.230.243.252 - 4/23/2015 11:05:05 AM
Key Words Intracranial hypertension · Craniectomy · Hydrocephalus
score of 8 to 11 but deteriorated after 2 weeks. A CT scan showed hydrocephalus (fig. 4). A VP shunt was carried out which led to an improvement in the coma score to 12 over a period of 3 months. Case 3 A 6-year-old boy had a sudden onset of left hemiplegia and drowsiness; a CT head scan showed malignant MCA infarction (fig. 5). He underwent decompressive craniotomy and improved in sensorium. After a few days he developed a wound bulge and was found to have hydrocephalus (fig. 6). A VP shunt was carried out and he was discharged after 8 days.
Discussion
In 1914, Dandy and Blackfan [13] published a report on post-traumatic hydrocephalus. Going through the literature, we found that the incidence of post-traumatic hydro-
Fig. 2. Hydrocephalus is seen with craniectomy defect.
288
Pediatr Neurosurg 2013;49:287–291 DOI: 10.1159/000363701
Wani/Ramzan/Tanki/Malik/Dar
Downloaded by: UCSF Library & CKM 169.230.243.252 - 4/23/2015 11:05:05 AM
Fig. 1. CT scan revealing right temporo-parietal acute subdural hematoma.
cephalus ranges from 0.7 to 29% [9, 11]. To diagnose cases as post-traumatic hydrocephalus various authors have suggested a variety of clinical and radiological diagnostic criteria. Hence, such a wide variation in the percentage of incidences may be because of differences in diagnostic criteria and classification systems. One important point which needs emphasis is that we first need to differentiate post-craniectomy hydrocephalus from simple ventriculomegaly, as in the latter CSF diversion procedures are not required since there is no associated elevation of intra-cranial pressure. However, it is difficult to determine whether post-craniectomy ventriculomegaly is because of atro-
phic-gliotic brain or hydrocephalus. Some authors propose that the diagnosis of true post-traumatic, post-craniectomy hydrocephalus requires the exhibition of large ventricles without sulci enlargement and the presence of associated clinical symptoms and signs like persistent impaired consciousness, no neurological improvement (or early improvement followed by deterioration a few days following surgery), dementia and incontinence. Although on clinical grounds a decision regarding CSF diversion procedures can be taken most of the time, various studies such as CT brain studies, MRI brain studies, SPECT studies, CSF dynamic studies, and temporary lumbar drainage
Fig. 4. Hydrocephalus is seen in the patient following decompressive craniotomy.
Hydrocephalus after Decompressive Craniotomy
Pediatr Neurosurg 2013;49:287–291 DOI: 10.1159/000363701
289
Downloaded by: UCSF Library & CKM 169.230.243.252 - 4/23/2015 11:05:05 AM
Fig. 3. CT scan showing right fronto-temporal acute subdural hematoma with midline shift.
Fig. 6. Scan showing craniectomy defect with hydrocephalus.
studies may guide us to differentiate post-traumatic ventriculomegaly due to hydrocephalus from ventriculomegaly due to cortical atrophy [14, 15]. Despite applying all these criteria, it is still difficult to predict whether such patients will benefit from CSF diversion or not. However, even in patients with post-craniectomy hydrocephalus the results of CSF diversion have not been encouraging [9]. Even after a thorough search we could not reach a conclusion regarding an appropriate treatment for post-traumatic, post-craniectomy hydrocephalus. In patients with head trauma who have undergone decompressive craniectomy, it is hypothesized that a large cranial defect can lead to turbulences in hydrodynamic CSF circulation and cerebral blood perfusion by atmospheric pressure, leading to the development of hydrocephalus [14–20]. Sometimes herniation of the brain can occur through the craniectomy defect, especially when there is associated hydrocephalus [21]. After head injury, there is often dilatation of ventricles due to posttraumatic cerebral atrophy (hydrocephalus en vacuo), but this entity is different from hydrocephalus because in the latter there is also associated raised intracranial pressure which is improved by CSF diversion procedures, including VP shunt, lumbar drainage and extra-ventricular drainage [22–24]. Regarding the pathophysiology of the
development of post-traumatic hydrocephalus, various factors such as altered intracranial pressure dynamics, inflammation of the arachnoid granulation by post-surgical debris or mechanical blockage have been implied by various studies [25–28]. In 2007, a study by Waziri et al. [28] suggested that decompressive craniectomy may play a role in the ‘flattening’ of the normally dicrotic intracranial pressure waveform in patients having undergone craniectomy due to the transmission of the pressure pulse out through the open cranium. Since the arachnoid granulations function as pressure-dependent one-way valves from the subarachnoid space to the draining venous sinuses, it is possible that disruption of pulsatile intracranial pressure dynamics secondary to opening the cranial vault results in decreased CSF outflow [29]. Hence, early cranioplasty may restore normal intracranial pressure dynamics and prevent the development or resolution of hydrocephalus. Some studies report that in cases of traumatic intracranial hematomas or traumatic subarachnoid haemorrhage, hydrocephalus may develop due to mechanical blockage or inflammation of arachnoid granulations. In some cases it has been seen that the obliteration of subarachnoid spaces with fibrous thickening of leptomeninges, especially in the sulci of the convexities and base of the brain, and obstruction around the convexities
290
Pediatr Neurosurg 2013;49:287–291 DOI: 10.1159/000363701
Wani/Ramzan/Tanki/Malik/Dar
Downloaded by: UCSF Library & CKM 169.230.243.252 - 4/23/2015 11:05:05 AM
Fig. 5. CT scan showing left MCA infarction with midline shift.
can result in hydrocephalus [25–27]. Shapiro et al. [30] attempted to offer an interesting but conceptually difficult hypothesis that the time constant (resistance to CSF outflow × compliance of cerebrospinal space) of cerebrospinal system hydrodynamics has a tendency to remain constant. Therefore, an increase in compliance after craniectomy tends to be followed by a decrease in the resistance to CSF outflow. This process may be reversed after cranioplasty – that is, a decrease in pressure volume index may be followed by an increase in the resistance to CSF outflow. Therefore, it is suggested that early cranioplasty can reduce the incidence of post-craniectomy hydro-
cephalus and also lead to an improvement in the level of consciousness and focal deficits. Various treatments have been suggested for post-craniectomy hydrocephalus but none has proved to be better than others. CSF diversion procedures like VP shunts with or without cranioplasty may be performed in such patients. Patients who undergo CSF diversion procedures like VP shunt or external ventricular drainage without cranioplasty develop ‘syndrome of sinking skin flap’ or ‘syndrome of trephine’ due to CSF over-drainage at atmospheric pressure and midline shift [18].
References
Hydrocephalus after Decompressive Craniotomy
10 Gudeman SK, Kishore PR, Becker DP, Lipper MH, Girevendulis AK, Jeffries BF, et al: Computed tomography in the evaluation of incidence and significance of post-traumatic hydrocephalus. Radiology 1981;141:397–402. 11 Hawkins TD, Lloyd AD, Fletcher GI, Hanka R: Ventricular size following head injury: a clinico-radiological study. Clin Radiol 1976; 27: 279–289. 12 Philippon J, George B, Visot A, Cophignon J: Post-operative hydrocephalus (in French). Neurochirurgie 1976;22:111–117. 13 Dandy W, Blackfan KD: Internal hydrocephalus. An experimental, clinical and pathological study. Am J Dis Child 1914;8:406–482. 14 Kishore PR, Lipper MH, Miller JD, Girevendulis AK, Becker DP, Vines FS: Post-traumatic hydrocephalus in patients with severe head injury. Neuroradiology 1978;16:261–265. 15 Marmarou A, Foda MA, Bandoh K, Yoshihara M, Yamamoto T, Tsuji O, et al: Posttraumatic ventriculomegaly: hydrocephalus or atrophy? A new approach for diagnosis using CSF dynamics. J Neurosurg 1996;85:1026–1035. 16 Fodstad H, Ekstedt J, Friden H: CSF hymodynamic studies before and after cranioplasty. Acta Neurochir Suppl (Wien) 1979;28:514–518. 17 Rish BL, Meacham WF: Elementary study of the intraventricular installation of radioactive gold. J Neurosurg 1967;27:15–20. 18 Yoshida K, Furuse M, Izawa A, Iizima N, Kuchiwaki H: Dynamics of cerebral blood flow and metabolism in patients with cranioplasty as evaluated by xenon,133, CT and P31 magnetic resonance spectroscopy. J Neurol Neurosurg Psychiatry 1996;61:166–171. 19 Alperin N, Vikingstad EM, Gomez-Anson B, Levin DN: Hemodynamically independent analysis of the CSF and brain motion observed with dynamic phase contrast MRI. Magn Reson Med 1996;35:741–754. 20 Ekstedt J: CSF hydrodynamic studies in man. 1. Method of constant pressure CSF infusion. J Neurol Neurosurg Psychiatry 1977;40:105–119.
21 Stein SC, Langfitt TW: Normal pressure hydrocephalus: predicting the results of cerebrospinal fluid shunting. J Neurosurg 1974; 41: 463–470. 22 Phuenpathom N, Ratanalert S, Saeheng S: Post-traumatic hydrocephalus: experience in 17 consecutive cases. J Med Assoc Thai 1999; 82:46–53. 23 Polin RS, Shaffrey ME, Bogaev CA, Tisdale N, Germanson T, Bocchicchio B, et al: Decompressive bifrontal craniectomy in the treatment of severe refractory posttraumatic cerebral edema. Neurosurgery 1997;41:84–94. 24 Bret P, Hor F, Huppert J, Lapras C, Fischer G: Treatment of cerebrospinal fluid rhinorrhea by percutaneous lumboperitoneal shunting: review of 15 cases. Neurosurgery 1985;16:44–47. 25 Foltz EL, Ward AA Jr: Communicating hydrocephalus from subarachnoid bleeding. J Neurosurg 1956;13:546–566. 26 Foroglou G, Zander E: Post-traumatic hydrocephalus and measurement of cerebrospinal fluid pressure (in French). Acta Radiol Diagn (Stockh) 1972;13:524–530. 27 Pedersen KK, Haase J: Isotope liquorgraphy in the demonstration of communicating obstructive hydrocephalus after severe cranial trauma. Acta Neurol Scand 1973;49:10–30. 28 Waziri A, Fusco D, Mayer SA, McKhann GM 2nd, Connolly ES Jr: Postoperative hydrocephalus in patients undergoing decompressive hemicraniectomy for ischemic or hemorrhagic stroke. Neurosurgery 2007; 61: 489–493, discussion 493–494. 29 Upton ML, Weller RO: The morphology of cerebrospinal fluid drainage pathways in human arachnoid granulations. J Neurosurg 1985;63: 867–875. 30 Shapiro K, Fried A, Takei F, et al: Effect of the skull and dura on neural axis pressure-volume relationships and CSF hydrodynamics. J Neurosurg 1985;63:76–81.
Pediatr Neurosurg 2013;49:287–291 DOI: 10.1159/000363701
291
Downloaded by: UCSF Library & CKM 169.230.243.252 - 4/23/2015 11:05:05 AM
1 Liao CC, Kao MC: Cranioplasty for patients with severe depressed skull bone defect after cerebrospinal fluid shunting. J Clin Neurosci 2002;9:553–555. 2 Winkler PA, Stummer W, Linke R, Krishnan KG, Tatsch K: Influence of cranioplasty on postural blood flow regulation, cerebrovascular reserve capacity, and cerebral glucose metabolism. J Neurosurg 2000;93:53–61. 3 Lee JH, Lim DJ, Kim SH, Park JY, Chung YG, Suh JK: Effects of decompressive craniectomy for the management of patients with refractory intracranial hypertension. J Korean Neurosurg Soc 2003;34:531–536. 4 Park JY, Seok KS, Cho JH, Kang DG, Kim SC: Early decompressive craniectomy for cerebral edema. J Korean Neurosurg Soc 2002; 31: 33– 38. 5 Shin HS, Kim JY, Kim TH, Hwang YS, Kim SJ, Park SK: Clinical significance of bifrontotemporal decompressive craniectomy in the treatment of severe refractory posttraumatic brain swelling. J Korean Neurosurg Soc 2000; 29: 1179–1183. 6 Yoo DS, Kim DS, Huh PW, Cho KS, Park CK, Kang JK: Intracranial pressure and cerebral blood flow monitoring after bilateral decompressive craniectomy in patients with acute massive brain swelling. J Korean Neurosurg Soc 2001;30:295–306. 7 Erban P, Woertgen C, Luerding R, Bogdahn U, Schlachetzki F, Horn M: Long-term outcome after hemicraniectomy for space occupying right hemispheric MCA infarction. Clin Neurol Neurosurg 2006;108:384–387. 8 Woertgen C, Rothoerl RD, Schebesch KM, Albert R: Comparison of craniotomy and craniectomy in patients with acute subdural haematoma. J Clin Neurosci 2006;13:718–721. 9 Cardoso ER, Galbraith S: Posttraumatic hydrocephalus – a retrospective review. Surg Neurol 1985;23:261–264.
Received: November 27, 2013 Accepted after revision: May 14, 2014 Published online: September 2, 2014
Hydrocephalus after Decompressive Craniotomy: A Case Series Abrar A. Wani Altaf U. Ramzan Humam Tanki Nayil K. Malik Bashir A. Dar Department of Neurosurgery, Sher-i-Kashmir Institute of Medical Sciences (SKIMS), Srinagar, India
Abstract Background: Post-craniectomy hydrocephalus in patients with intracranial hypertension is becoming a major concern for neurosurgeons because of the increasing number of hospital admissions for head trauma, stroke and other lesions which may lead to severe brain oedema requiring decompressive craniectomy. Methods: We collected records of all the paediatric patients who developed hydrocephalus following decompressive craniotomy from October 2011 to October 2013 and analysed their clinical profiles. Results: We had 3 patients in this group, ranging in age from 6 to 18 years; 1 patient died and the other 2 patients continue to remain in follow-up. Conclusion: Post-traumatic hydrocephalus is one of the rare complications of decompressive craniotomy; CSF diversion remains the only option for improvement in neurological status. © 2014 S. Karger AG, Basel
Introduction
Decompressive craniectomy, carried out either alone or in conjunction with the evacuation of any mass lesion, is one of the common procedures done in neurosurgical practice [1, 2]. Many studies have been conducted to date to gauge the effectiveness of wide decompressive craniectomy in decreasing intracranial pressure and improving © 2014 S. Karger AG, Basel 1016–2291/14/0495–0287$39.50/0 E-Mail [email protected] www.karger.com/pne
the outcome of such patients [3–6]. There is substantial evidence suggesting an improvement in long-term functional outcome and quality of life compared to standard medical therapies [7, 8]. However, such an extensive procedure is often associated with complications such as increased hospital stay, a cosmetically unacceptable cranial defect and the vulnerability of the underlying brain to injury and sometimes the development of hydrocephalus. The incidence of post-traumatic hydrocephalus has been found to range from 0.7 to 86% [9–12]. Various factors such as age, long duration of coma, associated subarachnoid haemorrhage and craniotomy have been reported to increase the risk of developing hydrocephalus.
Subjects and Methods Case 1 A 14-year-old boy presented with severe head injury with a Glasgow Coma Scale score of 6 and was found to have acute subdural hematoma with midline shift (fig. 1). He was operated on by right fronto-temporo-parietal decompressive craniotomy and evacuation of hematoma with duraplasty. Post-operatively, the patient improved gradually by a score of 2 but he started deteriorating after 10 days. A CT scan was done which showed hydrocephalus (fig. 2). A ventriculo-peritoneal (VP) shunt was carried out, after which the patient improved and is now on follow-up. Case 2 A young boy had a fall from a 2-storey house and was found to have acute subdural hematoma (fig. 3) in the right front temporal area. He was in a comatose condition and was operated on by fronto-temporo-parietal decompressive craniotomy and evacuation of hematoma with duraplasty. The patient improved from a coma
Dr. Abrar Ahad Wani Department of Neurosurgery Sher-i-Kashmir Institute of Medical Sciences Soura, 190001 Srinagar, Jammu and Kashmir (India) E-Mail abrarwani @ rediffmail.com
Downloaded by: UCSF Library & CKM 169.230.243.252 - 4/23/2015 11:05:05 AM
Key Words Intracranial hypertension · Craniectomy · Hydrocephalus
score of 8 to 11 but deteriorated after 2 weeks. A CT scan showed hydrocephalus (fig. 4). A VP shunt was carried out which led to an improvement in the coma score to 12 over a period of 3 months. Case 3 A 6-year-old boy had a sudden onset of left hemiplegia and drowsiness; a CT head scan showed malignant MCA infarction (fig. 5). He underwent decompressive craniotomy and improved in sensorium. After a few days he developed a wound bulge and was found to have hydrocephalus (fig. 6). A VP shunt was carried out and he was discharged after 8 days.
Discussion
In 1914, Dandy and Blackfan [13] published a report on post-traumatic hydrocephalus. Going through the literature, we found that the incidence of post-traumatic hydro-
Fig. 2. Hydrocephalus is seen with craniectomy defect.
288
Pediatr Neurosurg 2013;49:287–291 DOI: 10.1159/000363701
Wani/Ramzan/Tanki/Malik/Dar
Downloaded by: UCSF Library & CKM 169.230.243.252 - 4/23/2015 11:05:05 AM
Fig. 1. CT scan revealing right temporo-parietal acute subdural hematoma.
cephalus ranges from 0.7 to 29% [9, 11]. To diagnose cases as post-traumatic hydrocephalus various authors have suggested a variety of clinical and radiological diagnostic criteria. Hence, such a wide variation in the percentage of incidences may be because of differences in diagnostic criteria and classification systems. One important point which needs emphasis is that we first need to differentiate post-craniectomy hydrocephalus from simple ventriculomegaly, as in the latter CSF diversion procedures are not required since there is no associated elevation of intra-cranial pressure. However, it is difficult to determine whether post-craniectomy ventriculomegaly is because of atro-
phic-gliotic brain or hydrocephalus. Some authors propose that the diagnosis of true post-traumatic, post-craniectomy hydrocephalus requires the exhibition of large ventricles without sulci enlargement and the presence of associated clinical symptoms and signs like persistent impaired consciousness, no neurological improvement (or early improvement followed by deterioration a few days following surgery), dementia and incontinence. Although on clinical grounds a decision regarding CSF diversion procedures can be taken most of the time, various studies such as CT brain studies, MRI brain studies, SPECT studies, CSF dynamic studies, and temporary lumbar drainage
Fig. 4. Hydrocephalus is seen in the patient following decompressive craniotomy.
Hydrocephalus after Decompressive Craniotomy
Pediatr Neurosurg 2013;49:287–291 DOI: 10.1159/000363701
289
Downloaded by: UCSF Library & CKM 169.230.243.252 - 4/23/2015 11:05:05 AM
Fig. 3. CT scan showing right fronto-temporal acute subdural hematoma with midline shift.
Fig. 6. Scan showing craniectomy defect with hydrocephalus.
studies may guide us to differentiate post-traumatic ventriculomegaly due to hydrocephalus from ventriculomegaly due to cortical atrophy [14, 15]. Despite applying all these criteria, it is still difficult to predict whether such patients will benefit from CSF diversion or not. However, even in patients with post-craniectomy hydrocephalus the results of CSF diversion have not been encouraging [9]. Even after a thorough search we could not reach a conclusion regarding an appropriate treatment for post-traumatic, post-craniectomy hydrocephalus. In patients with head trauma who have undergone decompressive craniectomy, it is hypothesized that a large cranial defect can lead to turbulences in hydrodynamic CSF circulation and cerebral blood perfusion by atmospheric pressure, leading to the development of hydrocephalus [14–20]. Sometimes herniation of the brain can occur through the craniectomy defect, especially when there is associated hydrocephalus [21]. After head injury, there is often dilatation of ventricles due to posttraumatic cerebral atrophy (hydrocephalus en vacuo), but this entity is different from hydrocephalus because in the latter there is also associated raised intracranial pressure which is improved by CSF diversion procedures, including VP shunt, lumbar drainage and extra-ventricular drainage [22–24]. Regarding the pathophysiology of the
development of post-traumatic hydrocephalus, various factors such as altered intracranial pressure dynamics, inflammation of the arachnoid granulation by post-surgical debris or mechanical blockage have been implied by various studies [25–28]. In 2007, a study by Waziri et al. [28] suggested that decompressive craniectomy may play a role in the ‘flattening’ of the normally dicrotic intracranial pressure waveform in patients having undergone craniectomy due to the transmission of the pressure pulse out through the open cranium. Since the arachnoid granulations function as pressure-dependent one-way valves from the subarachnoid space to the draining venous sinuses, it is possible that disruption of pulsatile intracranial pressure dynamics secondary to opening the cranial vault results in decreased CSF outflow [29]. Hence, early cranioplasty may restore normal intracranial pressure dynamics and prevent the development or resolution of hydrocephalus. Some studies report that in cases of traumatic intracranial hematomas or traumatic subarachnoid haemorrhage, hydrocephalus may develop due to mechanical blockage or inflammation of arachnoid granulations. In some cases it has been seen that the obliteration of subarachnoid spaces with fibrous thickening of leptomeninges, especially in the sulci of the convexities and base of the brain, and obstruction around the convexities
290
Pediatr Neurosurg 2013;49:287–291 DOI: 10.1159/000363701
Wani/Ramzan/Tanki/Malik/Dar
Downloaded by: UCSF Library & CKM 169.230.243.252 - 4/23/2015 11:05:05 AM
Fig. 5. CT scan showing left MCA infarction with midline shift.
can result in hydrocephalus [25–27]. Shapiro et al. [30] attempted to offer an interesting but conceptually difficult hypothesis that the time constant (resistance to CSF outflow × compliance of cerebrospinal space) of cerebrospinal system hydrodynamics has a tendency to remain constant. Therefore, an increase in compliance after craniectomy tends to be followed by a decrease in the resistance to CSF outflow. This process may be reversed after cranioplasty – that is, a decrease in pressure volume index may be followed by an increase in the resistance to CSF outflow. Therefore, it is suggested that early cranioplasty can reduce the incidence of post-craniectomy hydro-
cephalus and also lead to an improvement in the level of consciousness and focal deficits. Various treatments have been suggested for post-craniectomy hydrocephalus but none has proved to be better than others. CSF diversion procedures like VP shunts with or without cranioplasty may be performed in such patients. Patients who undergo CSF diversion procedures like VP shunt or external ventricular drainage without cranioplasty develop ‘syndrome of sinking skin flap’ or ‘syndrome of trephine’ due to CSF over-drainage at atmospheric pressure and midline shift [18].
References
Hydrocephalus after Decompressive Craniotomy
10 Gudeman SK, Kishore PR, Becker DP, Lipper MH, Girevendulis AK, Jeffries BF, et al: Computed tomography in the evaluation of incidence and significance of post-traumatic hydrocephalus. Radiology 1981;141:397–402. 11 Hawkins TD, Lloyd AD, Fletcher GI, Hanka R: Ventricular size following head injury: a clinico-radiological study. Clin Radiol 1976; 27: 279–289. 12 Philippon J, George B, Visot A, Cophignon J: Post-operative hydrocephalus (in French). Neurochirurgie 1976;22:111–117. 13 Dandy W, Blackfan KD: Internal hydrocephalus. An experimental, clinical and pathological study. Am J Dis Child 1914;8:406–482. 14 Kishore PR, Lipper MH, Miller JD, Girevendulis AK, Becker DP, Vines FS: Post-traumatic hydrocephalus in patients with severe head injury. Neuroradiology 1978;16:261–265. 15 Marmarou A, Foda MA, Bandoh K, Yoshihara M, Yamamoto T, Tsuji O, et al: Posttraumatic ventriculomegaly: hydrocephalus or atrophy? A new approach for diagnosis using CSF dynamics. J Neurosurg 1996;85:1026–1035. 16 Fodstad H, Ekstedt J, Friden H: CSF hymodynamic studies before and after cranioplasty. Acta Neurochir Suppl (Wien) 1979;28:514–518. 17 Rish BL, Meacham WF: Elementary study of the intraventricular installation of radioactive gold. J Neurosurg 1967;27:15–20. 18 Yoshida K, Furuse M, Izawa A, Iizima N, Kuchiwaki H: Dynamics of cerebral blood flow and metabolism in patients with cranioplasty as evaluated by xenon,133, CT and P31 magnetic resonance spectroscopy. J Neurol Neurosurg Psychiatry 1996;61:166–171. 19 Alperin N, Vikingstad EM, Gomez-Anson B, Levin DN: Hemodynamically independent analysis of the CSF and brain motion observed with dynamic phase contrast MRI. Magn Reson Med 1996;35:741–754. 20 Ekstedt J: CSF hydrodynamic studies in man. 1. Method of constant pressure CSF infusion. J Neurol Neurosurg Psychiatry 1977;40:105–119.
21 Stein SC, Langfitt TW: Normal pressure hydrocephalus: predicting the results of cerebrospinal fluid shunting. J Neurosurg 1974; 41: 463–470. 22 Phuenpathom N, Ratanalert S, Saeheng S: Post-traumatic hydrocephalus: experience in 17 consecutive cases. J Med Assoc Thai 1999; 82:46–53. 23 Polin RS, Shaffrey ME, Bogaev CA, Tisdale N, Germanson T, Bocchicchio B, et al: Decompressive bifrontal craniectomy in the treatment of severe refractory posttraumatic cerebral edema. Neurosurgery 1997;41:84–94. 24 Bret P, Hor F, Huppert J, Lapras C, Fischer G: Treatment of cerebrospinal fluid rhinorrhea by percutaneous lumboperitoneal shunting: review of 15 cases. Neurosurgery 1985;16:44–47. 25 Foltz EL, Ward AA Jr: Communicating hydrocephalus from subarachnoid bleeding. J Neurosurg 1956;13:546–566. 26 Foroglou G, Zander E: Post-traumatic hydrocephalus and measurement of cerebrospinal fluid pressure (in French). Acta Radiol Diagn (Stockh) 1972;13:524–530. 27 Pedersen KK, Haase J: Isotope liquorgraphy in the demonstration of communicating obstructive hydrocephalus after severe cranial trauma. Acta Neurol Scand 1973;49:10–30. 28 Waziri A, Fusco D, Mayer SA, McKhann GM 2nd, Connolly ES Jr: Postoperative hydrocephalus in patients undergoing decompressive hemicraniectomy for ischemic or hemorrhagic stroke. Neurosurgery 2007; 61: 489–493, discussion 493–494. 29 Upton ML, Weller RO: The morphology of cerebrospinal fluid drainage pathways in human arachnoid granulations. J Neurosurg 1985;63: 867–875. 30 Shapiro K, Fried A, Takei F, et al: Effect of the skull and dura on neural axis pressure-volume relationships and CSF hydrodynamics. J Neurosurg 1985;63:76–81.
Pediatr Neurosurg 2013;49:287–291 DOI: 10.1159/000363701
291
Downloaded by: UCSF Library & CKM 169.230.243.252 - 4/23/2015 11:05:05 AM
1 Liao CC, Kao MC: Cranioplasty for patients with severe depressed skull bone defect after cerebrospinal fluid shunting. J Clin Neurosci 2002;9:553–555. 2 Winkler PA, Stummer W, Linke R, Krishnan KG, Tatsch K: Influence of cranioplasty on postural blood flow regulation, cerebrovascular reserve capacity, and cerebral glucose metabolism. J Neurosurg 2000;93:53–61. 3 Lee JH, Lim DJ, Kim SH, Park JY, Chung YG, Suh JK: Effects of decompressive craniectomy for the management of patients with refractory intracranial hypertension. J Korean Neurosurg Soc 2003;34:531–536. 4 Park JY, Seok KS, Cho JH, Kang DG, Kim SC: Early decompressive craniectomy for cerebral edema. J Korean Neurosurg Soc 2002; 31: 33– 38. 5 Shin HS, Kim JY, Kim TH, Hwang YS, Kim SJ, Park SK: Clinical significance of bifrontotemporal decompressive craniectomy in the treatment of severe refractory posttraumatic brain swelling. J Korean Neurosurg Soc 2000; 29: 1179–1183. 6 Yoo DS, Kim DS, Huh PW, Cho KS, Park CK, Kang JK: Intracranial pressure and cerebral blood flow monitoring after bilateral decompressive craniectomy in patients with acute massive brain swelling. J Korean Neurosurg Soc 2001;30:295–306. 7 Erban P, Woertgen C, Luerding R, Bogdahn U, Schlachetzki F, Horn M: Long-term outcome after hemicraniectomy for space occupying right hemispheric MCA infarction. Clin Neurol Neurosurg 2006;108:384–387. 8 Woertgen C, Rothoerl RD, Schebesch KM, Albert R: Comparison of craniotomy and craniectomy in patients with acute subdural haematoma. J Clin Neurosci 2006;13:718–721. 9 Cardoso ER, Galbraith S: Posttraumatic hydrocephalus – a retrospective review. Surg Neurol 1985;23:261–264.
