Vacuum assisted delivery

Vacuum assisted delivery

Towner et al. stated that tThe rate of intracranial hemorrhage is higher among infants delivered by vacuum extraction, forceps, or cesarean section during labor than among infants delivered spontaneously, but the rate among infants delivered by cesarean section before labor is not higher, suggesting that the common risk factor for hemorrhage is abnormal labor 1)

While cranial birth injury in term infants are well recognized, to date, only small case series have been described. In an attempt to further define the spectrum of cranial birth injuries, Pollina et al. analyzed 41 consecutive cranial birth injuries over the period 1991-1998. The most common clinical presentations were apnea (39%) and seizures (37%). Average Apgar scores were 5.7 at 1 min and 7.3 at 5 min; 54% of infants had abnormally low Apgar scores at 1 min and 31% had abnormally low scores at 5 min. The most common intracranial lesion was subdural hematoma, present in 73% of infants; most had either a tentorial subdural hematoma (57%) and/or interhemispheric subdural hematoma (50%) location. Operative treatment was required in 5 infants (12%). Two of the 41 infants (4.8%) died. The study group was compared with a control group of 63 randomly selected births without cranial injury. Using a stepwise logistic regression model, independently significant variables included neonatal birth weight, Apgar scores at 1 and 5 min and mode of delivery. Compared with the controls, the study group had a significantly higher incidence of obstetrical forceps and/or vacuum deliveries. Combining vacuum, forceps and urgent cesarean section deliveries together as ‘urgent’ and elective cesarean and spontaneous vaginal deliveries as ‘nonurgent’, they could find no significant differences between these two groups. This data conflict with those of Towner et al. [N Engl J Med 1999;341:1709-1714], and suggest that the method of assisted delivery, rather than the urgency of the delivery or dysfunctional labor per se, is a more important variable in cranial birth injuries 2).


Birth brachial plexus injury.


Subgaleal hematoma most commonly occurs after vacuum assisted delivery, but may also be seen following head trauma.


Low and mid station vacuum assisted deliveries (VAD) are delicate manual procedures that entail a high degree of subjectivity from the operator and are associated with adverse neonatal outcome. Little has been done to improve the procedure, including the technical development, traction force and the possibility of objective documentation.

Romero et al. aimed to explore if a digital handle with instant haptic feedback on traction force would reduce the neonatal risk during low or mid station VAD.

A two centre, randomised superiority trial at Karolinska University HospitalSweden, 2016-2018. Cases were randomised bedside to either a conventional or a digital handle attached to a Bird metal cup (50 mm, 80 kPa). The digital handle measured applied force including an instant notification by vibration when high levels of traction force were predicted according to a predefined algorithm. Primary outcome was a composite of hypoxic ischaemic encephalopathy, intracranial haemorrhage, seizures, death and/or subgaleal hematoma. Three hundred eighty low and mid VAD in each group were estimated to decrease primary outcome from six to 2 %.

After 2 years, an interim analyse was undertaken. Meeting the inclusion criteria, 567 vacuum extractions were randomized to the use of a digital handle (n = 296) or a conventional handle (n = 271). Primary outcome did not differ between the two groups: (2.7% digital handle vs 2.6% conventional handle). The incidence of primary outcome differed significantly between the two delivery wards (4% vs 0.9%, p < 0.05). A recalculation of power revealed that 800 cases would be needed in each group to show a decrease in primary outcome from three to 1 %. This was not feasible, and the study therefore closed.

The incidence of primary outcome was lower than estimated and the study was underpowered. However, the difference between the two delivery wards might reflect varying degree of experience of the technical equipment. An objective documentation of the extraction procedure is an attractive alternative in respect to safety and clinical training. To demonstrate improved safety, a multicentre study is required to reach an adequate cohort. This was beyond the scope of the study.

Trial registration: ClinicalTrials.gov NCT03071783 , March 1, 2017, retrospectively registered 3).


A newborn with a large, high parieto-frontally located mass after vacuum extraction. Imaging methods revealed a large subcutaneous collection of cerebrospinal fluid and hemorrhage. Traumatic dura lesions should be considered in neonates presenting with a large head lump after assisted delivery with vacuum extraction 4).


A child who was born by vacuum extraction delivery. Days after the birth, a frontal swelling, which was thought to be a caput succedaneum, enlarged. Imaging revealed an iatrogenic encephalocele with a large subcutaneous CSF collection. Surgical reconstruction was performed. A parasagittal dura defect was closed. There was no involvement of the superior sagittal sinus. Encephalocele is an infrequent complication of vacuum extraction delivery, rarely described in literature. The child had a good recovery after the operation, without neurologic deficits 5).


A newly-born infant with a congenital dural and bony defect and an associated short-segmented duplication of the superior sagittal sinus suffered from herniation and infarction of parietal brain tissue secondary to vacuum extraction. This ultimately led to the formation of a subgaleal cerebrospinal fluid (CSF) collection. Initial operative closure of the encephalocele was performed by attaching a galeal flap to the periostium surrounding the congenital defect. As the bony defect developed characteristics of a growing fracture later on, dural repair, transplantation of a split-bone flap and, finally, the insertion of a ventriculoperitoneal shunt became necessary. This case affirms that stringent indication and cautious usage of vacuum-assisted delivery is strongly recommended, especially in view of the possibility that undetected congenital cranial, vascular and/or cerebral alterations may be present 6).


Doward W, Sgouros S. Acute subdural haematomas following ventouse-assisted delivery. Pediatr Neurosurg. 2001 Dec;35(6):335. doi: 10.1159/000050448. PMID: 11786704.Doward W, Sgouros S. Acute subdural haematomas following ventouse-assisted delivery. Pediatr Neurosurg. 2001 Dec;35(6):335. doi: 10.1159/000050448. PMID: 11786704.


1)

Towner D, Castro MA, Eby-Wilkens E, Gilbert WM. Effect of mode of delivery in nulliparous women on neonatal intracranial injury. N Engl J Med. 1999 Dec 2;341(23):1709-14. doi: 10.1056/NEJM199912023412301. PMID: 10580069.
2)

Pollina J, Dias MS, Li V, Kachurek D, Arbesman M. Cranial birth injuries in term newborn infants. Pediatr Neurosurg. 2001 Sep;35(3):113-9. doi: 10.1159/000050403. PMID: 11641618.
3)

Romero S, Pettersson K, Yousaf K, Westgren M, Ajne G. Perinatal outcome after vacuum assisted delivery with digital feedback on traction force; a randomised controlled study. BMC Pregnancy Childbirth. 2021 Feb 26;21(1):165. doi: 10.1186/s12884-021-03604-z. PMID: 33637058; PMCID: PMC7913459.
4)

Poryo M, Yilmaz U, Linsler S, Gortner L, Meyer S. A newborn with a large mass: vacuum extraction-caused dura lesion. Clin Case Rep. 2015 Dec 6;4(1):101-2. doi: 10.1002/ccr3.428. PMID: 26783449; PMCID: PMC4706397.
5)

Jeltema HR, Hoving EW. Iatrogenic encephalocele: a rare complication of vacuum extraction delivery. Childs Nerv Syst. 2011 Dec;27(12):2193-5. doi: 10.1007/s00381-011-1600-0. Epub 2011 Oct 11. PMID: 21987344; PMCID: PMC3217141.
6)

Neumann JO, Herweh C, Halatsch ME. Congenital duplication of the superior sagittal sinus and parietal encephalocele after vacuum extraction delivery. Acta Neurochir (Wien). 2010 Apr;152(4):713-6. doi: 10.1007/s00701-009-0470-7. Epub 2009 Jul 29. PMID: 19639246.

Posttraumatic leptomeningeal cyst

Posttraumatic leptomeningeal cyst

Posttraumatic leptomeningeal cysts (PTLMC) (sometimes just traumatic leptomeningeal cysts), AKA growing skull fractures consists of a fracture line that widens with time.

The term cyst is actually a misnomer, as it is not a cyst, but an extension of the encephalomalacia 1).

Posttraumatic leptomeningeal cysts were first described in 18162).

Very rare, occurring in 0.05–0.6% of skull fracture3) 4). Usually requires both a widely separated fracture AND a dural tear.

Mean age at injury: < 1 year; over 90% occur before age 3 years 5) (formation may require the presence of a rapidly growing brain 6)), although rare adult cases have been described 7)8) 9) (a total of 5 cases in the literature as of 1998 10)).

The pathophysiology and some aspects of its management are still controversial.

It is thought they occur secondary to skull fractures causing dural tears allowing the leptomeninges and/or cerebral parenchyma to herniate into it

Pulsations from CSF erode the fracture margin, resulting in eventual expansion and non-union.

It occurs due to a wide skull defect with underlying dural defect and changes in pressure gradients within the skull cavity. Neglected cases may develop progressive neurological deficits and complications after second head trauma 11).

Enlarging scalp mass

Seizures

Focal neurological deficit

Headache

Most often presents as scalp mass (usually subgaleal), although there are reports of presentation with head pain alone 12).

Kitumba and Mascarenhas presented a rare case of an adult with excruciating headache secondary to a post-traumatic fronto-orbital leptomeningeal cyst 13)

PTLMCs rarely occur > 6 mos out from the injury. Some children may develop a skull fracture that seems to grow during the initial few weeks that is not accompanied by a subgaleal mass, and that heals spontaneously within several months; the term “pseudogrowing fracture” has been suggested for these 14).

They can rupture and cause diffuse subgaleal CSF collection 15).

Radiographic findings: progressive widening of fracture and scalloping (or saucering) of edges.

round or oval lucency with smooth margins

CT scan is the modality of choice for the evaluation of leptomeningeal cyst. It consists of a lytic calvarial lesion with scalloped edges, in which encephalomalacia invaginates. The following features may also be present

extracranial brain herniation

hydrocephalus

unilateral ventricular dilatation

porencephalic cyst.

Guler I, Buyukterzi M, Oner O, Tolu I. Post-traumatic leptomeningeal cyst in a child: computed tomography and magnetic resonance imaging findings. J Emerg Med. 2015 May;48(5):e121-2. doi: 10.1016/j.jemermed.2014.12.042. Epub 2015 Feb 3. PMID: 25662419.

Not to be confused with arachnoid cysts (AKA leptomeningeal cysts, which are not posttraumatic).

Posttraumatic intradiploic leptomeningeal cyst.

Skull tumor 16).

eosinophilic granuloma

calvarial metastases

epidermoid cyst

osteomyelitis

congenital calvarial defect

Although usually asymptomatic, the cyst may cause a mass effect with neurologic deficit.

Distal cortical artery aneurysms: often associated with an overlying s skull fracture, sometimes a growing skull fracture


Neglected GSF can rupture and cause diffuse subgaleal CSF collection 17).

If early growth of a fracture line with no subgaleal mass is noted, repeat skull films in 1–2 months before operating (to rule out pseudogrowing fracture). In young patients with separated skull fractures (the width of the initial fracture is rarely mentioned), consider obtaining follow-up skull film 6–12 mos post-trauma. However, since most PTLMCs are brought to medical attention when the palpable mass is noticed, routine follow-up X-rays may not be cost-effective.

Treatment of true PTLMC is surgical, with dural closure mandatory. Since the dural defect is usually larger than the bony defect, it may be advantageous to perform a craniotomy around the fracture site, repair the dural defect, and replace the bone 18).

The dural substitutes used are either autografts (which may not be enough) or artificial grafts (which are foreign-body implantations and which also may be too expensive in a low-resource practice).

Adeleye presented the surgical description of the use of the cyst capsule as a cost-free autologous graft in the surgical repair of the dural defects of two cases of traumatic leptomeningeal cyst 19).

Pseudogrowing fractures should be followed with X- rays and operated only if expansion persists beyond several months or if a subgaleal mass is present.

Liu et al. performed a retrospective review of 27 patients with GSF, who were grouped according to 3 different GSF stages.

Over a period of 20 years, 27 patients with GSF (16 males and 11 females) were treated in the authors’ department. The mean follow-up period was 26.5 months. Six patients were in the pre-phase of GSF (Stage 1), 10 patients in the early phase (Stage 2), and 11 in the late phase (Stage 3). All patients underwent duraplasty. All 6 patients at Stage 1 and 5 patients at Stage 2 underwent craniotomy without cranioplasty. Five patients at Stage 2 and all of the patients at Stage 3 underwent cranioplasty with autologous bone and alloplastic materials, respectively. Among all patients, 5 underwent ventriculoperitoneal shunt placement. Symptoms in all patients at Stages 1 and 2 were alleviated or disappeared, and the cranial bones developed without deformity during follow-up. Among patients with Stage 3 GSF, no obvious improvement in neurological deficits was observed. Three patients underwent additional operations because of cranial deformation or infection.

The authors identify the stages of GSF according to a new hypothesis. They conclude that accurately diagnosing and treating GSF during Stages 1 and 2 leads to a better prognosis 20)

Kulkarni et al. presented a 14-year-old child who developed sudden-onset, diffuse, soft, fluctuant, circumferential swelling of the head after a road traffic accident. He had sustained a head injury at the age of 3-months leading to an asymptomatic soft swelling over the skull which was left untreated. The present CT scan of the brain showed a bony defect with ragged edges and cerebrospinal fluid (CSF) collection in subgaleal space circumferentially. He underwent exploration, duroplasty, and cranioplasty and had a good outcome.

Neglected GSF can rupture and cause diffuse subgaleal CSF collection. It should be managed with dural repair and cranioplasty 21).

Kitumba D, Mascarenhas L. Rare case of an adult with excruciating headache secondary to post-traumatic fronto-orbital leptomeningeal cyst. Neurochirurgie. 2020 Nov;66(5):410-411. doi: 10.1016/j.neuchi.2020.06.126. Epub 2020 Aug 7. PMID: 32777233 22).


A 4-year-old boy was brought to the emergency department after suffering from head trauma caused by a fall from a rooftop where he was treated conservatively at a local hospital. Later, he developed swelling in the occipital region and was brought to the department of neurosurgery where he was operated on. After the first surgery, recurrence of swelling was seen after a postoperative period of 2 months, and a computed tomography scan reported persistent epidural hygroma with extension into the subcutaneous space. The second surgery was performed, and a 12-month follow-up did not show any recurrence of swelling in the patient 23).

A full-term infant born after a nontraumatic, forceps-assisted spontaneous delivery, who developed an increasing cystic swelling over the left frontoparietal area that crossed over coronal and sagittal sutures. The lesion was initially misinterpreted as cephalhematoma. Clinical and radiological follow-up established the correct diagnosis of leptomeningeal cyst.

The collection was initially tapped. Surgical treatment was undertaken thereafter, consisting of decompression and resection of the cyst and dural repair. Two months after follow-up, the patient remains asymptomatic and the porencephalic cavity remains isolated from the extradural space, with no evidence of new fluid collections 24).

A 53-year-old female presented with a post-traumatic leptomeningeal cyst manifesting as bulging of the scalp, dizziness, and tinnitus. She had known of the bulging of her forehead for about 20 years. She had suffered an injury to the head in childhood. Brain CT revealed a bone cyst associated with a round bone defect in the left frontal bone, bulging of the very thin outer layer, and the defective inner layer. She was treated surgically with a diagnosis of a skull tumor, but only gray cystic membranous tissue was found. The dural defect was repaired with fascia and the bone defect with bone cement. Bulging of the skull in adults can be caused by a bone cyst originating from a skull fracture 25).

12 patients diagnosed and treated between 1980 and 2002. 11 patients were under the age of 3 years and one patient was 5 years old at the moment of HI. The most common cause of injury was a fall from height. In the initial plain x-rayfilms, 11 patients showed a diastatic skull fracture and one patient only had a linear fracture. At this time, CT scan showed cortical contussion underlying the fracture in every case. The mean time between injury and presentation of GSF was 11.6 weeks. Diagnosis was made by palpation of the cranial defect and confirmed with skull x-rayfilms. The most frecuent location of GSF was in the parietal region. Associated lesions like hydrocephalus, encephalomalacia, leptomenigeal cysts, brain tissue herniation and ipsilateral ventricular dilatation, were found in the preoperative CT or MRI. All patients underwent a dural repair with pericranium or fascia lata. The cranial defect was covered with local calvarial bone fragments in every case. Only one patient needed a cranioplasty with titanium mesh. Every child with a skull fracture must be followed until the fracture heals. Patients under the age of 3 years with a diastatic fracture and a dural tear, demostrated by TC or MRI, are more prone to develop GSF. In these cases, early repair must be adviced in order to prevent progressive brain damage 26).

A growing skull fracture associated with cerebrospinal fluid rhinorrhoea following trauma sustained in adult life. The natural history of its development, diagnosis, and the results of surgery are discussed. The literature is reviewed with regard to aetiology, incidence, imaging characteristics and management of this rare post-traumatic complication 27).

A lump in the right parietal region of this 53-year-old man prompted a computed tomography (CT) scan. The patient denied any symptoms and was in good health. The examination confirmed a firm, non-tender, non-pulsatile mass in the right parietal region of the skull. The CT scan demonstrated a 4 x 3 cm area of irregular bone destruction involving both the inner and outer table of the skull. At operation a distinctly raised paper-thin outer table was noted, and underneath was a soft, tan-colored mass, which measured approximately 2 x 2 cm and was connected to the underlying brain through a 1 cm dural defect. The extradural portion of the mass was amputated, the dura repaired with a pericranium patch, the skull defect was repaired with a split-thickness bone graft, and the final pathology was congruent with a gliotic brain 28).

Meloche BR, Sansregret A, Grégoire H, Gagnon J, Massicotte P. Un cas de kyste leptoméningé post-traumatique [A case of post-traumatic leptomeningeal cyst]. Union Med Can. 1967 Oct;96(10):1214-9. French. PMID: 5601803.

PEYSER E, WEISSBERG D. Post-traumatic arachnoidal cyst. Report of an unusual case. J Neurosurg. 1961 Jul;18:551-3. doi: 10.3171/jns.1961.18.4.0551. PMID: 13735101.


2) , 7) , 10) , 28)

Britz GW, Kim DK, Mayberg MR. Traumatic leptomeningeal cyst in an adult: a case report and review of the literature. Surg Neurol. 1998 Nov;50(5):465-9. doi: 10.1016/s0090-3019(97)00233-4. PMID: 9842874.
3)

Ramamurthi B, Kalyanaraman S. Rationale for Surgery in Growing Fractures of the Skull. J Neurosurg. 1970; 32:427–430
4)

Arseni CS. Growing Skull Fractures of Children. A Particular Form of Post-Traumatic Encephalopathy. Acta Neurochir. 1966; 15:159–172
5)

Lende R, Erickson T. Growing Skull Fractures of Childhood. J Neurosurg. 1961; 18:479–489
6)

Gadoth N, Grunebaum M, Young LW. Leptomeningeal Cyst After Skull Fracture. Am J Dis Child. 1983; 137:1019–1020
8) , 12)

Halliday AL, Chapman PH, Heros RC. Leptomeningeal Cyst Resulting from Adulthood Trauma: Case Report. Neurosurgery. 1990; 26:150–153
9) , 18)

Iplikciglu AC, Kokes F, Bayar A, et al. Leptomeningeal Cyst. Neurosurgery. 1990; 27: 1027–1028
11)

Drapkin AJ. Growing skull fracture: a posttraumatic neosuture. Childs Nerv Syst. 2006 Apr;22(4):394-7. doi: 10.1007/s00381-005-1158-9. Epub 2005 Apr 22. PMID: 15856258.
13) , 22)

Kitumba D, Mascarenhas L. Rare case of an adult with excruciating headache secondary to post-traumatic fronto-orbital leptomeningeal cyst. Neurochirurgie. 2020 Nov;66(5):410-411. doi: 10.1016/j.neuchi.2020.06.126. Epub 2020 Aug 7. PMID: 32777233.
14)

Sekhar LN, Scarff TB. Pseudogrowth in Skull Fractures of Childhood. Neurosurgery. 1980; 6:285–289
15) , 17) , 21)

Kulkarni AV, Dikshit P, Devi BI, Sadashiva N, Shukla D, Bhat DI. Unusual Complication of a Neglected Growing Skull Fracture. Pediatr Neurosurg. 2021 Feb 24:1-5. doi: 10.1159/000513102. Epub ahead of print. PMID: 33626526.
16) , 25)

Kurosu A, Fujii T, Ono G. Post-traumatic leptomeningeal cyst mimicking a skull tumour in an adult. Br J Neurosurg. 2004 Feb;18(1):62-4. doi: 10.1080/02688690410001660463. PMID: 15040717.
19)

Adeleye AO. Posttraumatic leptomeningeal cyst capsule as a cost-free autograft for its repair: case illustrated technical reports. Neurosurg Rev. 2020 Aug 8. doi: 10.1007/s10143-020-01364-6. Epub ahead of print. PMID: 32772295.
20)

Liu XS, You C, Lu M, Liu JG. Growing skull fracture stages and treatment strategy. J Neurosurg Pediatr. 2012 Jun;9(6):670-5. doi: 10.3171/2012.2.PEDS11538. PMID: 22656261.
23)

Harsh V, Gond PK, Kumar A. Post-Traumatic Diploic Leptomeningeal Cyst with Bilateral Posterior Cranial Fossa Epidural Hygroma: A Management Dilemma? World Neurosurg. 2020 Aug;140:258-261. doi: 10.1016/j.wneu.2020.05.129. Epub 2020 May 21. PMID: 32445897.
24)

Miranda P, Vila M, Alvarez-Garijo JA, Perez-Nunez A. Birth trauma and development of growing fracture after coronal suture disruption. Childs Nerv Syst. 2007 Mar;23(3):355-8. Epub 2006 Oct 5. PubMed PMID: 17021730.
26)

Mierez R, Guillén A, Brell M, Cardona E, Claramunt E, Costa JM. [Growing skull fracture in childhood. Presentation of 12 cases]. Neurocirugia (Astur). 2003 Jun;14(3):228-33; discussion 234. Spanish. PubMed PMID: 12872172.
27)

Gupta V, Sinha S, Singh AK, Kumar S, Singh D. Growing skull fracture of ethmoid: a report of two cases. J Craniomaxillofac Surg. 2000 Aug;28(4):224-8. doi: 10.1054/jcms.2000.0141. PMID: 11110154.

Steroids for chronic subdural hematoma

Since glucocorticoids have been used for treatment of chronic subdural hematoma in 1962 their role is still discussed controversially in lack of evident data. On the basis of the ascertained inflammation cycle in cSDH dexamethasone will be an ideal substance for a short lasting, concomitant treatment protocol.

Berghauser et al. stated in 2013 that the proportion of patients primarily treated with corticosteroids are increasing year by year 1)

Patients with lower grades of CSDH can be treated successfully with steroids. Female patients seem to do better with steroids 2).


In 2020 in the The New England Journal of Medicine among adults with symptomatic chronic subdural hematoma, most of whom had undergone surgery to remove their hematomas during the index admission, treatment with dexamethasone resulted in fewer favorable outcomes and more adverse events than placebo at 6 months, but fewer repeat operations were performed in the dexamethasone group. (Funded by the National Institute for Health Research Health Technology Assessment Programme; Dex-CSDH ISRCTN number, ISRCTN80782810.) 3).

Surveys

Forty-two percent of surgeons never prescribe steroids and 55% prescribe them to those managed conservatively 4).

In another Canadian survey regarding neurosurgical practice of treatment of CSDH, <15% of neurosurgeons prefer using high-dose corticosteroid 5)

Current evidence implicates a potentially beneficial role of dexamethasone in the management of CSDH. However, it remains unclear whether the rate of crossover to surgery is reduced in patients treated with corticosteroids compared with those managed conservatively. A longer duration of study with detailed analysis of individual cases and appropriately randomized cohorts are necessary to draw more reliable conclusions 6)

Scerrati et al. performed a systematic review according to PRISMA criteria of the studies analyzing the nonsurgical strategies for CSDHs. They collected all papers in the English language published between 1990 and 2019 by searching different medical databases. The chosen keywords were “chronic subdural hematoma,” “conservative treatment/management,” “pharmacological treatment,” “non-surgical,” “tranexamic acid,” “dexamethasone,” “corticosteroid,” “glucocorticoid,” “middle meningeal artery,” “endovascular treatment,” and “embolization.”

The authors ultimately collected 15 articles regarding the pharmacological management of CSDHs matching the criteria, and 14 papers included the endovascular treatment.

The results showed that surgery still represents the mainstay in cases of symptomatic patients with large CSDHs; however, adjuvant and alternative therapies can be effective and safe in a carefully selected population. Their inclusion in new guidelines is advisable 7).


A meta-analysis of Holl et al. from 29019 suggested that the addition of corticosteroids to surgery might be effective in the treatment of CSDH. However, the results must be interpreted with caution in light of the serious risk of bias of the included studies. This study stresses the need for large randomized trials to investigate the use of corticosteroids in the management of CSDH 8)


In 2017 a study of Yao et al. had no enough evidence to support DX use as an effective alternation to surgical therapy. But adjuvant DX use may facilitate the surgical therapy by reducing chronic subdural hematoma recurrence. Further study focusing on adjuvant DX was required 9)

Among adults with symptomatic chronic subdural hematoma, most of whom had undergone surgery to remove their hematomas during the index admission, treatment with dexamethasone resulted in fewer favorable outcomes and more adverse events than placebo at 6 months, but fewer repeat operations were performed in the dexamethasone group. (Funded by the National Institute for Health Research Health Technology Assessment Programme; Dex-CSDH ISRCTN number, ISRCTN80782810.) 10).

see DECSA trial.

see SUCRE trial.

A study is designed as a double-blind randomized placebo-controlled trial 820 patients who are operated for cSDH and from the age of 25 years are included after obtaining informed consent. They are randomized for administration of dexamethasone (16-16-12-12-8-4 mg/d) or placebo (maltodextrin) during the first 48 hours after surgery. The type I error is 5% and the type II error is 20%. The primary endpoint is the reoperation within 12 weeks postoperative.

This study tests whether dexamethasone administered over 6 days is a safe and potent agent in relapse prevention for evacuated cSDH 11).

Mebberson et al. presented an interim analysis of the first registered prospective randomised placebo-controlled trial (PRPCT) of adjuvant DX on RR and outcome after CSDH surgery with post-operative drainage. Participants were randomised to either placebo or a reducing DX regime over 2 weeks, with CSDH evacuation and post-operative drainage. Post-operative mortality (POMT) and RR were determined at 30 days and 6 months; modified Rankin Score (mRS) at discharge and 6 months. Post-operative morbidity (POMB) and adverse events (AEs) were determined at 30 days. Interim analysis at approximately 50% estimated sample size was performed (n = 47). Recurrences were not observed with DX: only with placebo (0/23 [0%] v 5/24 [20.83%], P = 0.049). There was no significant between-group differences in POMT, POMB, LOS, mRS or AEs. CONCLUSIONS: In this first registered PRPCT, interim analysis suggested that adjuvant DX with post-operative drainage is both safe and may significantly decrease recurrences. A 12.5% point between-groups difference may be reasonable to power a final sample size of approximately n = 89. Future studies could consider adjuvant DX for longer than the arbitrarily-chosen 2 weeks 12).


Twenty patients with imaging-confirmed CSDH were recruited from a single center and randomized to receive dexamethasone (12 mg/day for 3 weeks followed by tapering) or placebo as a conservative treatment. Patients were followed for 6 months and the rate of success of conservative treatment with dexamethasone versus placebo was measured. Parameters such as hematoma thickness and clinical changes were also compared before and after treatment with chi-square tests. Adverse events and complications were documented.

Results: During the 6-month follow-up, one of ten patients treated with corticosteroids had to undergo surgical drainage and three of ten patients were treated surgically after placebo treatment. At the end of the study, all remaining patients had complete radiological resolution. No significant differences were observed in terms of hematoma thickness profile and impression of change; however, patients experienced more severe side effects when treated with steroids as compared with placebo. Dexamethasone contributed to many serious adverse events.

Given the small sample size, these preliminary results have not shown a clear beneficial effect of dexamethasone against placebo in our patients. However, the number of secondary effects reported was much greater for corticosteroids, and dexamethasone treatment was responsible for significant complications 13).

Sunet al. prospectively studied a group of 30 patients, who were managed non-operatively: 26 patients were treated with dexamethasone (Group 1) and four patients expectantly (Group 4). Nineteen patients (73%) from Group 1 were confused or had focal neurological deficits on admission. The mean maximum thickness of the CSDH was 12 mm. Only one of these cases (4%) required surgical drainage 6 weeks after steroid therapy. One patient died of an unrelated stroke (mortality = 4%). Two patients (8%) were left severely disabled. No significant complication from steroid therapy was documented. Out of the 85 surgically treated patients, 69 patients underwent surgical drainage in addition to steroid therapy (Group 2). Thirteen patients were treated with burr-hole drainage only (Group 3). The mean maximum thickness of the CSDH for these two groups were both 16 mm. Comparing with group 1, the redrainage rate of Group 2 [4% (3/69, p = 1)] and that of Group 3 [15% (2/13, p = 0.253)] were not significantly different. 50% of patients in Group 4 (2/4, p = 0.039) required delayed surgical drainage. The mortality rates of Groups 2, 3 and 4 were 3% (2/69, p = 1), 15% (2/13, p = 0.253) and 50% (2/4, p = 0.039), respectively. Our results suggest that steroid treatment in a selected group of patients is a good option, particularly in patients with co-morbidity 14).


1)

Berghauser Pont LM, Dippel DW, Verweij BH, Dirven CM, Dammers R. Ambivalence among neurologists and neurosurgeons on the treatment of chronic subdural hematoma: a national survey. Acta Neurol Belg. 2013 Mar;113(1):55-9. doi: 10.1007/s13760-012-0130-1. Epub 2012 Sep 14. PMID: 22975837.
2)

Thotakura AK, Marabathina NR. Nonsurgical Treatment of Chronic Subdural Hematoma with Steroids. World Neurosurg. 2015 Dec;84(6):1968-72. doi: 10.1016/j.wneu.2015.08.044. Epub 2015 Sep 2. PMID: 26342776.
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