Subgaleal hematoma

Subgaleal hematoma

Subgaleal hematoma is a type of cephalhematoma in the potential space between the periosteum and the galea aponeurosis.

They dont calcify.

Its occurrence beyond the neonatal period is rare and is often associated with head trauma involving tangential or radial forces applied to the scalp causing emissary veins traversing the subgaleal space to be ruptured 1).

In patients with traumatic intracranial hemorrhage or skull fractures, the incidence is increased.

In the newborn infant is rare, occurs early, and often bears serious consequences.

The diagnosis is generally a clinical one, with a fluctuant boggy mass developing over the scalp

Laboratory studies consist of a hematocrit evaluation.

Right frontotemporoparietal intracranial acute epidural hematoma, up to 1 cm. thick, underlying a broad line of right temporoparietal Right parietal subgaleal hematoma, up to 1cm. of thickness.

Hemorrhage under the scalp

Not to confuse with subperiosteal hematoma.


Small gyriform laminar hyperdensity is observed in the left superior frontal sulcus in relation to a small subarachnoid hemorrhage. Left parietal subgaleal hematoma up to 7 mm thick.

Although rare, rapid spontaneous resolution of epidural hematomas in the pediatric population has even been reported 2).

Numerous theories have been proposed to explain the pathophysiology behind these cases, including egress of epidural collections through cranial discontinuities (fractures/open sutures), blood that originates in the subgaleal space, and bleeding from the cranial diploic cavity after a skull fracture that preferentially expands into the subgaleal space 3)

Children born by use of vacuum extractor or forceps require careful monitoring by the nursing staff throughout their stay in the maternity unit 4).

In most cases, conservative treatment is the preferred option because adhesion between the galea aponeurotica and the periosteum restricts the extent of the hematoma. In special cases, however, the hematoma enlarges extraordinarily past these adhesions, and the patients thus affected suffer from progressive anemia followed by the lethargy and headache resulting from the excessive distension of the skin and the subcutaneous tissue. In such cases, hematoma removal is performed in order to relieve the symptoms 5).

The therapeutic strategy for massive subgaleal hematoma is individualized. However, treatment for massive subgaleal hematoma with skull fracture should not be considered the same as for hematoma without skull fracture. Emergent surgery is recommended before neurological deterioration is recognized in the patient if damage to the dural sinus is suspected 6).

Endoscopic techniques have been advanced along with the recent trend toward invasive neurosurgery. These minimally invasive techniques can allow sufficient removal of subgaleal hematoma with minimal morbidity, especially in patients such as ours. In addition, the utility of endoscopic techniques for the removal of subgaleal hematoma should be confirmed after long-term follow-up 7).

Usually starts as a small localized hematoma, and may become huge (with significant loss of circulating blood volume in age < 1 year, transfusion may be necessary).


A 3 kg baby was delivered by cesarean section after prolonged labor. He had massive subgaleal hematoma. He developed anemia requiring packed cell transfusions and hyperbilirubinemia requiring a total of seven exchange transfusions and highly intensive phototherapy. There were no adverse complications of the hyperbilirubinemia or the exchange transfusion 8).

A 39-year-old healthy worker came to our emergency department (ED) due to scalp lacerations from an accident that caused severe twisting of his hair. He denied head contusion and was conscious upon arrival. Physical examination showed three lacerations over his right temporal area. The wounds depth extended to the skull, with a 10-cm subperiosteal pocket beneath the lacerations. Primary sutures were performed immediately under local anesthesia, not only for wound closure but also for hemostasis. However, he returned to our ED 3 h after the first visit for a newly developed soft lump over the left side of his forehead. Computed tomography scan of brain illustrated a huge and diffuse SGH in the left temporal region with extension to periorbital region. Although the option of incision and drainage was discussed with a neurosurgeon and a search for some case reports was done, most of the hematoma could be self-limited. Conservative management with non-elastic bandage packing direct compression was applied. The patient was then admitted for close observation and conservative treatment for 1 week. There was no recurrence of SGH in the following 3 months. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: SGH is an uncommon phenomenon that is caused by tearing of the emissary veins in the loose areolar tissue located beneath the galeal aponeurosis. Conservative treatment with bandage compression is recommended for SGH. Surgery is reserved for cases where non-invasive management fails or severe complications 9).


1)

Vu TT, Guerrera MF, Hamburger EK, Klein BL. Subgaleal hematoma from hair braiding.Case report and literature review. Pediatr Emerg Cure. 2004;20:821–3
2)

Chida K, Yukawa H, Mase T, Endo H, Ogasawara K. Spontaneous slow drainage of epidural hematoma into the subgaleal space through a skull fracture in an infant–case report. Neurol Med Chir (Tokyo). 2011;51(12):854-6. PubMed PMID: 22198110.
3)

Tataryn Z, Botsford B, Riesenburger R, Kryzanski J, Hwang S. Spontaneous resolution of an acute epidural hematoma with normal intracranial pressure: case report and literature review. Childs Nerv Syst. 2013 Nov;29(11):2127-30. doi: 10.1007/s00381-013-2167-8. Epub 2013 May 26. Review. PubMed PMID: 23708934.
4)

Boumahni B, Ghazouani J, Bey KJ, Carbonnier M, Staquet P. [Subgaleal hematoma in 2 neonates]. Arch Pediatr. 2010 Oct;17(10):1451-4. doi: 10.1016/j.arcped.2010.07.011. Epub 2010 Sep 18. French. PubMed PMID: 20851581.
5)

Amar AP, Aryan HE, Meltzer HS, Levy ML. Neonatal subgaleal hematoma causing brain compression: Report of two cases and review of the literature. Neurosurgery. 2003;52:1470–4.
6)

Yamada SM, Tomita Y, Murakami H, Nakane M. Delayed post-traumatic large subgaleal hematoma caused by diastasis of rhomboid skull suture on the transverse sinus. Childs Nerv Syst. 2015 Apr;31(4):621-4. doi: 10.1007/s00381-014-2531-3. Epub 2014 Aug 21. PubMed PMID: 25142690.
7)

Hayashi Y, Kita D, Furuta T, Oishi M, Hamada J. Endoscopic removal of subgaleal hematoma in a 7-year-old patient treated with anticoagulant and antiplatelet agents. Surg Neurol Int. 2014 Jun 20;5:98. doi: 10.4103/2152-7806.134911. eCollection 2014. PubMed PMID: 25024898; PubMed Central PMCID: PMC4093743.
8)

Dutta S, Singh A, Narang A. Subgaleal hematoma and seven exchange transfusions. Indian Pediatr. 2004 Mar;41(3):267-70. PubMed PMID: 15064515.
9)

Chen CE, Liao ZZ, Lee YH, Liu CC, Tang CK, Chen YR. Subgaleal Hematoma at the Contralateral Side of Scalp Trauma in an Adult. J Emerg Med. 2017 Nov;53(5):e85-e88. doi: 10.1016/j.jemermed.2017.06.007. Epub 2017 Sep 20. PMID: 28941556.

Chronic subdural hematoma recurrence prevention

Chronic subdural hematoma recurrence prevention

In total, 402 studies were included in this analysis and 32 potential risk factors were evaluated. Among these, 21 were significantly associated with the postoperative recurrence of CSDH. Three risk factors (male, bilateral hematoma, and no drainage) had convincing evidence 1).

The single most important factor appears to be the residual subdural space after drainage of the chronic subdural hematoma and an effort should be made by the surgeon to facilitate the expansion of the underlying brain. The presence of a functioning drain for 48–72 h draining the subdural fluid and promoting brain expansion will reduce the subdural space, thus reducing the recurrence of the CSDH. Some of the relevant surgical nuances include placement of at least two burr holes with the burr holes located to drain multiple cavities, copious irrigation of the subdural space, placement of the drain in the dependent burr hole site, near-total filling of the subdural space with irrigation to prevent a pneumocephalus and placing a subdural drain. Closure of the site with a large piece of Gelfoam prevents the subgaleal blood to migrate into the subdural space.

Postoperative subdural drain of maximal 48 h is effective in reducing recurrent hematomas. However, the shortest possible drainage time without increasing the recurrence rate is unknown

see Subdural drain for chronic subdural hematoma

The effect of a physical property of irrigation solution (at body vs room temperature) on the chronic subdural hematoma recurrence rate needs further study.

Objective: To explore whether irrigation fluid temperature has an influence on cSDH recurrence.

Design, setting, and participants: This was a multicenter randomized clinical trial performed between March 16, 2016, and May 30, 2020. The follow-up period was 6 months. The study was conducted at 3 neurosurgical departments in Sweden. All patients older than 18 years undergoing cSDH evacuation during the study period were screened for eligibility in the study.

Interventions: The study participants were randomly assigned by 1:1 block randomization to the cSDH evacuation procedure with irrigation fluid at room temperature (RT group) or at body temperature (BT group).

Main outcomes and measures: The primary end point was recurrence requiring reoperation within 6 months. Secondary end points were mortality, health-related quality of life, and complication frequency.

Results: At 6 months after surgery, 541 patients (mean [SD] age, 75.8 [9.8] years; 395 men [73%]) had a complete follow-up according to protocol. There were 39 of 277 recurrences (14%) requiring reoperation in the RT group, compared with 16 of 264 recurrences (6%) in the BT group (odds ratio, 2.56; 95% CI, 1.38-4.66; P < .001). There were no significant differences in mortality, health-related quality of life, or complication frequency.

Conclusions and Relevance: In this study, irrigation at body temperature was superior to irrigation at room temperature in terms of fewer recurrences. This is a simple, safe, and readily available technique to optimize outcome in patients with cSDH. When irrigation is used in cSDH surgery, irrigation fluid at body temperature should be considered standard of care.

Trial registration: ClincalTrials.gov Identifier: NCT02757235 2).

A study aimed to evaluate the efficacy and safety of half-saline solution for irrigation in burr hole trephination for chronic subdural hematoma.

This randomized clinical trial was conducted in university hospital referral centers from 2020 to 2021. Sixty-three patients with chronic subdural hematoma eligible for burr hole trephination were primarily enrolled. Two patients were excluded because of concurrent stroke. Sixty-one patients were randomly allocated into case (HS=30) and control (normal-saline [NS]=31) groups. HS was used to irrigate the hematoma in the case group and NS was used in the control group. The patients were followed-up. Clinical variables including demographic and medical findings, postoperative computed tomography findings, postoperative complications, hospitalization period, recurrence rate, and functional status measured by the Barthel type B index were recorded.

Forty-six of 61 patients were male (75.4%), and the patients’ mean age was 65.4±16.9 years, with equal distribution between the 2 groups. Postoperative effusion and postoperative hospital stay duration were significantly lower in the HS group than in the NS group (p=0.002 and 0.033, respectively). The postoperative recurrence within 3 months in both groups was approximately equal (6.6%). In terms of functional outcomes and postoperative complications, HS showed similar results to those of NS.

Conclusion: HS as an irrigation fluid in BHC effectively reduced postoperative effusion and hospital stay duration without considerable complications.

Trial registration: Iranian Registry of Clinical Trials Identifier: IRCT20200608047688N1 3).


1)

Zhu F, Wang H, Li W, Han S, Yuan J, Zhang C, Li Z, Fan G, Liu X, Nie M, Bie L. Factors correlated with the postoperative recurrence of chronic subdural hematoma: An umbrella study of systematic reviews and meta-analyses. EClinicalMedicine. 2021 Dec 20;43:101234. doi: 10.1016/j.eclinm.2021.101234. PMID: 34988412; PMCID: PMC8703229.
2)

Bartley A, Bartek J Jr, Jakola AS, Sundblom J, Fält M, Förander P, Marklund N, Tisell M. Effect of Irrigation Fluid Temperature on Recurrence in the Evacuation of Chronic Subdural Hematoma: A Randomized Clinical Trial. JAMA Neurol. 2022 Nov 21. doi: 10.1001/jamaneurol.2022.4133. Epub ahead of print. PMID: 36409480.
3)

Mahmoodkhani M, Sharafi M, Sourani A, Tehrani DS. Half-Saline Versus Normal-Saline as Irrigation Solutions in Burr Hole Craniostomy to Treat Chronic Subdural Hematomata: A Randomized Clinical Trial. Korean J Neurotrauma. 2022 Sep 29;18(2):221-229. doi: 10.13004/kjnt.2022.18.e47. PMID: 36381457; PMCID: PMC9634318.

Moyamoya disease

Moyamoya disease

Moyamoya disease is a chronic, occlusive cerebrovascular disease, characterized by bilateral steno-occlusive changes at the terminal portion of the internal carotid artery and an abnormal vascular network at the base of the brain.

These diagnostic criteria of the moyamoya disease, stated by the Research Committee on Spontaneous Occlusion of the Circle of Willis (moyamoya disease) in Japan, are well established and generally accepted as the definition of this rare entity. On the contrary to the diagnosis of definitive moyamoya disease, there is some confusion in the terminology and understanding of quasi-moyamoya disease; moyamoya disease in association with various disease entities, such as atherosclerosis, autoimmune diseases, Down syndrome, etc. Although the clinical management is not affected by these semantic distinctions, terminological confusion may interfere with the international collaboration of the clinical investigation of these rare conditions 1).

The perforating arteries in the basal ganglia and thalamus markedly dilate and function as an important collateral circulation, called as “moyamoya” vessels. The posterior cerebral artery are also involved in a certain subgroup of patients. Therefore, cerebral hemodynamics is often impaired especially in the frontal lobe, leading to transient ischemic attack (TIa) and cerebral infarction. Furthermore, the dilated, fragile moyamoya vessels often rupture and cause intracranial hemorrhage 2) 3).

Unknown etiology.

A study indicated a higher overall autoimmune disease prevalence in unilateral than in bilateral MMD. Unilateral MMD may be more associated with autoimmune disease than bilateral MMD. Different pathogenetic mechanisms may underlie moyamoya vessel formation in unilateral and bilateral MMD 4).

The p.R4810K mutation in RNF213 gene confers a risk of MMD, but other factors remain largely unknown. Mineharu et al. tested the association of gut microbiota with MMD. Fecal samples were collected from 27 patients with MMD, 7 patients with non-moyamoya intracranial large artery disease (ICAD) and 15 control individuals with other disorders, and 16S rRNA were sequenced. Although there was no difference in alpha diversity or beta diversity between patients with MMD and controls, the cladogram showed Streptococcaceae was enriched in patient samples. The relative abundance analysis demonstrated that 23 species were differentially abundant between patients with MMD and controls. Among them, increased abundance of Ruminococcus gnavus > 0.003 and decreased abundance of Roseburia inulinivorans < 0.002 were associated with higher risks of MMD (odds ratio 9.6, P = 0.0024; odds ratio 11.1, P = 0.0051). Also, Ruminococcus gnavus was more abundant and Roseburia inulinivorans was less abundant in patients with ICAD than controls (P = 0.046, P = 0.012). The relative abundance of Ruminococcus gnavus or Roseburia inulinivorans was not different between the p.R4810K mutant and wildtype. The data demonstrated that gut microbiota was associated with both MMD and ICAD 5).

The histopathological features of the middle cerebral artery (MCA) and superficial temporal artery (STA) from moyamoya disease (MMD) and their relationships with gender, age, angiography stage were explored. The causes and the clinical significance of vasculopathy of STA were also discussed. The clinical data and specimens of MCA and STA from 30 MMD patients were collected. Twelve samples of MCA and STA from non-MMD patients served as control group. Histopathological examination was then performed by measuring the thickness of intima and media, and statistical analysis was conducted. The MCA and STA specimens from MMD group had apparently thicker intima and thinner media than those from the control group. There was no significant pathological difference between the hemorrhage group and non-hemorrhage group, and between the males and females in MMD patients. Neither the age nor the digital subtraction angiography (DSA) stage was correlated with the thickness of intima in MCA and STA. MMD is a systemic vascular disease involving both intracranial and extracranial vessels. Preoperative external carotid arteriography, especially super-selective arteriography of the STA, benefits the selection of donor vessel 6).

Quantification of the severity of vasculopathy and its impact on parenchymal hemodynamics is a necessary prerequisite for informing management decisions and evaluating intervention response in patients with moyamoya.

Computational fluid dynamics (CFD) analysis on eight patients (5 female, 3 male) with MMD treated by EDAS (encephalo-duro-arterio-synangiosis) between 2011 and 2012. All the eight patients presented with haemorrhage, with subsequent 4-12 month follow-up done using Magnetic Resonance Angiography (MRA) to capture auto-remodelling. Karunanithi et al. calculated percentage change in flow rate and pressure drop indicator (ΡDI) across the Left and Right ICA. Pressure drop indicator (PDI) is defined as the difference of pressure reduction within the carotid arteries, measured at post-op and follow up, using patient specific inflow rates. The measured percentage flow change and pressure reduction showed an increase at follow up for improved patients (characterised by angiography according to the method of Matsushima), who did not develop any complications after surgery. The inverse was observed in patients who were clinically classified as no change and retrogressed (according to the method of Matsushima) cases post-operation. This elucidates the findings of a new parameter that may well play a critical role as an assistive clinical decision making tool in MMD 7).

Artificial intelligence (AI) clustering was used to classify the articles into 5 clusters: (1) pathophysiology (23.5%); (2) clinical background (37.3%); (3) imaging (13.2%); (4) treatment (17.3%); and (5) genetics (8.7%). Many articles in the “clinical background” cluster were published from the 1970s. However, in the “treatment” and “genetics” clusters, the articles were published from the 2010s through 2021. In 2011, it was confirmed that a gene called Ringin protein 213 (RNF213) is a susceptibility gene for moyamoya disease. Since then, tremendous progress in genomictranscriptomics, and epigenetics (e.g., methylation profiling) has resulted in new concepts for classifying moyamoya disease. The literature survey revealed that the pathogenesis involves aberrations of multiple signaling pathways through genetic mutations and altered gene expression 8).


1)

Fujimura M, Tominaga T. Diagnosis of moyamoya disease: international standard and regional differences. Neurol Med Chir (Tokyo). 2015 Mar 15;55(3):189-93. doi: 10.2176/nmc.ra.2014-0307. Epub 2015 Feb 20. PubMed PMID: 25739428.
2)

Suzuki J, Takaku a: Cerebrovascular “moyamoya” disease. disease showing abnormal net-like vessels in base of brain. Arch Neurol 20: 288–299, 1969
3)

Kuroda S, Houkin K: Moyamoya disease: current concepts and future perspectives. Lancet Neurol 7: 1056–1066, 2008
4)

Chen JB, Liu Y, Zhou LX, Sun H, He M, You C. Increased prevalence of autoimmune disease in patients with unilateral compared with bilateral moyamoya disease. J Neurosurg. 2015 Sep 25:1-6. [Epub ahead of print] PubMed PMID: 26406790.
5)

Mineharu Y, Nakamura Y, Sato N, Kamata T, Oichi Y, Fujitani T, Funaki T, Okuno Y, Miyamoto S, Koizumi A, Harada KH. Increased abundance of Ruminococcus gnavus in gut microbiota is associated with moyamoya disease and non-moyamoya intracranial large artery disease. Sci Rep. 2022 Nov 24;12(1):20244. doi: 10.1038/s41598-022-24496-9. PMID: 36424438.
6)

Sun SJ, Zhang JJ, Li ZW, Xiong ZW, Wu XL, Wang S, Shu K, Chen JC. Histopathological features of middle cerebral artery and superficial temporal artery from patients with moyamoya disease and enlightenments on clinical treatment. J Huazhong Univ Sci Technolog Med Sci. 2016 Dec;36(6):871-875. PubMed PMID: 27924520.
7)

Karunanithi K, Han C, Lee CJ, Shi W, Duan L, Qian Y. Identification of a hemodynamic parameter for assessing treatment outcome of EDAS in Moyamoya disease. J Biomech. 2015 Jan 21;48(2):304-9. doi: 10.1016/j.jbiomech.2014.11.029. Epub 2014 Nov 29. PubMed PMID: 25498370.
8)

Kuribara T, Akiyama Y, Mikami T, Komatsu K, Kimura Y, Takahashi Y, Sakashita K, Chiba R, Mikuni N. Macrohistory of Moyamoya Disease Analyzed Using Artificial Intelligence. Cerebrovasc Dis. 2022 Feb 1:1-14. doi: 10.1159/000520099. Epub ahead of print. PMID: 35104814.
WhatsApp WhatsApp us
%d bloggers like this: