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Acute subdural hematoma case series


Kaestner et al., identified patients presenting between January 2012 and September 2017 with an aSDH. All patients treated conservatively were selected retrospectively, and the following parameters were documented: age, sex, chronification status, Glasgow Coma Scale score on admission and discharge, hematoma thickness and density, the degree of midline shift (MLS), prior anticoagulants and administration of procoagulants, thrombosis management, other coagulopathies, initial length of hospital stay, interval between discharge and readmission, and interval between initial injury and date of surgery and last follow-up. The cohort was divided into patients with complete resolution of their aSDH, and patients who needed surgery due to chronification.

A total of 75 conservatively treated patients with aSDH were included. A chronification was observed in 24 cases (32%). The process of chronification takes an average of 18 days (range: 10-98 days). The following factors were significantly associated with the process of chronification: age (p = 0.001), anticoagulant medication (acetylsalicylic acid [ASA], Coumadin, and novel anticoagulants [NOACs]) before injury (p = 0.026), administration of procoagulants (p = 0.001), presence of other coagulopathies such as thrombocytopenia (p = 0.002), low hematoma density at discharge (p = 0.001), hematoma thickness on admission and discharge (p = 0.001), and the degree of MLS (p = 0.044).

Chronification occurred in a third of all patients with conservatively treated aSDH, on average within 3 weeks. The probability of developing a cSDH is 0.96 times higher with every yearly increase in age, resulting in 56% chronification in patients ≥ 70 years. Hematoma thickness and impairment of the coagulation system such as anticoagulant medication (ASA, Coumadin, and NOACs) or thrombocytopenia are further risk factors for chronification 1).


Beynon et al. analyzed the medical records of consecutive patients treated at our institution for acute SDH during anticoagulation therapy with Direct oral anticoagulants (DOAC) or vitamin K antagonists (VKA) during a period of 30 months. Patient characteristics such as results of imaging and laboratory studies, treatment modalities and short-term patient outcomes were included.

A total of 128 patients with preadmission DOAC (n = 65) or VKA (n = 63) intake were compared. The overall 30-day mortality rate of this patient cohort was 27%, and it did not differ between patients with DOAC or VKA intake (26% vs. 27%; p = 1.000). Similarly, the rates of neurosurgical intervention (65%) and intracranial re-hemorrhage (18%) were comparable. Prothrombin complex concentrates were administered more frequently in patients with VKA intake than in patients with DOAC intake (90% vs. 58%; p < 0.0001). DOAC treatment in patients with acute SDH did not increase in-hospital and 30-day mortality rates compared to VKA treatment.

These findings support the favorable safety profile of DOAC in patients, even in the setting of intracranial hemorrhage. However, the availability of specific antidotes to DOAC may further improve the management of these patients 2)


A retrospective chart review of consecutive patients age ≥ 16 with Glasgow Coma Score (GCS) ≥ 13 and CT-documented isolated SDH presenting to a university affiliated, urban, 100,000-annual-visit ED from 2009-2015. Demographic, historical and physical exam variables were collected. Primary outcome was a composite of neurosurgical intervention, worsening repeat CT and neurological decline. Univariate analysis was performed and statistically important variables were utilized to create a logistic regression model.

644 patients with isolated SDH were reviewed, 340 in the derivation group and 304 in the validation set. Mortality was 2.2%. 15.5% of patients required neurosurgery. A decision instrument was created: patients were low risk if they had none of the following factors: SDH thickness ≥ 5mm, warfarin use, clopidogrel use, GCS < 14 and presence of midline shift. This model had a sensitivity of 98.6% for the composite endpoint, specificity of 37.1% and a negative likelihood ratio of 0.037. In the validation cohort, sensitivity was 96.3%, specificity was 31.5% and negative likelihood ratio was 0.127.

Subdural hematomas are amenable to risk stratification analysis. With prospective validation, this decision instrument may aid in triaging these patients, including reducing the need for transfer to tertiary centers 3).

Won et al. analyzed 139 patients with aSDH treated from 2007 until 2015. Baseline characteristics and clinical findings including Glasgow coma scale (GCS) at admission, 24 hours after operation, timing of operation, anticoagulation, Glasgow outcome scale (GOS) at hospital discharge and after 3 months were analyzed. Multivariate logistic regression analysis was performed to detect independent predictors of seizures and a scoring system was developed.

Of 139 patients, overall incidence of seizures was 38%, preoperatively 16% and postoperatively 24%. Ninety percent of patients with preoperative seizures were seizure-free after operation for 3 months. Independent predictors of seizures were GCS < 9 (OR 3.3), operation after 24 hours (OR 2.0) and anticoagulation (OR 2.2). Patients with seizures had a significant higher rate of unfavorable outcome at hospital discharge (p=0.001) and in 3 month follow-up (p=0.002). Furthermore a score system (GATE-24) was developed. In patients with GCS < 14, anticoagulation or surgical treatment 24 hours after onset a prophylactic antiepileptic treatment is recommended.

Occurrence of seizures affected severity and outcomes after surgical treatment of aSDH. Therefore, seizure prophylaxis should be considered in high-risked patient based on GATE-24 score to promote better clinical outcome 4).

Vilcinis et al. performed a prospective review of all adult patients with ASDH operated on by craniotomy from January 2009 to January 2016. Mortality and discharge outcomes (Glasgow Outcome Scale) were analyzed as a function of surgical method adjusting for age, admission Glasgow Coma Scale score, ASDH thickness and midline shift.

OC was performed in 394 (61%) patients, and DC was performed in 249 (39%) patients. Patients undergoing DC were younger, with lower Glasgow Coma Scale score, greater ASDH thickness, and greater midline shift (P < 0.001). Mortality rate (54% vs. 20%; P < 0.001) and proportion of patients with poor discharge outcomes (85% and 45%; P < 0.001) were greater in DC patients versus OC patients. Glasgow Outcome Scale score was lower and mortality rate was greater (P ≤ 0.048) in DC patients versus OC patients across all patient subgroups. Outcomes were similar between the 2 groups in patients with Glasgow Coma Scale score of 3 and midline shift of ≥2 cm. Adjusting for disease severity, DC remained associated with greater risk for in-hospital mortality (odds ratio = 3.442 [95% confidence interval 2.196-5.396], P < 0.001) and unfavorable discharge outcome (odds ratio = 5.277 [95% confidence interval 3.030-9.191], P < 0.001).

DC was performed more often in younger and more severely injured patients. DC is associated with greater mortality and handicap rates independent of disease severity. Clinical trials investigating optimal surgical management strategy of patients with ASDH are needed 5).


Renzi et al., present a retrospective analysis of 316 consecutive cases of post-traumatic aSDH operated on between 2003 and 2011.

Mortality was 67% (n = 212); a useful recovery was achieved in 16.4% cases (n = 52). Age >65 years, a preoperative Glasgow coma scale (GCS) ≤ 8, specific pre-existing medical comorbidities (hypertension, heart diseases) were found to be strong indicators of unfavorable outcomes and death during hospitalization.

The results, compared with those of the inherent literature, led the authors to question both the “aggressiveness” of neurosurgical care indications in certain subpopulations of patients being known to fare worse or even die regardless of the treatment administered and the relevance of the results concerning mortality and functional recovery reported by third authors 6).

Kaestner S, van den Boom M, Deinsberger W. Frequency of and Risk Factors for Chronification in Traumatic Acute Subdural Hematoma following Conservative Therapy. J Neurol Surg A Cent Eur Neurosurg. 2019 Jun 10. doi: 10.1055/s-0039-1685188. [Epub ahead of print] PubMed PMID: 31181579.
Beynon C, Brenner S, Younsi A, Rizos T, Neumann JO, Pfaff J, Unterberg AW. Management of Patients with Acute Subdural Hemorrhage During Treatment with Direct Oral Anticoagulants. Neurocrit Care. 2018 Oct 31. doi: 10.1007/s12028-018-0635-4. [Epub ahead of print] PubMed PMID: 30382531.
Pruitt P, Van Ornam J, Borczuk P. A Decision Instrument to Identify Isolated Traumatic Subdural Hematomas at Low Risk of Neurological Deterioration, Surgical Intervention or Radiographic Worsening. Acad Emerg Med. 2017 Sep 4. doi: 10.1111/acem.13306. [Epub ahead of print] PubMed PMID: 28871614.
Won SY, Dubinski D, Herrmann E, Cuca C, Strzelczyk A, Seifert V, Konczalla J, Freiman TM. Epileptic seizures in patients following surgical treatment of acute subdural hematoma - incidence, risk factors, patient outcome and development of a new scoring system for prophylactic antiepileptic treatment (GATE 24-score). World Neurosurg. 2017 Feb 14. pii: S1878-8750(17)30186-9. doi: 10.1016/j.wneu.2017.02.024. [Epub ahead of print] PubMed PMID: 28213197.
Vilcinis R, Bunevicius A, Tamasauskas A. The Association of Surgical Method with Outcomes of Acute Subdural Hematoma Patients: Experience with 643 Consecutive Patients. World Neurosurg. 2017 May;101:335-342. doi: 10.1016/j.wneu.2017.02.010. Epub 2017 Feb 13. PubMed PMID: 28216211.
Lenzi J, Caporlingua F, Caporlingua A, Anichini G, Nardone A, Passacantilli E, Santoro A. Relevancy of positive trends in mortality and functional recovery after surgical treatment of acute subdural hematomas. Our 10-year experience. Br J Neurosurg. 2016 Sep 6:1-6. [Epub ahead of print] PubMed PMID: 27596026.
acute_subdural_hematoma_case_series.txt · Last modified: 2019/12/12 08:11 by administrador