Patients with cSDH presenting with new or worsening neurological deficits, especially if they are debilitating and adversely affecting quality of life require urgent medical and surgical attention. Neurological and neurosurgical critical care team need to stabilize the patient by reversing any underlying coagulopathy states in order to prevent further hematoma expansion.In the event of brain herniation and presumed ICP elevation and CPP compromise, step-wise ICP management should be instituted promptly.Seizure prophylaxis treatment is reasonable. Timing of surgical evacuation is not always easy to determine but the presence of significant neurological deficits with impending herniation require immediate surgical Intervention. Consideration of the clot density along with patient’s current neurological status would determine the timing and type of surgical interventions. Postoperative critical care management is not trivial. In addition to detecting any changes in neurological conditions, timely initiation (typically within the first 48 hours if clinical and radiographic conditions are stable with no co-existing coagulopathy) of venous thromboembolism prophylaxis is essential. Resuming antiplatelets and anticoagulants are warranted for those with clear indications including atrial fibrillation, atrial thrombus, known deep vein thrombosis, mechanical heart valves and other preexisting hypercoagulable conditions, but it is generally advised to hold antiplatelets and anticoagulants for about 10-14 post injury and/or surgical intervention.
Key points
- •
A chronic subdural hematoma (cSDH) is a collection of old (>3 weeks) blood products and blood breakdown products that have accumulated in the subdural space, which is a potential space between the dura mater and the arachnoid layers of the meninges.
- •
cSDH is increasingly common due to the combination of more frequent use of anticoagulant and antiplatelet agents and the advanced age of many people in the population.
- •
The incidence of cSDH is estimated to be between 3.4 and 58 per 100,000 person-years, depending on the age of the population, with the average presenting age 63 years.
- •
The United Nations predicts that the percentage of the population above the age of 65 is expected to double between 2010 and 2050.
- •
cSDH is more prevalent in men, with a 3:1 male-to-female ratio.
Case presentation
A 50-year-old man with a history of hypertension and alcohol abuse with prior withdrawal-related seizures presented to an outside hospital facility with confusion and headache after a witnessed fall. Further questioning revealed that he suffered a fall approximately 8 weeks prior to presentation. Since then he has been experiencing progressive dizziness and intermittent headaches. For the 10 days prior to presentation, he noticed progressive right arm weakness. On the day of presentation, after drinking a few beers, bystanders noted that he was confused and then suffered a fall from standing without head strike or loss of consciousness. The emergency medical service was activated, and he was taken to an outside hospital facility for evaluation. Initial vital signs were notable for no fever with blood pressure 152/105 mm Hg and a pulse of 102 beats per minute. He was awake and alert but confused. He was able to state his name and provide the history surrounding his fall but was unable to state his current location or the date. He was very combative. His right pupil was 6 mm and left pupil was 5 mm and both were reactive to light. He had pronator and downward drift in the right arm with decreased strength in all muscle groups. He had full strength in the left arm and both legs. His Glasgow Coma Scale (GCS) score was 14. His initial blood testing was notable for normal electrolytes, slightly elevated liver function tests, and mild anemia with normal platelet count and normal coagulation studies. CT scan of the head showed large left-sided cSDH ( Fig. 1 ). He was immediately transported to the authors’ facility for further management.
Case presentation
A 50-year-old man with a history of hypertension and alcohol abuse with prior withdrawal-related seizures presented to an outside hospital facility with confusion and headache after a witnessed fall. Further questioning revealed that he suffered a fall approximately 8 weeks prior to presentation. Since then he has been experiencing progressive dizziness and intermittent headaches. For the 10 days prior to presentation, he noticed progressive right arm weakness. On the day of presentation, after drinking a few beers, bystanders noted that he was confused and then suffered a fall from standing without head strike or loss of consciousness. The emergency medical service was activated, and he was taken to an outside hospital facility for evaluation. Initial vital signs were notable for no fever with blood pressure 152/105 mm Hg and a pulse of 102 beats per minute. He was awake and alert but confused. He was able to state his name and provide the history surrounding his fall but was unable to state his current location or the date. He was very combative. His right pupil was 6 mm and left pupil was 5 mm and both were reactive to light. He had pronator and downward drift in the right arm with decreased strength in all muscle groups. He had full strength in the left arm and both legs. His Glasgow Coma Scale (GCS) score was 14. His initial blood testing was notable for normal electrolytes, slightly elevated liver function tests, and mild anemia with normal platelet count and normal coagulation studies. CT scan of the head showed large left-sided cSDH ( Fig. 1 ). He was immediately transported to the authors’ facility for further management.
Introduction
A cSDH is a collection of old (>3 weeks) blood products and blood breakdown products that have accumulated in the subdural space, which is a potential space between the dura mater and the arachnoid layers of the meninges. cSDH is increasingly common due to the combination of more frequent use of anticoagulant and antiplatelet agents and the advanced age of many people in the population. The incidence of cSDH is estimated to be between 3.4 and 58 per 100,000 person-years, depending on the age of the population. The average presenting age is 63 years. The United Nations predicts that the percentage of the population above the age of 65 is expected to double between 2010 and 2050. The US census reported that 12% of the population (or 35.9 million people) were over the age of 65 in 2003. This is expected to rise to approximately 20% of the population (or 72 million people) by the year 2030. The incidence of cSDH is expected to follow accordingly. In elderly individuals, cSDH has been identified as a sentinel event linked to underlying systemic pathology with 1-year mortality similar to that of a hip fracture. cSDH is more prevalent in men, with a 3:1 male-to-female ratio. cSDH is bilateral in 20% to 25% of cases.
cSDH occurs at the dural border cell layer, which is between the dura mater and arachnoid mater ( Fig. 2 ). Generally, 2 predisposing factors must be present for a cSDH to develop: (1) decreased brain volume (eg, in elderly patients and patients abusing alcohol) and (2) previous head trauma. Experts believe there are several causes that lead to the formation of cSDH. The 2 most common are thought to be an acute subdural hematoma and a subdural hygroma (a collection of cerebral spinal fluid in the subdural space). In acute subdural hematoma, incomplete resorption of the blood products leads to the formation of cSDH. In both causes, a substantial inflammatory response infiltrates the subdural space. This inflammation includes angiogenic factors that lead to neovascularization. Although these friable capillaries are forming, they are subject to microhemorrhages, which result in cSDH. Many risk factors are thought to contribute to the formation of cSDH, including advanced age, history of falls, alcohol abuse (due to brain atrophy, increased fall risk, and coagulopathy), epilepsy, low intracranial pressure states, and hemodialysis. As discussed previously, there has been an increase in the use of anticoagulants and antiplatelet agents. This has led to a higher incidence of both atraumatic cSDH (whereby the antecedent trauma is so minor that it is not recalled) and recurrent cSDH.
Some sources refer to cSDH as the “great imitator” given its heterogenous presenting symptoms and that its symptom onset can range from days to weeks prior to presentation. In a pooled cohort of 205 randomized controlled trial participants, presenting symptoms included gait disturbance and falls, cognitive decline, limb weakness, and acute confusion ( Box 1 ). In the same cohort, a majority of patients presented with a GCS score 13 to 15 (81%) whereas 12% had a GCS score 9 to 12, and 7% had a GCS score less than or equal to 8. A diagnosis of cSDH is usually made using CT scan of the head, on which cSDH usually appears as a hypodense, crescent-shaped collection along the convexity of the brain. There may be the presence of hyperdense or isodense material associated with the hypodense collection owing to the descriptive terms, acute-on-chronic hematoma and subacute-on-chronic subdural hematoma, respectively.
- •
Acute confusion
- •
Aphasia
- •
Collapse
- •
Drowsiness or coma
- •
Falls
- •
Gait disturbance
- •
Headache
- •
Incontinence
- •
Limb weakness
- •
Mental deterioration
- •
Seizure
- •
Speech impairment
- •
Status epilepticus
- •
Visual disturbance
- •
Vomiting
Preoperative management
Initial assessment of a patient with a cSDH should include evaluations of the airway, breathing, and circulation. Any acutely life-threatening issues should be appropriately managed. As a general rule, a GCS score of less than 8 warrants endotracheal intubation. A detailed history should be obtained with a focus on prior falls and head trauma as well as the use of antiplatelet or anticoagulant agents. A physical examination should be conducted, including a calculation of GCS score and evaluation for focal neurologic deficits. Initial laboratory evaluation should include chemistries and electrolytes, complete blood cell count, liver function tests, and coagulation studies. A noncontrast CT scan of the head should be completed to make a diagnosis of cSDH.
Reversal of Coagulopathies
Once the patient is stabilized, the focus should move to the management of any coagulopathies. The initial step is the cessation of any anticoagulant or antiplatelet agents. The next step is the decision to reverse any coagulopathy that may exist. One series of 88 patients showed that patients with cSDH who presented on anticoagulant medications experienced a significantly longer hospital stay (11 vs 7.5 days, P = .040), although the percentage with a good modified Rankin scale at discharge was not significantly different between the groups. General consensus is that patients with cSDH presenting on anticoagulant medications should undergo rapid reversal to prevent hematoma expansion and to allow for urgent neurosurgical intervention; this even applies to patients on anticoagulation for prosthetic heart valves. Oral warfarin, a vitamin K antagonist, is the most frequently used anticoagulant medication associated with cSDH. The vitamin K antagonists are reversed using prothrombin complex concentrate (PCC), fresh frozen plasma (FFP), and vitamin K. Traditionally, FFP has been the first-line therapy in the reversal of vitamin K antagonists. Its use, however, can predispose to additional medical complications given its large volume of infusion. Alternatively, PCC can be infused over a few minutes and has a volume exponentially smaller than FFP. With both PCC and FFP, vitamin K should be used an adjunctive therapy to facilitate the liver in producing new clotting factors. For cases in which a more gradual reversal technique is acceptable, vitamin K can be used as monotherapy. Most institutions have guidelines on the use of these agents. The clinical situation and the acuity of any necessary surgical intervention guide the decision on which agents to use.
Novel oral anticoagulants (NOACs) include factor Xa inhibitors and direct thrombin inhibitors. There is limited experience with the reversal of these agents. The best antidote for NOACs is time in the absence of life-threatening acute hematoma expansion or the need for emergent surgical intervention. The Neurocritical Care Society guidelines suggest using activated charcoal and PCC for NOAC reversal, but this is based on low-quality evidence and this decision should be made with input from a hematologist. The direct thrombin inhibitor dabigatran now has a Food and Drug Administration–approved antidote, idarucizumab. It is suggested that the reversal of dabigatran involve activated charcoal, hemodialysis, and PCC (all low-quality evidence) and idarucizumab (moderate-quality evidence). Laboratory assays have been developed that can aid in assessing the anticoagulant effect of NOACs. Diluted thrombin time for direct thrombin inhibitors and factor Xa levels for factor Xa inhibitors are inconsistently available and the extent of their clinical use is not fully established.
For antiplatelet therapy, it has been established that 7 to 10 days are necessary to allow for the production of fully functional platelets to replace the inhibited ones in circulation. When emergent surgical intervention is necessary, platelet transfusion is recommended to acutely reverse the effects of antiplatelet agents although there is scant evidence to support this. Some centers combine platelet transfusion with a single dose of desmopressin, but this too is based on minimal evidence.
Mannitol and Hypertonic Saline
Mannitol and hypertonic saline are agents used to create an osmotic gradient between the brain and the plasma, ultimately removing free water from the brain in an effort to decrease the intracranial pressure. In acute subdural hematoma, there is a theoretic concern of SDH expansion with the use of hypertonic and hyperosmotic agents because it is thought that the full brain has a tamponade effect on the SDH. Despite this theoretic concern, the temporary use of hypertonic and hyperosmotic agents in patients actively experiencing cerebral herniation or impending herniation should be advocated as a temporizing measure prior to surgical intervention.
Seizure Prophylaxis
Only a few studies have examined the rate of seizures in patients with cSDH. The preoperative incidence of seizures ranged from 2% to 19%; postoperative seizure incidence was 1% to 23%. Two studies reported no significant difference in the seizure rate related to the use of prophylactic anticonvulsive medications (ACMs). The investigators concluded that there was no benefit in using prophylactic ACM except in patients at high risk of seizures, such as patients abusing alcohol. A third study showed that 2.4% of patients treated with therapeutic prophylactic ACMs experienced a seizures compared with 32% of patients who were not adequately treated with prophylactic ACMs. The investigators concluded that this significantly increased the morbidity and mortality for the patients who experienced new-onset seizures and therefore recommended the use of prophylactic ACMs in cSDH. A fourth study found that preoperative administration of prophylactic ACMs was the only independent predictor of decreased incidence of postoperative seizures. Despite this, there was no effect on discharge outcomes, suggesting that, if given, prophylactic ACMs should be administered prior to surgical intervention. Given these mixed results, practices vary in their use of prophylactic ACMs. The authors’ practice is to treat with seizure prophylaxis for 7 days, especially in patients who are undergoing surgical intervention or have an increased risk of seizures, such as alcoholics or those with significant underlying traumatic brain injury.
Corticosteroids
Because inflammation plays a role in the pathophysiology of cSDH, multiple studies have examined the use of corticosteroids as monotherapy to avoid surgery and in combination to surgical intervention. Medical management of cSDH is discussed in a See Jan Claassen’s article, “ Chronic Subdural Medical Management ”, in this issue, so monotherapy is not discussed in this article. European studies have shown the use of preoperative and postoperative steroids reduces the rate of cSDH recurrence after surgical treatment and decreases 6-month mortality. An additional retrospective study suggests that local application of methylprednisolone into the hematoma cavity at the time of surgery may reduce hematoma recurrence. The evidence is insufficient, however, to draw any significant conclusions, and further study with randomized controlled trials should be conducted. It is the authors’ practice not to use steroids as monotherapy or as adjunctive therapy to surgical intervention in the treatment of cSDH. The use of corticosteroids in the treatment of cSDH is generally not recommended due to lack of evidence.
Indication for Surgical Intervention
Clinical presentation and radiographic appearance both influence the decision for surgical intervention. A small cSDH in an asymptomatic patient is best managed with clinical and radiographic observation in a closely monitored setting. Should a patient develop significant neurologic symptoms, however, surgical intervention is advised. Although the radiographic size of the cSDH plays a role in the decision for surgery, there is no absolute size greater than which a surgical intervention is mandated. The spontaneous resolution of cSDHs of significant size has been reported in a few case series. The investigators described these patients as advanced in age (>70 years) with significant cerebral atrophy and no clinical or radiographic evidence of increased intracranial pressure.
Management of asymptomatic patients with cSDHs large enough to cause brain compression and/or midline shift remains a controversial topic. Despite the lack of evidence to establish a size cutoff, it is generally accepted that hematoma volume with a maximum thickness greater than 1 cm, or greater than the thickness of the skull, should undergo surgical evacuation.
Patients with neurologic symptoms that can be attributed to a radiographically proved cSDH warrant immediate surgical evacuation. These symptoms are dictated by the location of the cSDH but can include aphasia, neglect, contralateral hemiparesis, and partial seizures. For patients with a large cSDH causing mass effect on the left frontotemporal convexity, it is not uncommon to observe a profound aphasia; some of these patients have severe global aphasia with or without contralateral hemiparesis. An isolated aphasia with intact level of alertness is often due to the chemical irritation of the dominant hemisphere and does not necessarily mean the patient is experiencing a stroke or status epilepticus. Although it is prudent to rule out acute ischemic stroke and seizures for anyone with acute aphasia, such a symptom is frequently seen with dominant hemispheric convexity subdural hematomas — whether acute or chronic. Large hematomas, or those in a frontotemporal location, can lead to brainstem compression resulting in anisocoria, coma, and death. The presence of these symptoms associated with a cSDH necessitates emergent surgical intervention. Surgical options include burr hole craniostomy, twist drill craniostomy, and craniotomy, all of which are discussed in See William Mack’s article, “ Minimally Invasive Surgical Approaches for Chronic Subdural Hematomas and See Louis Kim’s article, Craniotomy for treatment of chronic subdural hematoma ”, in this issue.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
