traumatic brain injury ( tbi ) is the most frequent reason for neurosurgical consultation in the emergency room .
minor or mild tbi is common in elderly patients , many of whom are treated on anticoagulant .
the common practice is to discharge these patients if computed tomography ( ct ) of the brain is normal .
however , a small subgroup of these patients may experience a delayed intracranial bleeding2,4 ) . here
, we describe a patient on anticoagulant therapy that developed an acute subdural haematoma ( sdh ) 48 hours after a mild head injury .
furthermore , this case report wishes to raise the awareness among emergency department physicians and neurosurgeons that treat elderly anticoagulated patients , for a possible delayed onset of intracranial haematoma , even if the initial assessment is normal .
a 66-year - old male presented to the emergency department after a fall and a mild head trauma .
the patient had a history of atrial fibrillation and was on acenocoumarol ( sintrom ) .
initial ct scan of the brain was without any sign of intracranial hemorrhage or cranial fracture ( fig .
1 ) . the laboratory workup revealed an international normalized ratio ( inr ) of 2.5 .
forty - eight hours later the patient was transferred to the emergency room with a decreased level of consciousness and vomiting . on neurological examination
he had a score of 9/15 on the glasgow coma scale ( e2v2m5 ) and a dilated left pupil unresponsive to light .
a ct scan of the brain revealed a large left acute sdh with midline shift ( fig .
the point of the haemorrhage was some bridging veins to the transverse sinus , which were promptly coagulated .
postoperatively , the left pupil became small and reactive and a ct scan demonstrated complete removal of sdh .
the patient progressively improved and one month after the operation he was discharged for further physiotherapy ( fig .
this case is another example of the very low risk of delayed subdural haematoma after minor head injury in patients , who are treated with anticoagulants .
some reports of delayed haematomas after minor head injury in adults , with a negative initial ct scan , have already been described .
however , the incidence has turned out to be extremely low ( < 0.02% ) .
it is generally accepted that elderly tbi patients are at greater risk for clinically important brain injury .
furtherrmore , oral anticoagulation is associated with a significant risk of intracranial bleeding , even after a minor head trauma2,3 ) .
there have been previously five well - documented reports of delayed subdural haematoma after tbi2,5 ) .
the clinical and radiologic characteristics are summarized in table 1 . as it is shown in the above table
more specifically , there were two deaths , two patients remained with severe and one with moderate disability , while one had a good recovery .
one commonly discussed mechanism for the development of acute sdh is the rupture of bridging veins , which empty into the dural sinuses .
as the veins cross the subdural space , they have little supporting structure , and are therefore more vulnerable to injury at this point . in elderly patients with cerebral atrophy , bridging veins are stretched and transverse a greater distance in the subdural space .
doherty suggests that rupture of these veins is the mechanism for delayed sdh in patients with trauma - induced hypotension and cerebral edema .
in addition , there is a delayed tamponade effect since the atrophied brain is shrunken away from the inner table of the skull . in these patients with hypotension ,
matsuda et al.4 ) suggest , that inflammation or vasoparalysis resulting from local hypoxia after a head trauma may increase the permeability of the vessels and may form coalescent small perivascular haemorrhages . in this case
, the patient had been straining to tighten a bolt of his football helmet when he suffered the acute subdural hemorrhage .
this valsalva maneuver might have caused increased intracranial pressure , hypercapnia , and subsequent venous congestion , resulting in subdural hemorrhage because of a rupture of coalescent vessels . in our patient , it was found intraoperatively that the cause of the subdural hematoma was the tearing of some bridging veins to the transverse sinus .
it is believed that these bridging veins were damaged by the primary injury and 48-hours later , a valsalva maneuver and a temporary increase of the icp could have caused the tearing of the bridging veins and the subsequent development of the haematoma .
therefore , an overnight observation period and a negative first ct scan do not entirely eliminate the possibility that the patient will later develop an intracranial haematoma .
this possibility , according to the persisting literature , seems to be greater for the patients over the age of 65 , who are under anticoagulant therapy .
the nice guidelines6 ) state that it is safe to discharge the abovementioned patients if imaging is normal . however , as it was explained above , these patients may be then exposed to comparatively high risks of delayed deterioration
. currently , there are no specific guidelines regarding the anticoagulated patients with a negative initial ct scan4 ) . one recent paper from menditto et al.5 ) also underlines the need for reevaluation of the current guidelines after a head injury on patients receiving anticoagulant therapy .
they suggest a 24-hour observation period for all the patients under anticoagulants followed by a second ct scan .
both of them had an inr greater than 3.0 and age over 65 years old .
based on the current literature and on our experience we propose a modification of this protocol .
we suggest all the patients receiving anticoagulants to be hospitalized for 24 hours followed by a second ct scan . for the subgroup of patients over the age of 65 and with an inr greater than 2.5
, we suggest to extend the observation period to 48 hours followed by a ct scan . as long as
we can not prevent primary injuries , we should not fail to prevent fatal deterioration if at all possible .
our case report underlines the need , that physicians and neurosurgeons should maintain a high level of vigilance in anticoagulated patients , after a mild tbi , due to a possible delayed onset of intracranial haematoma , even if the initial assessment is normal .
we recommend that all anticoagulated patients , who experience a head injury , should be hospitalized for a 24-hour neurological observation followed by a second ct scan .
for the subgroup of patients over the age of 65 and with an inr greater than 2.5 , we suggest to extend the observation period to 48 hours followed by a ct scan .
 mild traumatic brain injury is common in elderly patients , many of whom are on anticoagulant . 
 the common practice is to discharge these patients from the emergency room if the computed tomography ( ct ) of the brain is normal . 
 however , a very small proportion of these patients may develop a life threatening intracranial haematoma in the following days . 
 we present here a case of a 66-year - old male on anticoagulant therapy that developed a subdural haematoma 48 hours after a mild head injury , with a normal initial ct scan of the brain . 
 the patient underwent a craniotomy with evacuation of a large subdural clot . 
 postoperatively he had progressively improved and six months later has a glasgow outcome score of three . 
 this case is characterized by the delayed onset of a subdural haematoma in a patient on anticoagulation and we discuss here the possible pathogenesis related to this phenomenon . 
 we also briefly review the pertinent literature and the current guidelines for the management of this type of head injuries . 