A peripheral IV was placed, and the patient was connected to a cardiac monitor, which showed atrial fibrillation and a heart rate of 70 beats/minute, which is a rare presentation but could be attributed to adequate management of rate, per the RACE II studies.1 A F.A.S.T. exam was negative. While undergoing CT, the patient suddenly decompensated and became more obtunded, though still arousable. He began to vomit and became incontinent of urine. His blood pressure elevated to >200/100 mm Hg, and his heart rate decreased to 48 to 50 beats/minute.
CT of the cervical spine revealed no acute pathology. CT imaging of the brain revealed an acute 1.3-cm subdural hematoma over the right convexity and 1.5 cm of midline shift to the left. The right lateral ventricle and third ventricle were effaced (see Figure 1). No masses were present, and there was no sign of epidural hematoma or subarachnoid hemorrhage. Neurosurgery staff arrived and repeated the physical examination. The patient now had no response to stimuli, became unresponsive, and his GCS was rated at 3.
Figure 1. CT of the brain
A relative of the patient arrived at the hospital and provided a medical history of atrial fibrillation, which was treated with warfarin. There was no other known past medical or surgical history for this patient. His primary languages were Spanish and English.
The patient was returned to the trauma bay for immediate endotracheal intubation, and a right femoral central line was placed. A chest radiograph confirmed proper tube placement. The patient’s initial INR was 2.89, and activated prothrombin complex concentrate was administered, which corrected the INR to 1.14. The patient was taken to the operating room for an emergent craniectomy and decompression, as his status had deteriorated, there was 1.5cm of midline shift, and there was effacement of the ventricles.
Two days later, the patient was awake, alert, and oriented with full sensorimotor function in all extremities. CT of the brain showed postsurgical changes of right frontal temporoparietal craniectomy. A small right subdural hematoma was noted overlying the posterior temporal and occipital lobe and tracking along the posterior interhemispheric fissure. There was no midline shift (see Figure 2). Six days later, the patient was expected to make a full to near-full recovery. He had been extubated, was tolerating a regular diet, and speaking fluently in Spanish and English. He was transferred to a rehabilitation unit.
Figure 2. Postoperative CT of the brain
This patient’s history and physical examination were limited by a presumed language barrier. The patient was Hispanic, and it was assumed that he was speaking a dialect. Translation services were ordered during the patient’s arrival, but he deteriorated prior to having someone available to effectively communicate with him. However, his language, cognition, and speech were impaired by the mass effect due to the subdural hematoma. This patient’s cranial examination was atraumatic of physical examination, even though he had sustained head trauma. The quick availability of translators or translation systems may have led to a more accurate assessment and prompt assessment of this patient prior to the CT scan.
The diagnosis of subdural hematoma was made with CT imaging. Subarachnoid hemorrhage and epidural hematoma were likely differential diagnoses, but the CT imaging was able to rule out these alternatives. While a cerebral mass was a possible diagnosis, the traumatic presentation made this differential less likely. CT imaging was also able to exclude that this patient’s symptoms were due to a cerebral mass.
Treatment options for patients with traumatic subdural hematoma include watchful waiting versus surgical intervention (see Table 1).
Table 1. Indication for immediate surgical intervention
|Midline shift||Greater than or equal to 5 mm|
|Thickness||Greater than 10 mm|
|Glasgow Coma Scale score||GCS score decreases by 2 or more points between the time of injury and hospital evaluation|
|Pupils||Patient presents with fixed and dilated pupils|
|Intracranial pressure||ICP exceeds 20 mm Hg|
Modified from Bullock et al, 2006.2
Traumatic subdural hematoma is a risk factor for patients who sustain a head trauma and are taking anticoagulation medications. In the United States, admission rates for traumatic subdural hematoma increased 154% from 1993 to 2006.3 However, in-hospital deaths decreased from 16.4% to 11.6% for traumatic subdural hematoma during this same time frame.3 There is a 31% mortality rate for patients who sustain a traumatic subdural hematoma when taking warfarin.4 Emergent diagnosis and treatment in these patients is critical for patient survival.
Lindsay Gietzen, PA-C, is an assistant professor (clinical), physician assistant studies, Department of Health Care Sciences at Wayne State University in Detroit, and Kevin Ryan, PA-C, is a physician assistant with the University of Michigan Health System in Ann Arbor.
- Heist EK, Mansour M, Ruskin JN. Rate control in atrial fibrillation: targets, methods, resynchronization considerations. Circulation. 2011;124:2746-2755.
- Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell DW, et al. Surgical management of acute subdural hematomas. Neurosurgery. 2006;58(3 Suppl):S16-S24.
- Kalanithi P, Schubert RD, Lad SP, Harris OA, Boakye M. Hospital costs, incidence, and inhospital mortality rates of traumatic subdural hematoma in the United States. J Neurosurg. 2011;115:1013-1018.
- Hart RG, Diener H, Yang S, Connolly SJ, Wallentin L, Reilly PA, et al. Intracranial hemorrhage in atrial fibrillation patients during anticoagulation with warfarin or dabigatran: The RE-LY Trial. Stroke. 2012;43:1511-1517.