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Hemodynamic stroke caused by strangulation
Abstract
We report a case of watershed ischemic stroke in a 36-year-old male secondary to manual strangulation. The patient presented with a right hemiparesis with grade IV motor deficit and an expressive aphasia. Radiological investigation revealed an ischemic stroke on the left distal middle cerebral artery territory and in watershed areas of the left anterior and posterior cerebral arteries. There was no evidence of injury of cervical vessels. The hemodynamic mechanism and associated brain injury secondary to manual strangulation is described and discussed based on a literature review.
Introduction
Strangulation describes the process whereby an external force is applied to the neck that results in a depressed or complete loss of consciousness. The external force can be the use of the bare hands (manual), ligature (a cord-like object), and gravity (near-hanging). The manual strangulation is a common injury found in domestic violence [1,2], in which the victim is almost always the woman.
Case reports and case series have been published [1,3] in the literature describing symptoms [4], radiology in surviving patients [5], post-mortem examination [6], and different precipitating factors of the ischemic stroke [7-11] secondary to strangulation. However there are no reports that describe the low cerebral blood flow without apparent injury to large cervical vessels as the mechanism of brain injury.
We report a case of a patient who was victim of manual strangulation and presented with ischemic stroke due to low cerebral blood flow. The hemodynamic mechanism is described and occurrence of brain injuries secondary to manual strangulation is discussed based on a literature review.
Case report
After a group assault, a 36-year-old man was taken to the emergency department of a local hospital. According to the rescue team report, the patient was attacked by 3 men and suffered manual strangulation.
He was transferred to our service, a high complexity trauma hospital, for medical evaluation and treatment after two days. The patient was admitted with normal and stable vital signs, with minor wounds on both arms. The neurological examination revealed a right hemiparesis with grade IV motor deficit and an incomplete expressive aphasia. It was noted a wound on the cervical region (zone II) with semicircular bruising, and lesions compatible with nail printing. Moreover, he had subconjunctival hemorrhage and bilateral periorbital ecchymosis (Figure 1). There was no dysphonia, dysphagia nor odynophagia.
Photography of the patient showing in (A) Subconjunctival hemorrhage and bilateral periorbital ecchymosis. In (B) Wound on the cervical region (zone II) with semicircular bruising, and lesions compatible with nail printing.
The head computed tomography (CT) showed hypoattenuation in cortical and subcortical areas of the left cerebral hemisphere compatible with watershed infarct. It also showed fracture of the left orbital floor and an intact hyoid bone (Figure 2).
The head computed tomography (CT) showed hypoattenuation in cortical and subcortical areas of the left cerebral hemisphere compatible with watershed infarct.
The investigation was complemented with magnetic resonance imaging (MRI) of the brain about 20 days after the trauma, which showed restriction on diffusion weighted imaging of the left distal middle cerebral artery territory and in watershed areas of the left anterior and posterior cerebral arteries, confirming the findings of subacute ischemic stroke.
A Doppler ultrasound and angiography of the extracranial carotid and vertebral arteries was done due to the mechanism of injury, and showed no abnormalities. Cardiovascular evaluation with electrocardiography, chest radiography and transthoracic echocardiography excluded comorbidities that could have contributed to the occurrence of cerebral ischemic injury.
After completion of the investigation, the patient remained neurologically stable with a grade IV motor deficit and improvement of the expressive aphasia. He was discharged to outpatient rehabilitation clinic.
Discussion
Asphyxia is defined as a syndrome resulting from the absence or low concentration of oxygen in the air breathed, including any form of oxygen deprivation [12]. Strangulation is a mixed type of mechanical asphyxia, in which circulatory, ventilatory and nervous phenomena overlap. The use of bare hands as the instrument of compression of neck structures (vessels and airways) is defined as manual strangulation [12,13].
The most frequent signs of manual strangulation are usually reported only in autopsies. Unfortunately, clinical findings are evident in approximately 50% of surviving patients [14]. Yen et al., described the CT and MRI findings in patients who survived manual strangulation with ischemia or hemorrhage [5].
The mechanism of death in cases of constriction of the neck may involve several factors [15]: cardiac arrhythmia by compression of the carotid sinus, obstruction of blood flow by compression of the carotid arteries, obstruction of venous return and consequent congestion secondary to the jugular veins compression, and obstruction of the airflow by compression of larynx. There may be some variables related to the way the force are applied to the neck: the area, the force magnitude, the duration and the region where force was applied [15]. However, the fatal outcome is almost always multifactorial. The classical sequence of events defined for death secondary to manual strangulation includes a mild cervical compression resulting in venous stasis and congestion associated with hypoxia due to loss of consciousness. This event leads to loss of cervical tone, ultimately causing arterial and airway obstruction (anoxic anoxia) and death [16]. There is also the arrhythmia caused by stimulation of the carotid sinus, which is observed in cases of sudden death [4,17].
The literature indicates that brain damage may occur in survivors of manual strangulation in an acute or late onset. Among the causative factors of brain injury, the cervical carotid artery dissection with or without thrombosis is the most described mechanisms [7-9]. However, there are reports of patients with brain lesions without evidence of a cervical vascular abnormality. The lesions described include: brain death on post-mortem examination (hypoxic ischemic encephalopathy), ischemic and hemorrhagic stroke (embolic or occlusive etiology) and ischemic stroke lesions of the basal ganglia [11,18].
To our knowledge, this is the first report that describes the hemodynamic mechanism without injury of large cervical vessels as the cause of brain injury. Our case showed signs suggestive of constriction of the neck (cervical bruising,and subconjunctival hemorrhage). In addition, the radiological features of ischemia suggest that the low blood flow was responsible for the injury in this patient. The significant decrease in cerebral blood flow for an unknown period of time was sufficient to cause an irreversible brain injury. Considering that the investigation showed no vascular abnormalities, one could assume that the temporary arterial stenosis due to mechanical cervical compression was the most likely mechanism of injury.
Conclusion
Although there are reports of surviving patients with brain injury secondary to manual strangulation, this is the first report that describes the low cerebral blood flow (hemodynamic) without apparent injury to large cervical vessels as the mechanism of brain injury. The extrinsic constriction of the cervical carotid artery due to manual strangulation may result in decreased cerebral blood flow, causing ischemia in watershed areas of cerebral arteries.
Disclosure of conflict of interest
None.