From the Guidelines
Autonomic dysreflexia (AD) in spinal cord injuries (SCI) is primarily caused by a noxious stimulus below the level of injury, triggering an exaggerated sympathetic nervous system response that the body cannot properly regulate due to the spinal cord damage. This condition can lead to severe hypertension, which is a significant concern in terms of morbidity, mortality, and quality of life. According to the study by 1, when a normal bladder is distended beyond approximately 300 mL, sympathetic nervous system stimulation may cause a substantial increase in blood pressure, particularly in patients with high spinal cord injuries.
Key Factors Contributing to AD
- Noxious stimuli below the level of injury, such as a full bladder or bowel distention, can trigger AD
- The inability of the body to properly regulate the sympathetic nervous system response due to spinal cord damage
- The use of sympatholytic drugs, such as 1-blockers (e.g., terazosin, doxazosin, or prazosin), can help improve blood pressure control by indirectly dilating prostatic and urinary sphincter smooth muscle and lowering blood pressure, as noted in the study by 1
Clinical Implications
The mechanism of AD highlights the importance of regular bladder and bowel management, pressure relief, and avoiding triggers that could cause this dangerous condition. Immediate identification and removal of the triggering stimulus, along with appropriate medical management, are crucial to prevent severe complications and improve quality of life. In clinical practice, it is essential to prioritize the management of AD to minimize its impact on morbidity, mortality, and quality of life.
From the Research
Mechanism of Autonomic Dysreflexia (AD) in Spinal Cord Injuries (SCI)
The mechanism of autonomic dysreflexia (AD) in spinal cord injuries (SCI) involves the loss of normal autonomic and cardiovascular control due to the disruption of sensory and motor function 2. This can result in a syndrome known as autonomic dysreflexia (AD), which is defined as episodic hypertension and concomitant baroreflex-mediated bradycardia initiated by unmodulated sympathetic reflexes in the decentralized cord 2.
Key Factors Contributing to AD
Some key factors that contribute to the development of AD include:
- Injury at or above the sixth thoracic spinal cord segment, which segregates critical spinal sympathetic neurons from supraspinal modulation 2
- Noxious yet unperceived visceral or somatic stimuli below the injury level, which can trigger AD 2, 3
- Maladaptive plasticity of neural circuits mediating abnormal sympathetic reflexes and hypersensitization of peripheral vasculature, which collectively contribute to abnormal hemodynamics after SCI 2
Systemic Effects of AD
The systemic effects of recurrent AD can be severe and include:
- High risk of cerebral or retinal hemorrhage, seizures, heart failure, or pulmonary edema 3
- Cardiac irregularities and death 4
- Intracranial and retinal haemorrhage, convulsions 4
Trigger Mechanisms
Some common trigger mechanisms for AD include: