Autonomic Dysreflexia | Pathophysiology | Causes | Symptoms | Diagnose | Treatment

TLDR;

This video provides a detailed explanation of Autonomic Dysreflexia, a potentially life-threatening condition characterized by an overreaction of the autonomic nervous system to stimuli below the level of a spinal cord injury. The video covers the definition, causes, pathophysiology, symptoms, diagnostic tests, and management of this condition. Key points include the importance of understanding the autonomic nervous system, identifying triggers, and promptly managing the condition to prevent severe complications.

• Autonomic Dysreflexia is a life-threatening condition requiring immediate action.
• It primarily affects individuals with spinal cord injuries at or above the T6 level.
• Common triggers include bladder distension, bowel distension, and skin breakdown.
• Management involves identifying and removing the trigger, along with medical interventions to lower blood pressure.

Introduction to Autonomic Dysreflexia [0:00]

Autonomic Dysreflexia is a nervous system disorder characterized by abnormal reflex actions due to disturbances in the autonomic nervous system, specifically the sympathetic nervous system. This condition is life-threatening and requires immediate attention. It typically occurs in patients with spinal cord injuries, particularly at or above the T6 level. The injury leads to an overreaction of the autonomic nervous system in response to stimuli below the level of injury.

Understanding the Autonomic Nervous System [3:31]

The autonomic nervous system controls involuntary bodily functions such as heart rate and digestion. It is divided into two main parts: the sympathetic and parasympathetic nervous systems. The sympathetic nervous system prepares the body for fight or flight responses during stressful situations, while the parasympathetic nervous system promotes rest and digestion. When the sympathetic nervous system is activated, it dilates pupils, inhibits salivation, increases heart rate, and raises blood pressure. Conversely, the parasympathetic nervous system constricts pupils, stimulates salivation, decreases heart rate, and lowers blood pressure.

Pathophysiology of Autonomic Dysreflexia [6:04]

In individuals with spinal cord injuries at or above T6, the connection between the spinal cord below the injury and the brain is disrupted. This disconnection means that stimuli below T6 cannot transmit signals to the brain. However, local sensory nerves still function and can trigger responses in the spinal cord. When a trigger occurs below T6, such as a full bladder, it irritates the spinal nerves, activating the sympathetic nerves. This activation leads to widespread vasoconstriction and a significant increase in blood pressure. Normally, the brain would use the parasympathetic nervous system to counteract this effect, but the signal is blocked at the site of the spinal cord injury.

The Process of Autonomic Dysreflexia [10:50]

The process begins with a stimulus below the T6 level, such as a full bladder, triggering the spinal cord. The sympathetic nerves below T6 become activated, leading to vasoconstriction and increased blood pressure. Baroreceptors in the carotid arteries and aorta detect the hypertension and send signals to the brain. The brain attempts to activate the parasympathetic nervous system via the vagus nerve to slow the heart rate, but the signal to lower blood pressure is blocked at the T6 injury site. As a result, the sympathetic nerves continue to fire, causing widespread vasoconstriction and dangerously high blood pressure.

Effects Above and Below the Injury Level [15:51]

Above the level of injury, vasodilation occurs due to the parasympathetic nervous system's attempt to regulate blood pressure, leading to flushing, sweating, and headache. Below the level of injury, vasoconstriction predominates due to the unopposed sympathetic nervous system activity, resulting in pale and cold skin. This mismatch of symptoms is characteristic of autonomic dysreflexia. The high blood pressure increases the risk of stroke, seizures, and cardiac arrest, making it an emergency condition.

Causes and Triggers of Autonomic Dysreflexia [18:25]

Common causes of autonomic dysreflexia include bladder distension (e.g., blocked catheter, urinary tract infection), bowel distension (e.g., constipation, fecal impaction), and skin breakdown (e.g., pressure sores, tight clothing). Other potential triggers include sexual activity, menstrual cramps, and fractures below T6.

Signs and Symptoms of Autonomic Dysreflexia [19:25]

Symptoms above the level of injury include severe pounding headache, nasal stuffiness, flushed face, sweating, nasal congestion, and bradycardia. Below the level of injury, symptoms include pale and cool skin, goosebumps, and the absence of pain, touch, or temperature sensations. Overall, hypertension is a key sign, with systolic blood pressure rising 20-40 mmHg above baseline or exceeding 200 mmHg in severe cases.

Diagnostic Tests for Autonomic Dysreflexia [21:19]

Diagnosis is primarily clinical, based on medical history and signs and symptoms. Tests include a physical examination to identify triggers such as a full bladder, bowel distension, or skin breakdown. Additional tests may include urine tests to detect bladder stones or urinary tract infections, blood tests to assess cardiac causes of hypertension, abdominal ultrasound to evaluate bladder and bowel distension, CT scans or MRIs to rule out other conditions, and ECG to check heart activity.

Management of Autonomic Dysreflexia [23:03]

Immediate management involves monitoring vital signs (especially blood pressure), seating the patient upright in a high Fowler's position to lower blood pressure, and loosening any tight clothing. The next step is to identify and address the trigger, such as checking for catheter blockages, managing bowel impaction, or addressing skin issues. If these measures do not provide relief, medical management includes administering calcium channel blockers like nifedipine sublingually for rapid vasodilation, applying nitroglycerin paste topically above the level of injury, and, in severe cases, using intravenous hydralazine or diazoxide for hypertensive crisis.