Study guide
3.3 Autonomic Dysreflexia & Acute Complications
ABPMR Physical Medicine and Rehabilitation Board Exam Study Guide Exam
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1 Chapter 1: Introduction & Exam Overview
1.1 ABPMR Part I Exam Overview & Format 1.2 Board Review Strategy & Content Blueprint Breakdown
2 Chapter 2: Musculoskeletal Medicine
2.1 Shoulder & Upper Extremity Diagnostics 2.2 Knee, Hip & Lower Extremity Conditions 2.3 Spine Pathology, Radiculopathy & Myelopathy 2.4 Inflammatory Arthritis, Tendinopathies & Concussion 2.5 Bone Health, Osteoporosis & Metabolic Bone Disease 2.6 Thoracic Outlet Syndrome & Peripheral Nerve Entrapment 2.7 Fracture Rehabilitation & Immobilization Complications 2.8 Overuse Tendinopathies & Regenerative Medicine 2.9 Gait Analysis & Abnormal Gait Patterns
3 Chapter 3: Spinal Cord Injury Rehabilitation
3.1 ASIA Examination & Impairment Scale 3.2 Spinal Cord Injury Syndromes 3.3 Autonomic Dysreflexia & Acute Complications 3.4 Neurogenic Bladder, Bowel & Secondary Complications
4 Chapter 4: Stroke & Neuromuscular Rehabilitation
4.1 Stroke Vascular Syndromes & Acute Assessment 4.2 Stroke Motor Recovery & Hemiplegic Complications 4.3 Spasticity Assessment & Multimodal Management 4.4 ALS, GBS, CIDP & Neuromuscular Disease Rehab 4.5 Multiple Sclerosis & Demyelinating Disease Rehabilitation 4.6 Parkinsonism, Movement Disorders & Functional Neurologic Disorder
5 Chapter 5: Electrodiagnostics (EMG/NCS)
5.1 Nerve Conduction Studies Principles & Physics 5.2 Needle Electromyography & MUAP Analysis 5.3 Mononeuropathies & Radiculopathy Patterns 5.4 Neuromuscular Junction Disorders & Myopathies
6 Chapter 6: Traumatic Brain Injury
6.1 TBI Severity Classification, Glasgow Coma Scale, and Pathophysiology 6.2 Rancho Los Amigos Levels of Cognitive Functioning and Disability Rating Scale 6.3 Neurobehavioral Sequelae and Agitation Management 6.4 Concussion Evaluation, Vestibular-Ocular Dysfunction, and Return-to-Play/Work Protocols
7 Chapter 7: Chronic Pain & Interventional Spine
7.1 Fluoroscopic Spine Interventions 7.2 Opioid Stewardship & Controlled Substance Compliance 7.3 Complex Regional Pain Syndrome, Fibromyalgia & Myofascial Pain 7.4 Spinal Cord Stimulation & Intrathecal Therapy
8 Chapter 8: Amputee Rehabilitation & Prosthetics
8.1 Amputation Surgical Levels & Medicare K-Levels 8.2 Socket Designs & Suspension Systems 8.3 Prosthetic Feet & Microprocessor Knee Mechanisms 8.4 Post-Amputation Care, Residual Limb & Phantom Pain
9 Chapter 9: Pediatric Rehabilitation
9.1 Cerebral Palsy Classification & GMFCS 9.2 Spina Bifida & Myelomeningocele Management 9.3 Muscular Dystrophies & Neuromuscular Disease in Children 9.4 Pediatric Brachial Plexopathy & Congenital Disorders
10 Chapter 10: Prosthetics, Orthotics & Assistive Technology
10.1 Lower Limb Orthoses — AFOs & KAFOs 10.2 Spinal & Upper Extremity Orthoses 10.3 Upper Limb Prosthetics — Body-Powered vs Myoelectric 10.4 Wheelchairs, Seating Systems & Pressure Mapping
11 Chapter 11: Medical Rehabilitation & Outcomes
11.1 Dysphagia Assessment & Management 11.2 Neurogenic Bladder & Bowel Management 11.3 Pressure Injuries & Wound Management 11.4 Outcome Measures & Medical Complications 11.5 Cancer Rehabilitation & Oncologic Rehabilitation 11.6 Burns, Endocrine/Metabolic & Medical Complications Rehabilitation
12 Chapter 12: Cardiopulmonary Rehabilitation
12.1 Cardiac Rehabilitation Phases & Metabolic Equivalents 12.2 Pulmonary Rehabilitation & COPD Management
13 Chapter 13: Foundational Rehabilitation Concepts
13.1 Kinesiology, Biomechanics & Functional Anatomy 13.2 Rehabilitation Pharmacology & Medication Management 13.3 Research Methodology, Biostatistics & Evidence-Based Practice 13.4 Nutrition, Metabolism & Energy Expenditure in Rehabilitation 13.5 Diagnostic Procedures: Imaging, MSK Ultrasound, Urodynamics & Neuropsych Assessment
3.3 Autonomic Dysreflexia & Acute Complications
Key Takeaways Explain This Topic AI
Autonomic Dysreflexia (AD) is a life-threatening medical emergency occurring in SCI at or above T6, triggered by noxious stimuli below the lesion.
The classic AD presentation includes severe paroxysmal hypertension, pounding headache, profuse sweating and cutaneous flushing above the injury level, and reflex bradycardia.
Bladder distension (due to Foley catheter blockage, urinary retention, or UTI) is the single most common cause of AD, followed by bowel fecal impaction.
Immediate non-pharmacological management requires sitting the patient upright (90 degrees) to induce orthostatic pooling, loosening tight garments, and rapidly identifying/removing the offending stimulus.
If systolic blood pressure remains elevated above 150 mmHg despite conservative interventions, short-acting antihypertensives such as sublingual nitropaste (1/2 to 1 inch) should be administered.
Last updated: July 2026
3.3 Autonomic Dysreflexia & Acute Complications
Spinal cord injuries at or above the T6 spinal level interrupt descending central autonomic pathways, leaving sympathetic preganglionic neurons isolated from brainstem inhibitory control. This autonomic disorganization predisposes patients to Autonomic Dysreflexia (AD) , a hypertensive emergency that requires immediate recognition and systematic management. In addition to AD, acute medical management of SCI encompasses cardiovascular dysregulation (orthostatic hypotension) and venous thromboembolism (VTE) prevention.
- Autonomic Dysreflexia (AD)
- Pathophysiology & Mechanisms
Autonomic Dysreflexia occurs almost exclusively in individuals with SCI at T6 or above , because the major sympathetic splanchnic outflow originates between T5 and L2.
Noxious Stimulus : A sensory stimulus below the level of injury (e.g., bladder or bowel distension) sends afferent pain impulses up the spinal cord.
Uninhibited Sympathetic Response : The impulses reach the isolated thoracolumbar sympathetic chain, triggering widespread sympathetic vasoconstriction of the splanchnic vascular bed.
Severe Hypertension : Massive vasoconstriction causes a rapid, dangerous rise in systemic blood pressure (systolic BP can exceed 200-300 mmHg).
Baroreceptor Reflex : Carotid sinus and aortic arch baroreceptors detect the acute surge in BP and send signals via cranial nerves IX and X to the vasomotor center in the medulla.
Parasympathetic Activation Above Lesion : The medulla responds by increasing parasympathetic (vagal) output to the heart, inducing reflex bradycardia , and sending descending inhibitory signals down the cord. However, descending inhibition is blocked at the SCI lesion site.
Clinical Dichotomy : Vasodilation and sweating occur above the level of injury (flushing, sweating, nasal congestion), while vasoconstriction and piloerection persist below the level of injury (cool, pale skin, goosebumps).
Clinical Presentation & Diagnostic Triad
Hypertension : Acute elevation of systolic BP >20 to 40 mmHg above baseline. Note that baseline resting BP in tetraplegic patients is normally low (80-100/50-60 mmHg); thus, a BP of 130/80 mmHg may represent severe AD in a high SCI patient.
Pounding Headache : Severe, sudden onset throbbing frontal or occipital headache.
Profuse Diaphoresis & Flushing : Sweating and red blotchiness above the NLI level.
Reflex Bradycardia : Relative or absolute bradycardia (though tachycardia occurs in up to 20% of cases).
Nasal Congestion & Blurred Vision : Secondary to cranial vasodilators.
Complications of Untreated AD : Hypertensive encephalopathy, intracranial hemorrhage, retinal detachment, seizures, cardiac arrhythmias, myocardial infarction, and death.
Triggers of Autonomic Dysreflexia
System Common Causes
Urological (#1 Cause ~85%) Bladder distension, blocked/kinked Foley catheter, urinary tract infection (UTI), bladder calculi, detrusor sphincter dyssynergia, cystoscopy.
Gastrointestinal (#2 Cause ~10%) Fecal impaction, rectal distension, bowel program stimulation, hemorrhoids, acute abdomen, appendicitis, cholecystitis.
Integumentary Pressure injuries, ingrown toenails, tight clothing, restrictive abdominal binders/leg bags, contact burns, sunburn.
Musculoskeletal & Reproductive Long bone fractures, heterotopic ossification, uterine contractions/labor, ejaculation, pregnancy, pelvic exam.
Stepwise Acute Management Protocol
When a patient at or above T6 develops signs of AD, the physiatrist and nursing staff must immediately execute a mandatory, standardized protocol:
Positioning : Immediately sit the patient upright at 90 degrees with lower extremities dangling dependent. This utilizes orthostatic venous pooling to decrease venous return and lower blood pressure.
Remove Restraints : Loosen tight clothing, abdominal binders, elastic compression stockings, and leg bag straps.
Monitor Vital Signs : Measure BP and HR every 2 to 5 minutes.
Check Bladder (#1 Trigger) :
If an indwelling Foley catheter is present, check for kinks or blockages. Irrigate gently with 15-30 mL of warm sterile saline. If blocked, replace the catheter immediately.
If no catheter is present, perform immediate straight catheterization using topical 2% lidocaine jelly as a lubricant (allow 3-5 minutes for local anesthesia to avoid triggering further dysreflexia).
Check Bowel (#2 Trigger) : If BP remains elevated after addressing the bladder, perform a digital rectal examination (DRE) for fecal impaction. Always instill 2% lidocaine jelly into the rectum and wait 5 minutes prior to digital intervention.
Pharmacotherapy : If systolic BP remains elevated (>150 mmHg or >20-40 mmHg above baseline) despite non-pharmacological measures:
First-line Agent : Nitroglycerin 2% Ointment (Nitropaste) , 1/2 to 1 inch applied topically above the level of injury. Advantage : Can be rapidly wiped off if blood pressure drops precipitous once the offending trigger is removed.
Alternative Agents : Immediate-release sublingual nifedipine (10 mg; note: avoid bite-and-swallow capsule forms due to stroke risk), captopril (25 mg sublingual), or intravenous hydralazine in monitored settings.
Caution : Never administer nitrates if the patient has taken a phosphodiesterase-5 (PDE-5) inhibitor (e.g., sildenafil, tadalafil) within the past 24-48 hours.
Orthostatic Hypotension in SCI
Loss of sympathetic vasoconstrictor tone and absence of lower extremity skeletal muscle pump activity produce profound orthostatic hypotension in acute and subacute SCI (especially T6 and above).
Symptoms : Lightheadedness, dizziness, presyncope, fatigue, blurry vision when elevating head.
Non-Pharmacological Management : Gradual verticalization using tilt tables, abdominal binders (compresses splanchnic bed), thigh-high compression stockings, and aggressive oral hydration.
Pharmacological Interventions :
Midodrine : Direct alpha-1 adrenergic agonist (5-10 mg TID, taken during daytime hours; avoid before bedtime to prevent supine hypertension).
Fludrocortisone : Mineralocorticoid promoting sodium and water retention (0.1 to 0.2 mg daily).
Droxidopa : Synthetic amino acid precursor of norepinephrine.
Venous Thromboembolism (VTE) Prophylaxis
Patients with acute SCI are at extraordinarily high risk for Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) due to Virchow's triad: stasis (flaccid paralysis), hypercoagulability (acute trauma reaction), and endothelial injury.
Peak Risk Window : First 2 to 12 weeks post-injury.
Prophylactic Regimen : Low-Molecular-Weight Heparin (LMWH, e.g., enoxaparin 30 mg SC BID or 40 mg SC daily) combined with mechanical prophylaxis (Sequential Compression Devices [SCDs]).
Recommended Duration : Minimum of 8 to 12 weeks for motor-complete SCI (AIS A and B) or until discharge from acute rehabilitation.