Medical Complications in Spinal Cord Injury

Original Editor - George Prudden

Top Contributors - Naomi O'Reilly, Kim Jackson, Admin, George Prudden, Tarina van der Stockt, Rucha Gadgil and Vidya Acharya  

Introduction

Spinal cord injury results not only in motor and sensory deficits but also in autonomic dysfunctions as a result of the disruption between higher brain centers and the spinal cord. Autonomic dysfunction can include compromised cardiovascular, respiratory, urinary, gastrointestinal, thermoregulatory, and sexual activities. Maintaining optimal health and well-being after sustaining a spinal cord injury can be a challenge. Common secondary health conditions like pressure sores, spasms, chronic pain, and urinary tract infections often negatively affect quality of life and social participation.

Autonomic Dysfunction

Neurogenic Shock

Neurogenic shock, sometimes referred to as vasogenic shock, can occur after damage to the central nervous system, such as an acute spinal cord injury, typically in individuals with a lesion at T6 or above.  Reported incidence of neurogenic shock was 19.3% in cervical injuries, 7% in thoracic injuries and and 3% in lumbar injuries, typically occurring within 24 hours of injury and lasting from one to five weeks.

Consequences of neurogenic shock are loss of sympathetic stimulation to the blood vessels and unopposed vagal activity leading to an imbalance of autonomic control, which can mimic or co-exist with Hypovolemic.This results in a haemodynamic triad of severe hypotension with systolic blood pressures of < 90 mmHg insupine position, bradycardia and peripheral vasodilation, which places an individual at risk for secondary neurological injury and pulmonary, renal, and cerebral insults leading to organ dysfunction and death if not promptly recognized and treated.

Restoration of intravascualar volume is the focus of initial treatment with the goal being to maintain Mean Arterial Pressure (MAP) at 85 to 90mmHg, followed by inotropic supports such as dopamine if symptoms of neurogenic shock do not resolve with initial volume resuscitation to maintain adequate spinal cord perfusion. 

Spinal Shock

Autonomic Dysreflexia

Autonomic dysreflexia, also referred to as autonomic hyperreflexia, is a potentially life-threatening condition that can affect people who have had a spinal cord injury at the level of T6 or above, and occurs more frequently in those with a complete injury over those with an incomplete injury, presenting more commonly during the chronic phase of spinal cord injury, around 3 - 6 months. Often unrecognised by many medical professionals, autonomic dysreflexia should be considered a medical emergency that requires immediate intervention. If not treated promptly and correctly, it can lead to significant complications, including stroke, seizures, myocardial ischaemia, and even death.  

It is an acute syndrome characterised by a sudden excessive increase in Systolic Blood Pressure triggered by an ascending sensory, usually "noxious” stimuli below the level of the lesion. Noxious stimuli can include bladder infection, urinary stasis, bowel obstruction, pressure on bony areas or pressure sores, improper positioning, tight clothing, catheter blockage, twisted intercostal drainage tubes, after sudden violent hip range of motion, and extreme hot weather with the most common causes resulting from bladder and bowel related problems.

The noxious stimulus send nerve impulses to the spinal cord, where they travel upward until they are blocked by the lesion at the level of the spinal cord injury. Since the impulses cannot reach the brain, a reflex is activated that increases activity of the sympathetic portion of the autonomic nervous system. This results in severe vasoconstriction, which causes a sudden rise in blood pressure. Baroreceptors in the heart and blood vessels detect this rise in blood pressure and send a message to the brain. The brain sends a message to the heart, causing the heartbeat to slow down and the blood vessels above the level of injury to dilate. However, the brain cannot send messages below the level of injury, due to the spinal cord lesion, and therefore the blood pressure cannot be regulated. The brain is unable to check the sympathetic response resulting in increased systemic blood pressure.  

This overstimulation of the autonomic nervous system is characterised by sudden onset of severe high blood pressure known as paroxysmal hypertension at least 20 to 40 mmHg above normal resting systolic level. (It is important to remember that Blood Pressure for individuals with tetraplegia or high paraplegia is usually low, around 90 to 100/60 mmHg while lying down and possibly lower whilst sitting). This manifests itself with flushing of the skin, pounding headache, blurred vision, spots in visual field, irritability, pilo erection (goose bumps), profuse sweating above the level of the injury, dry and pale skin caused by vasoconstriction below the level of the injury, blurred vision, nasal congestion, bradycardia, cardiac arrhythmias, atrial fibrillation and often associated with anxiety and feeling sof apprehension. Silent autonomic dysreflexia can also occur with minimal or no symptoms despite elevated blood pressure. (PVA 2001)

A variety of non-pharmacological and pharmacological strategies can be used to treat autonomic dysreflexia. Immediate treatment recommends identification and removal of the triggering stimuli as soon as possible prior to pharmacological strategies since autonomic Dysreflexia tends to resolve once the inciting stimulus is removed. Sitting the individual upright and with legs over the bedside can reduce help to blood pressure levels and provide partial symptom relief. Tight clothing and stockings should be removed. Catheterization of the bladder, or relief of a blocked urinary catheter tube may resolve the problem. The rectum should be cleared of stool impaction, using anaesthetic lubricating jelly. If the noxious precipitating trigger cannot be identified, drug treatment is sometimes needed until further studies can identify the cause. When non-pharmacologic treatment methods are not successful in an acute episode of autonomic dysreflexia, pharmacologic agents are required and may include nifedipine, nitrates, and captopril.  Only nifedipine has been supported by controlled trials.

Temperature Regulation

Respiratory Dysfunction

Impaired respiratory function is common following a spinal cord injury. Respiratory function of people with is primarily determined by neurological level of the injury. Paralysis or partial paralysis of key muscles has a marked impact on respiratory function. Respiratory complications in spinal cord injury are common with complications directly correlated with mortality, and both are related to the level of neurologic injury. Pulmonary complications of spinal cord injury include the following:

• Atelectasis secondary to decreased vital capacity and decreased functional residual capacity
• Ventilation-perfusion (V/Q) mismatch due to sympathectomy and/or adrenergic blockade
• Increased work of breathing secondary to decreased compliance
• Decreased cough, which increases the risk of retained secretions, atelectasis, and pneumonia
• Hypoventilation
• Muscle Paralysis
• Muscle Fatigue

Cardiovascular Dysfunction

Deep Vein Thrombosis and Pulmonary Embolism

Orthostatic Hypotension

Gastrointestinal Dysfunction

Paralytic Ileus

Neurogenic Bowel

Urological Dysfunction

Neurogenic Bladder

Sexual Dysfunction

Fertility

Erectile Dysfunction

Bone Metabolism Dysfunction

Osteoporosis

Heterotrophic Ossification

Heterotopic ossification is when a bone is formed in or around a joint resulting to the absence of movements of that joint this is commonly seen in spinal cord injury patients. It usually presents within joints like shoulder, elbow, knee etc.its first sign is swelling around the joint and reduced range of motion, pain and with or without fever.

Pressure Sores

The National Pressure Ulcer Advisory Panel, U.S (NPUAP) defines a pressure ulcer as an area of unrelieved pressure over a defined area, usually over a bony prominence, resulting in ischemia, cell death, and tissue necrosis. A pressure ulcer is localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear. A pressure sore can develop in a few hours, but the results can last for many months and even cause death. A number of contributing or confounding factors are also associated with pressure ulcers; the significance of these factors is yet to be elucidated.

Read more on the Guidelines on Prevention and Management of Pressure Ulcers

Pain

The most widely accepted and current definition of pain, established by the International Association for the Study of Pain (IASP), is "an unpleasant sensory and emotional experience associated with acutal or potential tissue damage, or described in terms of tissue damage, or both." Although several theoretical frameworks have been proposed to explain the physiological basis of pain, not one theory has been able to exclusively incorporate the entirety of all the aspects of pain perception.

Nociceptive

Nociceptive pain is associated with the activation of peripheral receptive terminals of primary afferent neurons in response to noxious chemical (inflammatory), mechanical or ischemic stimuli.

Neuropathic

Peripheral

Peripheral neuropathic pain is initiated or caused by a primary lesion or dysfunction in the peripheral nervous system (PNS) and involves numerous pathophysiological mechanisms associated with altered nerve functioning and responsiveness. Mechanisms include hyperexcitability and abnormal impulse generation and mechanical, thermal and chemical sensitivity.

Central

Central pain is pain initiated or caused by a primary lesion or dysfunction in the Central Nervous System (CNS).

Psychological

Depression

Anxiety

Post Traumatic Stress Disorder

References