Medical Complications in Spinal Cord Injury: Difference between revisions

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== Urological Dysfunction ==
== Urological Dysfunction ==
Urological dysfunction occurs in up to 80% of individuals with a spinal cord injury including uriary retention, urinary tract infection (UTI), upper and lower urinary tract deterioration, bladder or renal stones, incontinence, neurogenic bladder.During the acute stage of spinal cord injury there is an increased risk of urological complications secondary to spinal shock. The bladder becomes atonic, with no conscious awareness of bladder filling. The micturition reflex is interrupted and leads to urinary retention, which needs to be managed with clean intermittant catheteristion or with an indwelling cather, while neurogenic bladder, is a major problem long term both in terms of physical and psychological wellbeing.<ref name=":5" /><ref name=":10" /><ref name=":7" />


=== Neurogenic Bladder ===
=== Neurogenic Bladder ===

Revision as of 15:32, 1 January 2019

Original Editor - George Prudden

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

Introduction[edit | edit source]

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. [1][2]

Autonomic Dysfunction[edit | edit source]

Autonomic dysfunction is common following a spinal cord injury, particularly in those with a lesion at mid-thoracic levels (T6) and above. During the acute phase of spinal cord injury the main forms of autonomic dysfunction present are neurogenic and spinal shock. Although frequently used interchangeably, true definitions of neurogenic and spinal shock are hard to identify with multiple definition used. Biering-Sørensen et al (2018) suggest that while the symptoms and signs of spinal shock and neurogenic shock may occur simultaneously, it should be noted that these are two distinctly different clinical conditions and should be treated as such. [3] While Autonomic Dysreflexia and thermoregulation dysfunction is more common in the sub-acute and chronic spinal cord injury.

Spinal Shock[edit | edit source]

Spinal shock, first described by Whytt in 1750, is a temporary loss of all neurological activity including motor, sensory and reflex activity below the level of the spinal cord lesion that can occur immediately following the onset of an acute spinal cord injury. Reflexes above the level of the spinal cord injury remain unaffected while those below the level of injury are either depressed (hyporeflexia) or absent (areflexia). The extent of disruption to reflexes is variable, both in terms of reflexes involved and timeframe for recovery, and as a result the precise definition and duration of spinal shock is debated. Appearance of bulbocavernosus reflex, normally within the first few days post injury, is seen by some clinicians as the end point for spinal shock, while others suggest it ends with the recovery of either deep tendon reflexes within a few weeks or much later with the recovery of bladder reflexes within 2 months of injury. [3][4]

Overall there is general agreement that spinal shock resolves in a series of stages lasting anywhere from a few days to a few months, with mean duration around 4 - 6 weeks. The following model consists of four evolving phases for in recovery from spinal shock with both clinical and physiological descriptions. [5]

Phase Timeframe Clinical Description Underlying Physiological Mechanism
1 0 - 1 Day Areflexia / Hyporeflexia with Flaccid Paralysis Spinal Neuron Hyperpolarisation
2 1 - 3 Days Initial Reflex Return Denervation Supersensitivity / Receptor Upregulation
3 4 Days - 1 Month Early Hypereflexia Synapse Growth

Short Axons and/or Axon Supplied

4 1 - 12 Months Spasticity / Hypereflexia Synapse Growth

Long Axons and Soma Supplied

Gradual development of spasticity in those with an upper motor lesion is evident as spinal shock resolve, which may also be associated with neurophysiological and physical changes, and has important implications for physiotherapy management particularly in relation to contractures. [4][5]
[6]

Neurogenic Shock[edit | edit source]

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. [7][1][8] 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 and commonly can occur simultaneously with spinal shock. [3][9]

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. [7][1]

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. [1][10][11]

Autonomic Dysreflexia[edit | edit source]

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. [12][13] 

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. [13]

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. [12] 

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. [13][14][15]

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. [14][13][16]
[17]
[18]

Thermoregulation[edit | edit source]

Thermoregulation is a process that allows your body to maintain its core internal temperature, with baseline temperature normally between 37°C (98°F) and 37.8°C (100°F). Thermoregulation mechanisms are designed to return your body to homeostasis and maintain a state of equilibrium. A sophisticated thermoregulatory center in the hypothalamus regulates thermogenesis by activating or inhibiting the sympathetic nervous system to maintain core body temperature. When your internal temperature changes, sensors in the central nervous system send messages to the hypothalamus. In response, it sends signals to various organs and systems in the body, which respond with a range of different mechanisms to either heat or cool the body. These mechanisms include: [1][19]

Heating Mechanisms
Sweating Sweat glands release sweat, which cools your skin through evaporation.
Vasodilation Blood vessels under the skin dilate, which increases blood flow to the skin where it is cooler releasing heat through radiation.
Cooling Mechanisms
Vasoconstriction Blood vessels under the skin constrict, which decreases blood flow to the skin, enabling heat retention. 
Thermogenesis Production of heat by the muscles, organs, and brain e.g. shivering, brown adipose tissue
Thyroid gland releases hormones to increase metabolism, which increases the energy your body creates and the amount of heat it produces.

Individuals with a spinal cord injury, particularly those with a cervical or high thoracic lesion, have impaired thermoregulation and are unable to respond appropriately to the changing temperatures of their surrounding environments. This is largely as a result of damage to the afferent and efferent pathways of the sympathetic nervous system causing reduced sensory input to the thermoregulatory center and loss of supra spinal control, which lead to dysregulation in vasomotor tone, skeletal muscle shivering and sweating dysfunction below the level of the spinal cord injury. [1][19]

Core temperature and body surface temperature receptors have an effect on body temperature regulation in individuals with a lesion at T7 or below, while the most severe dysfunction in body temperature regulation against external temperature change occurs in individuals with a lesion at T6 or above as their body temperature is controlled by Central Thermoreceptors. Poikilothermia, which is the inability to regulate core body temperature is common among individuals with a spinal cord injury and individuals with a lesion at T6 or above are prone to fluctuating temperature, hypothermia and hyperthermia, which are potentially fatal complications of exposure to environmental extremes. [19]

Respiratory Dysfunction[edit | edit source]

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[edit | edit source]

Deep Vein Thrombosis and Pulmonary Embolism[edit | edit source]

Orthostatic Hypotension[edit | edit source]

Gastrointestinal Dysfunction[edit | edit source]

Gastrointestinal dysfunction including constipation, straining, diahorrea, distention, abdominal pain, incontenence, rectal bleeding, hemorrhoids, and autonomic dysreflexia during bowel movementsoccur in 27% to 62% of individualswith a spinal cord injury. During the acute stage of spinal cord injury there is an increased risk of gastrointestinal complications within the first few days post injury, including gastrointestinal hemorrhage, perforation, and paralytic ileus, while neurogenic bowel, affecting almost half of those with a spinal cord injury (46.9%) is a major problem long term both in terms of physical and psychological wellbeing. [1][2][20]

Paralytic Ileus[edit | edit source]

Paralytic Ileus, often associated with spinal shock post an acute spinal cord injury,is an obstruction of the intestine secondary to paralysis of the intestinal muscles with no evidence of mechanical obstruction, which like spinal shock can last from a few days to a few weeks. The paralysis does not need to be complete to cause ileus, but the intestinal muscles must be so inactive that it prevents the passage of food, and leads to a functional blockage of the intestine, which causes abdominal distension. A distended abdomen increases the work of breathing but also may cause vomiting, which increase the risk for aspiration pneumonia and further respiratory complications. Individuals with a paralytic ileus are typically managed Nil by Mouth (NPO) with nasogastric suction to regularly aspirate the stomach contents. [1][4][20]

Neurogenic Bowel[edit | edit source]

Neurogenic bowel dysfunction with changes to bowel motility, sphincter control, coupled with impaired mobility and hand dexterity, is a major physical and psychological problem for many individuls with a spinal cord injury, as well as major source of morbidity. Neurogenic bowel occurs secondary to a lack of central nervous control of the bowel resulting in dysfunction of the colon, with two distinct clinical presentations. [2][21]

Upper Motor Neuron (UMN) Bowel Syndrome, occurring in a spinal cord injury above the conus medullaris results in a hyperreflexic bowel, characterised by increased colonic wall and anal tones, with disrupted voluntary external anal sphincter control. Typically associated with constipation and fecal retention at least in part due to external anal sphincter activity. [2][21]

Lower Motor Neuron (LMN) Bowel Syndrome, occurring in a spinal cord injury at the injury at the conus medullaris or cauda equina results in an areflexic bowel, characterised by loss of spinal cord-mediated peristalsis and slow stool propulsion with an atonic external anal sphincter. Typically associated with constipation and a significant risk of incontinence due to flaccid paralysis of the external anal sphincter and redcued motor control of levator ani. [2][21]

Successful bowel management is multi-dimensional and needs to be specific to each individual requiring careful assessment for accurate diagnoses and prescription of treatments for bowel management following spinal cord injury, recognising that completeness of injury also has a significant impact on bowel function.Key strategies for bowel management include a high-fibre diet although further research to examine the optimal level, adequate fluid intake and a regular routine for bowel evacuation, which may incorporate digital stimulation or manual evacuation.Transanal irrigation is also now seen as a promising technique to reduce constipation and fecal incontinence. Prokinetic agents such as cisapride, prucalopride, metoclopramide, neostigmine, and fampridine are supported by strong evidence for the treatment of chronic constipation in individuals with a spinal cord injury in those where conservative management is not effective. [2][4][21]
[22]
[23]

Urological Dysfunction[edit | edit source]

Urological dysfunction occurs in up to 80% of individuals with a spinal cord injury including uriary retention, urinary tract infection (UTI), upper and lower urinary tract deterioration, bladder or renal stones, incontinence, neurogenic bladder.During the acute stage of spinal cord injury there is an increased risk of urological complications secondary to spinal shock. The bladder becomes atonic, with no conscious awareness of bladder filling. The micturition reflex is interrupted and leads to urinary retention, which needs to be managed with clean intermittant catheteristion or with an indwelling cather, while neurogenic bladder, is a major problem long term both in terms of physical and psychological wellbeing.[1][2][4]

Neurogenic Bladder[edit | edit source]

[24]
[25]

Sexual Dysfunction[edit | edit source]

Fertility[edit | edit source]

Erectile Dysfunction[edit | edit source]

Bone Metabolism Dysfunction[edit | edit source]

Osteoporosis[edit | edit source]

Heterotrophic Ossification[edit | edit source]

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[edit | edit source]

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. [26] 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. [27] 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[edit | edit source]

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. [28][29]

Nociceptive[edit | edit source]

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[edit | edit source]

Peripheral[edit | edit source]

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[edit | edit source]

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

Psychological[edit | edit source]

Depression[edit | edit source]

Anxiety[edit | edit source]

Post Traumatic Stress Disorder[edit | edit source]

References[edit | edit source]

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Hagen EM. Acute Complications of Spinal Cord Injuries. World Journal of Orthopedics. 2015 Jan 18;6(1):17.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Sezer N, Akkuş S, Uğurlu FG. Chronic Complications of Spinal Cord Injury. World Journal of Orthopedics. 2015 Jan 18;6(1):24.
  3. ↑ 3.0 3.1 3.2 Biering-Sørensen F, Biering-Sørensen T, Liu N, Malmqvist L, Wecht JM, Krassioukov A. Alterations in Cardiac Autonomic Control in Spinal Cord Injury. Autonomic Neuroscience. 2018 Jan 1;209:4-18.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 Harvey L. Management of Spinal Cord Injuries: A Guide for Physiotherapists. Elsevier Health Sciences; 2008 Jan 10.
  5. ↑ 5.0 5.1 Ditunno JF, Little JW, Tessler A, Burns AS. Spinal Shock Revisited: A Four-Phase Model. Spinal Cord. 2004 Jul;42(7):383.
  6. ↑ New Zealand Spinal Trust. Spinal 101 - Spinal Shock. Available from: http://vimeo.com/230390246[last accessed 30/10/87]
  7. ↑ 7.0 7.1 Krassioukov A, Claydon VE. The Clinical Problems in Cardiovascular Control following Spinal Cord Injury: An Overview. Prog Brain Res. 2006;152:223–229. [PubMed]
  8. ↑ Ahuja CS, Cadotte DW, Fehlings M. Chapter 33 Spinal Cord Injury. In Principles of Neurological Surgery (Fourth Edition) 2018 (pp. 518-531).
  9. ↑ Guly HR, Bouamra O, Lecky FE. The Incidence of Neurogenic Shock in Patients with Isolated Spinal Cord Injury in the Emergency Department. Resuscitation. 2008;76:57–62. [PubMed]
  10. ↑ Koffi M. Kla, Lorri A. Lee. Perioperative Anesthetic and ICU Considerations for Spinal Surgery. In Neurocritical Care Management of the Neurosurgical Patient, 2018
  11. ↑ Shank CD, Walters BC, Hadley MN. Management of Acute Traumatic Spinal Cord Injuries. In Handbook of Clinical Neurology 2017 Jan 1 (Vol. 140, pp. 275-298). Elsevier.
  12. ↑ 12.0 12.1 Eldahan KC, Rabchevsky AG. Autonomic Dysreflexia after Spinal Cord Injury: Systemic Pathophysiology and methods of management. Autonomic Neuroscience. 2018 Jan 1;209:59-70.
  13. ↑ 13.0 13.1 13.2 13.3 Krassioukov A, Warburton DE, Teasell R, Eng JJ, Spinal Cord Injury Rehabilitation Evidence Research Team. A Systematic Review of the Management of Autonomic Dysreflexia after Spinal Cord Injury. Archives of physical Medicine and Rehabilitation. 2009 Apr 1;90(4):682-95.
  14. ↑ 14.0 14.1 Khastgir J, Drake MJ, Abrams P. Recognition and Effective Management of Autonomic Dysreflexia in Spinal Cord Injuries. Expert Opinion on Pharmacotherapy. 2007 May;8(7):945–56.
  15. ↑ Consortium for Spinal Cord Injury Medicine. Acute Management of Autonomic Dysreflexia: Individuals with Spinal Cord Injury Presenting to Health Care Facilities. Journal Spinal Cord Med. 2002 Spring; 25 Suppl 1:S67-88.
  16. ↑ Squair JW, Phillips AA, Harmon M, Krassioukov AV. Emergency Management of Autonomic Dysreflexia with Neurologic Complications. Canadian Medical Association Journal. 2016 Oct 18;188(15):1100-3.
  17. ↑ Craig Hospital. What is Autonomic Dysreflexia?. Available from: https://youtu.be/2qGBVp3Ipvo[last accessed 30/10/18]
  18. ↑ Rick Hansen Institute. Best Practices - Diagnosis and Management of Autonomic Dysreflexia. Available from: https://youtu.be/iau-G2DHVtA[last accessed 30/10/18]
  19. ↑ 19.0 19.1 19.2 Song YG, Won YH, Park SH, Ko MH, Seo JH. Changes in Body Temperature in Incomplete Spinal Cord Injury by Digital Infrared Thermographic Imaging. Annals of Rehabilitation Medicine. 2015 Oct 1;39(5):696-704.
  20. ↑ 20.0 20.1 Ebert E. Gastrointestinal Involvement in Spinal Cord Injury: A Clinical Perspective. Journal of Gastrointestinal & Liver Diseases. 2012 Mar 1;21(1).
  21. ↑ 21.0 21.1 21.2 21.3 Krassioukov A, Eng JJ, Claxton G, Sakakibara BM, Shum S. Neurogenic Bowel Management after Spinal Cord Injury: A Systematic Review of the Evidence. Spinal Cord. 2010 Oct;48(10):718.
  22. ↑ SCIUcourses. Bowel 1.3 - Neurogenic Bowel. Available from: https://youtu.be/AYQo1R-sFHk[last accessed 30/10/18]
  23. ↑ SCIUcourses. Bowel 2.1 - The Perfect Program. Available from: https://youtu.be/2K7DByoxias[last accessed 30/10/18]
  24. ↑ SCIUcourses. Bladder 1.3 - Neurogenic Bladder. Available from: https://youtu.be/AVYFkgyZv-8[last accessed 30/10/18]
  25. ↑ SCIUcourses. Bladder 2.2 - Emptying Your Bladder. Available from: https://youtu.be/wR1vJmrZPP8[last accessed 30/10/18]
  26. ↑ http://emedicine.medscape.com/article/190115-overview
  27. ↑ http://www.npuap.org/wp-content/uploads/2012/01/NPUAP-Pressure-Ulcer-Stages-Categories.pdf
  28. ↑ Moayedi M, Davis KD. Theories of Pain: From Specificity to Gate Control. J Neurophysiol 2013;109:5-12.
  29. ↑ Smart KM, Blake C, Staines A, Doody C. Clinical Indicators of 'Nociceptive', 'Peripheral Neuropathic' and 'Central' Mechanisms of Musculoskeletal Pain. A Delphi Survey of Expert Clinicians. Man Ther 2010;15:80-7
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