Dermatomes – Physiopedia

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A dermatome is an area of skin that is mainly supplied by a single spinal nerve. There are 8 cervical nerves (note C1 has with no dermatome), 12 thoracic nerves, 5 lumbar nerves and 5 sacral nerves. Each of these spinal nerves relay sensation from a particular region of the skin to the brain.^[1]

^[2]

The nerves from the

• C2 to C4 supply the skin of the neck.

• C5 to T1 nerves supply the arms. 

• T2 to L2 nerves supply the chest and abdomen. 

• L3 to S1 nerves supply the skin of the legs. 

• S1 to S4 nerves go to the groin.

Testing of dermatomes is part of the neurological examination looking for radiculopathy as sensation changes within a specific dermatome may help in determining the pathological disc level.

Dermatome Testing is done ideally with a pin and cotton wool. Ask the patient to close their eyes and give the therapist feedback regarding the various stimuli. Testing should be done on specific dermatomes and should be compared to bilaterally.

• Pinprick test (pain sensation) – Gently touches the skin with the pin ask the patient whether it feels sharp or blunt

• Light touch test (light touch sensation) – Dab a piece of cotton wool on an area of skin ^[4]

During the review of systems, asking the patient to carefully describe the pattern or distribution of sensory symptoms (e.g., tingling, numbness, diminished, or absent sensation) provides the therapist with preliminary information to help guide the examination and to assist in identifying the dermatome(s) and nerve(s) involved.^[5]

Peripheral nerve injuries generally present sensory impairments that parallel the distribution of the involved nerve and correspond to its pattern of innervation.For example, if a patient presents with complaints of numbness on the ulnar half of the ring finger, the little finger, and the ulnar side of the hand, the therapist would be alerted to carefully address ulnar nerve (C8 and T1) integrity during the sensory examination. Complaints of sensory disturbances on the palmar surface of the thumb and the palmar and distal dorsal aspects of the index, middle, and the radial half of the ring finger would be indicative of median nerve (C6–8 and T1) involvement.^[5]

There exist some discrepancies among published dermatome maps based on the methodologies used to identify skin segment innervation. In a clinical commentary, Downs and Laporte discuss the history of dermatome mapping, including the variations in methodologies employed, and the inconsistencies in the dermatome maps used in education and practice.^[5][[Laporte C. Conflicting dermatome maps: educational and clinical implications. journal of orthopaedic & sports physical therapy. 2011 Jun;41(6):42^[6]7-34.]]

Dermatomes – Physiopedia

Original Editor – Your name will be added here if you created the original content for this page.

Lead Editors  

A dermatome is an area of skin that is mainly supplied by a single spinal nerve. There are 8 cervical nerves (note C1 has with no dermatome), 12 thoracic nerves, 5 lumbar nerves and 5 sacral nerves. Each of these spinal nerves relay sensation from a particular region of the skin to the brain.^[1]

^[2]

The nerves from the

• C2 to C4 supply the skin of the neck.

• C5 to T1 nerves supply the arms. 

• T2 to L2 nerves supply the chest and abdomen. 

• L3 to S1 nerves supply the skin of the legs. 

• S1 to S4 nerves go to the groin.

Testing of dermatomes is part of the neurological examination looking for radiculopathy as sensation changes within a specific dermatome may help in determining the pathological disc level.

Dermatome Testing is done ideally with a pin and cotton wool. Ask the patient to close their eyes and give the therapist feedback regarding the various stimuli. Testing should be done on specific dermatomes and should be compared to bilaterally.

• Pinprick test (pain sensation) – Gently touches the skin with the pin ask the patient whether it feels sharp or blunt

• Light touch test (light touch sensation) – Dab a piece of cotton wool on an area of skin ^[4]

During the review of systems, asking the patient to carefully describe the pattern or distribution of sensory symptoms (e.g., tingling, numbness, diminished, or absent sensation) provides the therapist with preliminary information to help guide the examination and to assist in identifying the dermatome(s) and nerve(s) involved.^[5]

Peripheral nerve injuries generally present sensory impairments that parallel the distribution of the involved nerve and correspond to its pattern of innervation.For example, if a patient presents with complaints of numbness on the ulnar half of the ring finger, the little finger, and the ulnar side of the hand, the therapist would be alerted to carefully address ulnar nerve (C8 and T1) integrity during the sensory examination. Complaints of sensory disturbances on the palmar surface of the thumb and the palmar and distal dorsal aspects of the index, middle, and the radial half of the ring finger would be indicative of median nerve (C6–8 and T1) involvement.^[5]

There exist some discrepancies among published dermatome maps based on the methodologies used to identify skin segment innervation. In a clinical commentary, Downs and Laporte discuss the history of dermatome mapping, including the variations in methodologies employed, and the inconsistencies in the dermatome maps used in education and practice.^[5][[Laporte C. Conflicting dermatome maps: educational and clinical implications. journal of orthopaedic & sports physical therapy. 2011 Jun;41(6):42^[6]7-34.]]

Low Back and Leg Pain is Lumbar Radiculopathy

Approximately 80% of the population is plagued at one time or another by back pain, especially lower back pain. Associated leg pain (called lumbar radiculopathy or sciatica) occurs less frequently. Pain can be bothersome and debilitating, limiting daily activities. Leg and back pain can be caused by a variety of reasons, not all of which originate in your spine.

For the purpose of this article, we will focus on lumbar radiculopathy, which refers to pain in the lower extremities in a dermatomal pattern (see image below). A dermatome is a specific area in the lower extremity that has nerves going to it from a specific lumbar nerve. This pain is caused by compression of the roots of the spinal nerves in the lumbar region of the spine. Diagnosing leg and lower back pain begins with a detailed patient history and examination.

Dermatomes (above): Where you feel back and/or leg pain
may help your doctor diagnose nerve compression. Photo Source: SpineUniverse.com.

Medical History: Important when Diagnosing Lower Back Pain and Sciatica

Your medical history helps the physician understand the problem. It is important to be specific when answering medical questions related to pain onset but remembering every detail is often not critical. Keeping records of your medical history, including medical problems, medications you are taking and surgeries you have had in the past is helpful.

Journal Your Back and Leg Pain
Regarding your leg and back pain, it may be helpful to keep a journal of your activities, documenting when the pain began, the activities that aggravate your pain and those that relieve your symptoms. It is also important to determine whether your back pain is more bothersome than your leg pain or visa versa. You may be asked if you are experiencing any numbness or weakness in your legs or any difficulty walking. Remember, understanding the cause of your problem is based on the information you provide.

Most people describe radicular pain as a sharp or burning pain that shoots down the leg. This is what some people call sciatica. This pain may or may not begin in the low back. Leg pain caused by compressed nerve roots generally has specific patterns. These patterns of pain depend on the level of the nerve being compressed. After reviewing your history, your physician will perform a physical examination. This will help the physician determine if your symptoms are due to a problem that is caused by spinal nerve root compression. To help you understand the exam performed by your physician lets pause for a quick anatomy lesson.

Spinal Anatomy: Helpful for Understanding Your Lower Back Pain

The spine is comprised of 33 vertebrae (bones stacked on top of each other in a “building-block” fashion) that have 4 distinct regions: cervical (neck), thoracic (upper/mid back), lumbar (low back), and sacrum (pelvis).

Discs are cushion-like tissues that separate most vertebrae and act as the spine’s shock absorbing system. Each disc is comprised of a tough outer ring of fibers called the annulus fibrosus, and a soft gel-like center called the nucleus pulposus.
Each disc is comprised of a tough outer ring of fibers called the annulus fibrosus, and a soft gel-like center called the nucleus pulposus. Photo Source: SpineUniverse.com.There are 7 flexible cervical (neck) vertebrae that help to support the head. Twelve thoracic vertebrae attach to ribs. Next, are 5 lumbar vertebrae; they are large and carry the majority of the body weight. The sacral region helps distribute the body weight to the pelvis and hips.

The spinal cord is housed within the protective elements of spinal canal. Spinal nerves branch from the spinal cord and exit the spinal canal through passageways between the vertebral bodies. The passageways are called neuroforamen. Nerves provide sensory (allowing you to touch and feel) and motor information (allowing the muscles to function) to the entire body.

In the next article (click the Continue Reading link below), we discuss how your doctor determines what is causing your lower back pain and sciatica, which is essential to the proper treatment plan and symptom relief.

Commentary by Curtis A. Dickman, MD

Lumbar radiculopathy is a common problem that results when nerve roots are compressed or irritated. This excellent article discusses the basic anatomy and clinical manifestations of lumbar radiculopathy, which is often referred to generically as sciatica. These symptoms can be due to a variety of causes such as disc bulges, degenerative narrowing of the space for the nerves (spinal stenosis or foraminal stenosis), spinal instability, deformity of the vertebrae, or herniated disc fragments outside of the disc space.

In 70-80% of patients, sciatica is transient, and resolves with non-surgical treatments such as anti-inflammatory medications, physical therapy, exercise, spinal manipulation, or other nonsurgical modalities. A proportion of patients with sciatica require surgical intervention in instances where nonsurgical therapies have failed to provide adequate pain relief, and there is pathology [cause] that is present compressing the nerves. A very small proportion of patients require urgent surgery. If a very large lumbar disc herniation causes severe nerve damage, with paralysis or acute bowel or bladder incontinence, then emergency surgery may be required.

Sensation Testing – Peripheral Nerve Lesion — Rayner & Smale

Documentation

The final aspect of sensory testing that I wanted to cover with this blog is terminology (O’Sullivan et al., 2013). Here are a few words…

Words relating to pain:

• Analgesia – the complete loss of pain sensitivity.
• Dysesthesia – touch sensation experienced as pain.
• Hyperalgesia – increased sensitivity to pain and hypalgesia – decreased sensitivity to pain.
• Allodynia – pain provoked by non-noxious stimulus.
• Causalgia – painful burning sensation (usually along the distribution of a nerve).

Words relating to sensation:

• Atopognosia – inability to localise a sensation.
• Hyperesthesia – increase sensitivity to a sensory stimuli and hypesthesia – decreased sensitivity to a sensory stimuli.
• Paraesthesia – abnormal sensation such as pins and needles, numbness, tingling.
• Thigmanesthesia – loss of light touch sensibility .

Words relating to temperature:

• Thermanalgesia – inability to perceive heat.
• Thermanesthesia – inability to perceive sensations of heat or cold.
• Thermhyperesthesia – increased sensitivity to temperature and thermhypesthesia – decreased temperature sensibility.

When I think back to my university days, I remember being quite overwhelmed with the number of sensory tests we learnt in neurology and musculoskeletal subjects. Always remember that when put in the context of a full neurological screen (deep tendon reflexes, strength and sensation) the clinical patterns are much easier to recognise. However, it is definitely important to know the purpose and method for these sensory assessments and the most common tests you will use such as light touch, sharp/blunt discrimination, and temperature. The focus initially is to rule out any sensory impairment during a neurological exam and once sensory impairment has been detected, you can then be more specific in your mapping of the distribution and description of the symptoms. 

Sian

References:

Adams RD, Victor M and Ropper MD (2001): Principles of Neurology (7th ed.) New York: McGraw Hill. (Chapter 3 & 9).

Fredericks C and Saladin L (1996): Pathophysiology of the Motor Systems: Principles and Clinical Presentations. Philadelphia: F.A Davis pp. 275 – 288.

Kingsley R.E (2000): Concise Text of Neuroscience. (2nd ed.) Philadelphia: Lippincott, Williams & Wilkins. (Chapter 6, Appendix 2).

Nolte J (1999): The Human Brain: An Introduction to its Functional Anatomy. (4th ed.) St Louis: Mosby Year Book. (Chapter 10).

Nolte J and Angevine JB (1995): The Human Brain in Photographs and Diagrams. (1st ed.) St Louis: Mosby Year Book Inc.

O’Sullivan, S. B., Schmitz, T. J., & Fulk, G. (2013). Physical rehabilitation. FA Davis.

The History of Dermatome Mapping

Peripheral nervous system origin of phantom limb pain
Apostol Vaso a, Haim-Moshe Adahan b, Artan Gjika a, Skerdi Zahaj a, Tefik Zhurda a, Gentian Vyshka c,
Marshall Devor d,⇑
a Pain and Rehabilitation Clinic, National Trauma Center, Trauma University Hospital and Galenus Clinic, Tirana, Albania
b Pain Rehabilitation Unit, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
c Biomedical and Experimental Department, Faculty of Medicine, University of Medicine, Tirana, Albania
d Department of Cell and Developmental Biology, Institute of Life Sciences and Center for Research on Pain, The Hebrew University of Jerusalem, Jerusalem 91904, Israel
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
a r t i c l e i n f o
Article history:
Received 31 December 2013
Received in revised form 6 April 2014
Accepted 14 April 2014
Keywords:
DRG
Ectopic firing
Electrogenesis
Intraforaminal
Neuropathic pain
Phantom limb pain

a b s t r a c t
Nearly all amputees continue to feel their missing limb as if it still existed, and many experience chronic
phantom limb pain (PLP). What is the origin of these sensations? There is currently a broad consensus
among investigators that PLP is a top-down phenomenon, triggered by loss of sensory input and caused
by maladaptive cortical plasticity. We tested the alternative hypothesis that PLP is primarily a bottom-up
process, due not to the loss of input but rather to exaggerated input, generated ectopically in axotomized
primary afferent neurons in the dorsal root ganglia (DRGs) that used to innervate the limb. In 31 amputees,
the local anesthetic lidocaine was applied intrathecally and/or to the DRG surface (intraforaminal epidural
block). This rapidly and reversibly extinguished PLP and also nonpainful phantom limb sensation (npPLS).
Control injections were ineffective. For intraforaminal block, the effect was topographically appropriate.
The suppression of PLP and npPLS could also be demonstrated using dilute lidocaine concentrations that
are sufficient to suppress DRG ectopia but not to block the propagation of impulses generated further distally
in the nerve. PLP is driven primarily by activity generated within the DRG.Werecommend the DRGas a
target for treatment of PLP and perhaps also other types of regional neuropathic pain.
� 2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
1. Introduction
The origin of phantom limb pain (PLP) remains uncertain. Religious
and psychiatric interpretations once predominated [54,58],
but these have since been supplanted by neurobiological and cognitive
theories. The fact that pressure on amputation stump neuromas
provokes PLP (Tinel sign), and the discovery that neuromas
generate ectopic impulse discharge (ectopia), favored the stump
as the pain generator [5,14,29,49,50,55,56,63]. However, PLP frequently
persists despite neuroma infiltration and nerve/plexus
block [4,27,46]. For this reason most investigators have abandoned
peripheral nervous system (PNS) explanations in favor of the
hypothesis that PLP is a consequence of maladaptive cortical plasticity
induced by loss of input from the limb [1,23,28,39,46,48].
The cortical origin of PLP has considerable empirical support.
For example, limb amputation or corresponding nerve injury leads
to conspicuous neuroplastic remapping of somatotopic representations
in the primary somatosensory cortex (S1) [16,21,24,25,31,32,
53,66], with the extent of remapping proportional to the intensity
of the pain [22]. Likewise, distortions in body schema perception
occur when conflict is induced experimentally between the
appearance of an individual’s limb and proprioceptive feedback.
In the rubber hand illusion, for example, the perceptual integration
of the rubber hand is so striking that threatening it with injury
evokes anxiety and pain affect–related cortical activations [18].
Some subjects report unpleasant sensations, perhaps even pain,
due to such sensory–sensory mismatch [28]. Resolving this mismatch,
as implemented in mirror box therapy, can relieve PLP, at
least temporarily [48,53].
However, a second PNS source, outside of the stump, has never
been adequately considered. For decades there has been direct
electrophysiological evidence that afferent somata in the dorsal
root ganglia (DRGs) also generate ectopia [33,37,52,62]. Indeed,
in head-to-head comparisons, the DRG has proved to be a more
robust source of spontaneous firing than neuromas [2,42].
Evidence, if indirect, is even available in humans [38,40,49,50].
For example, Nystrom and Hagbarth [50] showed that blocking
http://dx.doi.org/10.1016/j.pain.2014.04.018
0304-3959/� 2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
⇑ Corresponding author. Address: Department of Cell & Developmental Biology,
Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904,
Israel. Tel.: +972 2 6585085; fax: +972 2 6586027.
E-mail address: [email protected] (M. Devor).
www.elsevie r .com/ locate/pain
PAIN� 155 (2014) 1384–1391

History of the Dermatomes with Focus on the Contributions from the Lumbar Plexus

A dermatome is defined as an area of skin innervated by a single dorsal nerve root. ¹ Knowledge of dermatomes is derived from the work of Sir Henry Head, Otfrid Foester, ² Jay Keegan, Frederic Garrett, and others. ³ Many different methods were used by these authors and may have contributed to the variable findings and representations of what is understood as “the precise boundaries” of dermatomes. The differences could have also arise because several of these methods were based on physiology rather than anatomy.⁶ The ability of the central nervous system to suppress, facilitate, and reorganize the activities of primary sensory neurons may also account for differences in mapping. ⁴ Additionally, sensory neurons with a ganglion cell at one level through intersegmental anastomoses among posterior spinal rootlets are allowed to enter the spinal cord at another level, ^{4,​5,​6,​7,​8} resulting in differences in skin supply by the dorsal roots, dorsal root ganglia, and spinal nerves. ⁴ In this chapter, the history of the discovery of dermatomes is explored.

In 1893, William Thorburn, a surgical registrar in the Manchester Royal Infirmary, after observing patients with spinal cord lesions published detailed maps of the lumbar and sacral dermatomes (▶ Fig. 20.1). ^{4,​9,​10,​11,​12} Thorburn speculated that the dermatomes existed because of contributions from “certain serial sections of the nervous system.” He went on to state that “it remains to be proved that these ‘sections’ are spinal segments, nerve roots, or other serial arrangements.” ^4,​12

Fig. 20.1 Thorburn’s representation of the lumbar and sacral dermatomes. L4 is extended proximally and S1 is assigned to the medial foot. (Reproduced with permission from Thorburn. ¹²)

In 1892, maps of the dermatomes was also constructed by Professor M. Allen Starr of the College of Physicians and Surgeons in New York after examining patients with cauda equina syndrome (▶ Fig. 20.2). ^4,​13

Fig. 20.2 M. Allen Starr’s representation of the lumbar and sacral dermatomes. L2 (labeled VII) extends distally and S1 does not extend below the knee. (Reproduced with permission from Starr. ¹³)

From identifying the locations of afflicted skin in herpes zoster patients and from monitoring patients with visceral nonneurological disorders and spinal cord injuries, Sir Henry Head also constructed dermatomal maps (▶ Fig. 20.3). ⁴ His initial work on the association between cutaneous tenderness and visceral disease began in 1893, and he created charts outlining what others refer to as “Head’s zones,” which show the distribution of cutaneous tenderness in many diseases. ¹⁴ Through examining cases of herpes zoster, Head observed that the areas of herpetic eruptions matched the “area of tenderness” he had described. ^4,​14 Consequently, he made the deduction that the “areas of tenderness” corresponded to spinal cord segments. ⁴ By observing a case of sensory loss due to a “fracture of the 1st and 2nd lumbar vertebrae” L1 was determined. ¹⁴ Head found that the upper border of L1 matched the upper border of the sensory loss and that this area coincided with the upper border of the “gluteocrural area,” one of his proposed “areas of tenderness.” He inferred that these areas were the same and that the lower border of L1 must be the lower border of the “gluteocrural area.” After deriving such conclusions at L1 and later S1 to S5, Head noticed that the lateral area of the leg had no designated dermatome. He deduced that this area must be L5 because it was located next to the sacral skin segments. Using a case of presumed spinal cord injury, L4 was determined and a case of herpes zoster rash determined L3. The three dermatomes L3–L5 were proposed by Head to be involved after observing the pattern of the rash. As a result, L3 was assigned to the area outside the already determined areas, L4 and L5. Later, he speculated that L2 must be between L1 and L3. In 1900, Head and Campbell studied 500 cases of shingles and sketched a map showing the distribution of cutaneous lesions. ¹⁵ They also found that there were overlaps between adjacent nerve territories and considered that body shape influences differences in the shape of the affected skin. ¹⁶ The roots involved in most cases of herpes zoster could not be identified; however, they were able to identify them in 16 autopsy cases. Eight segments in those 16 cases (between T1 and L1) were represented. Head had no confirmation for C5 to C8 or areas below L1, and therefore there were uncertainties when it came to mapping the arm and leg. ^4,​15

Fig. 20.3 Sir Henry Head’s dermatomal maps. (Reproduced with permission from Head. ¹⁴)

Using the “method of remaining sensibility,” Sir Charles Scott Sherrington studied the dermatomes in monkeys and produced dermatomal maps in 1893 and 1898. ⁴ Sherrington found that after many roots above and below a given nerve root had been sectioned the remaining areas of sensation in the skin indicated input from the unsectioned root. ^{4,​17,​18} Sherrington also found evidence to support Herringham’s ventral axial line. ¹⁹ He found gaps where contiguous dermatomes were missing in the proximal portions of the dorsal and ventral parts of both the upper and the lower limbs. According to Sherrington, “the gap” formed an axial line that coursed downwards from the midline at the level of the sternal angle to the forearm. ^16,​17

Otfrid Foester, a German neurologist and neurosurgeon, adopted Sherrington’s approach but applied it to humans. He severed multiple nerve roots and electrically stimulated the distal end of the divided root that resulted in vasodilatation in the dermatomal area. ¹ One of the shortcomings of Foester was his lack of awareness that removing a nerve most likely resulted in pain due to input to the central nervous system, probably resulting in death in his patients. ¹ In the words of Dr. Robert Wartenburg, “he helped his patients, but they had to pay the price by being subjected to physiological experimentation.” ²⁰ Foester found from his research that removing a single root did not result in loss of sensibility, so he made the deduction that dermatomes in humans overlap. He also observed that only one rootlet from the entire posterior root was needed for sensibility within a dermatome and identified different dermatomes for different sensory modalities. ⁴ He found that the areas of vasodilatation matched the dermatomes determined by anesthesia. This finding presented similarities in distribution to the map drawn by Head from his studies of shingles. ¹⁶

Following the association made between disc herniation and back and leg pain in 1934, ²¹ Keegan and Garrett contradicted Sherrington and Foester’s hypothesis about nerve roots and cutaneous sensibility. They proposed that decreased sensibility of the skin resulted from disc compression of a single nerve root. ^{22,​23,​24,​25,​26,​27} They observed patients with different herniations of the cervical and lumbar areas and made maps reflecting the areas of decreased sensibility on the limbs. From the upper limbs studied in 165 cases, 47 cases showed that a single root was affected. Note that 707 cases showed that a single nerve root was affected out of 1,264 cases of the lower limb studied. They also used Novacain injection to test a single lower cervical nerve root in 10 medical students volunteers. ¹⁶ The maps constructed by Keegan and Garrett, like Head’s maps, showed no overlap of dermatomes (▶ Fig. 20.4). ⁴ Keegan and Garrett dismissed Foester’s claim that removing a single nerve root caused no sensory loss. ^16,​22 They also disagreed with Sherrington and concluded that “dermatomic loops” and “dorsal axial lines do not exist.” ²² Last ²⁸ analyzed Keegan and Garrett’s publications and found the following limitations in their findings:

“(1) The subjective method of mapping a dermatome by hypoalgesia must be open to wide error. (2) The lack of overlap of adjacent dermatomes is difficult to accept in face of the almost unanimous opinions of countless observers. (3) No mention is made of variability yet prefixation and post fixation of the plexuses are known to be common. (4) Their claim that an isolated nerve root is affected in their case of disc protrusions or injected medical students is not convincing; there may well have been some involvement of adjacent nerve roots.” ²⁸

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Related

The Organization of the Dermatome and Afferent Myotome on JSTOR

Abstract

Single fibres were dissected from the dorsal spinal roots of the nerves serving the brachial plexus in African green monkeys. The dermatomal organization of these spinal nerves was deduced from data concerning the receptive fields of 2834 single afferent fibres. These data were collected in an attempt to reconcile some of the discrepancies that exist in published descriptions of the dermatomes in primates; our results and the literature reviewed suggest that the cutaneous region served by one spinal nerve is actually much wider and much more variable in location than is generally recognized. This makes any summary diagram a misleading indicator of the true complexity of the spinal innervation of the upper limb. In spite of this variability among individuals, within any specific individual there is a regular and orderly progression of innervation which allows prediction of the region served by a particular spinal nerve when information concerning the site of innervation of adjacent nerves is available. The territory of each myotome tended to be larger than the dermatome of the same spinal nerve. Most muscles of the limb received afferent innervation from three to four different spinal nerves. Further, the territory of the myotome did not of necessity coincide with the dermatome of the same spinal nerve. Even those nerves innervating the hand still innervated axial muscles. These observations have important implications for the diagnosis of spinal nerve injuries.

Publisher Information

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Spinal stenosis

Stenosis of the lumbar spine

Spinal stenosis is a disease involving a combination of narrowing of the spinal canal according to either computed tomography (CT), magnetic resonance imaging (MRI) or spinal x-ray (spondylography) and characteristic clinical symptoms. During MRI of persons over 60 years old, it was noted that 21% of them had radiological signs of narrowing of the spinal canal at the lumbar level.Only one third (33%) presented complaints characteristic of stenosis.

The introduction of CT and MRI into wide clinical practice has led to a significant increase in the diagnosis of this pathology.

Classification

• Distinguish by anatomical criteria
• central stenosis – a decrease in the distance from the posterior surface of the vertebral body to the nearest opposite point on the arch at the base of the spinous process
• lateral stenosis – narrowing of the radicular canal and intervertebral foramen to 4 mm and less
• Distinguish by etiology
• congenital or idiopathic stenosis; achondroplasia
• acquired stenosis
• combined stenosis – any combination of congenital and acquired stenosis

Epidemiology

Spinal stenosis at the lumbar level is a very common disease.Its frequency increases sharply in people over 50 and in this age group ranges from 1.8 to 8%. According to Danish authors, stenosis of the lumbar spine occurs with a frequency of 272 cases per 1,000,000 population per year. Every year, 9.7 per 100,000 population are operated on for this problem in the Scandinavian countries.

Etiology

Congenital stenosis is caused by the anatomical features of the structure of the spine in humans and manifests itself

• by shortening of the vertebral arch
• achondroplasia (increase in the thickness of the arch of the vertebra, shortening of the leg and decrease in the height of the vertebral body)
• cartilaginous and fibrous diastematomyelia

The causes of acquired stenosis are different.The main ones are:

• spondyloarthrosis deformans with hypertrophy of intervertebral joints, formation of marginal osteophytes
• Ossified herniated discs
• hypertrophy and ossification of the yellow ligament
• Forestier disease (diffuse idiopathic hyperostosis of rheumatoid nature)
• ankylosing spondylitis
• spondylolisthesis of degenerative-dystrophic genesis
• iatrogenic stenosis – formation of subarachnoid adhesions and / or postoperative scars
• “steel stenosis” – the introduction of metal structures into the lumen of the spinal or radicular canal

Central stenosis occurs due to pathological processes in the anatomical structures that form the spinal canal (in particular, intervertebral discs, intervertebral joints, ligamentum flavum, posterior longitudinal ligament), which contains a spinal sac with nerve roots included in it.

Lateral stenosis can occur in one or more of three anatomical zones: the entry zone (lateral recessus), the middle zone, and the exit zone (intervertebral foramen).

Pathogenesis

Pathophysiological mechanisms causing the development of characteristic complaints are due to a combination of three groups of factors – increased epidural pressure, aseptic inflammation and ischemia. The emergence of each of them is due to chronic compression of the neurovascular structures of the spinal canal.

Due to chronic compression, there is a mismatch of blood flow to the nerve structures of the spinal canal. The level of incoming blood decreases and, accordingly, ischemia of the nerve root (with lateral stenosis) and cauda equina (with central stenosis) occurs. With combined stenosis, a combination of ischemia of both the cauda equina and the nerve root is observed. It is noted that the phenomena of ischemia cause demyelination processes, the formation of adhesions between the pia mater and arachnoid meninges, the development of interstitial fibrosis and cicatricial adhesive epiduritis.

The demand for oxygen increases with the intensification of biochemical processes. This explains the fact that complaints of pain in the back and / or legs, weakness with stenosis of the spinal canal occur when walking.

The discrepancy between the volume of neurovascular structures and the volume of the spinal canal causes an increase in epidural pressure and, as a consequence, causes an inflammatory process. Epidural pressure increases when walking, which causes the production of ectopic nerve impulses and is manifested by the occurrence of pain

With flexion, the height of the intervertebral foramen increases by 12%, with extension, it decreases by 15%.This explains the characteristic complaint, which consists in regression of pain up to complete disappearance when sitting down, bending over. Moreover, on the basis of this symptom, a differential diagnosis is made between neurogenic (with stenosis of the spinal canal) and vascular intermittent claudication. So, with neurogenic intermittent claudication, in contrast to vascular, a person can work on an exercise bike for a long time, do not experience complaints during prolonged driving.

Stenosis of the spinal canal as a consequence of osteochondrosis

The most common acquired stenosis of the spinal canal is the last 4th stage of osteochondrosis of the spine.Its occurrence is characterized by the fact that against the background of instability of the spinal motion segment (3rd stage of osteochondrosis), compensatory processes develop, aimed at its stabilization. These include the proliferation of bone tissue in the form of osteophytes, arthrosis of the intervertebral joints. The intervertebral joints limit both the spinal canal and the entry zone of the nerve root, the intermediate zone and the intervertebral foramen. Accordingly, the proliferation of intervertebral joints leads to a narrowing of the above anatomical structures and, accordingly, to the development of stenosis.

Clinic

In the study of a group of patients with spinal stenosis at the lumbar level, it was noted that the leading complaints are:

• back pain (95%)
• neurogenic intermittent claudication syndrome (91%)
• radicular pain in one or two legs (71%)
• weakness in one or two legs (33%)

In patients who noted a combination of pain in the leg and lower back, 70% noted the same intensity of pain in the leg and lower back, in 25% leg pain prevailed.In 58% of cases, the pain was in one leg and in 42% it was bilateral. The majority of patients had radiculopathy of several nerve roots. Basically, pain in spinal stenosis spreads in dermatomes L5 (91%) and SI (63%), less often in dermatomes L1-L4 (28%).

In the monograph by Yu. A. Zozuli et al., A table of the frequency of occurrence of various complaints in patients with spinal stenosis is given.

Neurogenic intermittent claudication is a pathognomonic symptom that makes it possible to assume the presence of spinal stenosis even before additional examination methods.It is characterized by the appearance of pain when walking, which regresses when sitting down or bending the body forward. After that, a person can again walk a certain distance until painful sensations appear. In a sitting position, the patient can perform any work (exercise bike, driving a car) without pain. The intensity of neurogenic intermittent claudication is estimated in the distance (meters) that a person can walk before the onset of pain.

Diagnostics

The diagnosis of stenosis of the spinal canal can be established on the basis of a combination of clinical complaints and narrowing of the lumen of the spinal canal according to the data of additional research methods.

Narrowing of the spinal canal (anteroposterior dimension less than 12 mm) can be detected by magnetic resonance imaging, computed tomography and radiography (spondylography) of the spine.

Treatment

Treatment of spinal stenosis can be conservative and operative.

Conservative treatment

Conservative treatment includes the appointment of antalgic, vascular, anti-inflammatory drugs. However, it is not effective enough in the treatment of spinal stenosis, as it leads to an improvement in well-being in 32-45% of patients.

Surgical treatment

Surgical treatment of spinal stenosis has a number of features. First, there are several types of operations used for stenosis:

• decompression laminectomy
• Installation of stabilizing systems
• Installation of interspinous fixation systems

Secondly, stenosis of the spinal canal is often combined with other types of spinal pathology, such as instability and herniated intervertebral discs.

Decompressive laminectomy

Decompressive laminectomy involves resection of structures that compress the nerve root and / or cauda equina by the posterior approach, namely the spinous process. arches of the vertebrae, yellow ligament, intervertebral joints.

Historically, decompression laminectomy was the first type of surgery used to treat spinal stenosis.

At the same time, decompression laminectomy has a number of disadvantages that lead to its insufficient effectiveness.So, as a result of this operation, the structures that form the third support column of the spine according to Denis or the second support column of the spine according to Holdsworth are removed. The result in a large number of cases is the development of spinal instability, which leads to unsatisfactory treatment results, syndrome of unsuccessfully operated spine. Various sources indicate a 13-43% risk of developing instability after decompression laminectomy.

Insufficient efficiency of decompressive laminectomy, due to the development of spinal instability, led to its addition in many cases with stabilizing operations.

Stabilizing operations

Proponents of spinal fixation after laminectomy refer to biomechanical data. It was found that laminectomy leads to an increase in the volume of movement in flexion by 16% (P <0.05), extension by 14% (P <0.04) of axial rotation by 23% (P <0.03). With flexion, the tension of the annulus fibrosus after interlaminar decompression increases by 20%, and after laminectomy by 130%.

Supplementation of decompression laminectomy with stabilization systems (anterior or posterior) significantly improved the results of surgical treatment of spinal stenosis.

At the same time, the use of stabilizing systems is not without its drawbacks. In addition to possible complications, during their installation, there are violations of the biomechanics of the spinal motion segments adjacent to the stabilized ones, which are manifested by their hypermobility. This, in turn, leads to the development of the so-called “disease of the adjacent level.” It includes the development of spondylolisthesis, spinal stenosis, fractures, scoliosis.

Insufficient efficiency of decompression laminectomy due to the development of spinal instability, the development of an “adjacent level disease” with the addition of decompression by installing stabilizing systems led to the search for alternative methods of surgical treatment of spinal stenosis.

Interspinous fixation systems

The concept of dynamic stabilization is based on the fact that the trigger mechanism for spinal stenosis is a decrease in the height of the intervertebral disc due to degenerative changes, which in turn causes a redistribution of the axial load from the anterior support pillars to the posterior ones (up to 70%). The use of dynamic interspinous fixation provides a decrease in the load on the posterior support columns and an expansion of the area of ​​the spinal canal, which contributes to the reduction or disappearance of the lumbodynia syndrome caused by the facet syndrome.

The technique of installing dynamic interspinous fixation systems consists in carrying out posterior decompression (Cophlex, DIAM, WALLIS systems), followed by insertion of implants into the interspinous space, which, on the one hand, restore the posterior supporting column (according to Denis) of the spine, and on the other, retain the ability to bend and extension both in the operated and in adjacent spinal motion segments.

The efficiency of surgical interventions for spinal stenosis, in which microsurgical decompression and dynamic interspinous stabilization are combined, is 87%, they can significantly reduce the recovery time.

A feature of dynamic interspinous fixation systems is the ability to perform both flexion and extension in the spinal motion segment, which prevents the development of diseases of adjacent levels in patients

When installing implants in the interspinous space, the load on the intervertebral joints is also reduced, axial decompression of the roots occurs due to an increase in the height of the intervertebral foramen. Reducing the load on the joints promotes relaxation of the ligamentous apparatus

A contraindication to the use of interspinous dynamic stabilization is instability in the spinal motion segment.Since they stabilize only the posterior support pillars (according to Denis), their therapeutic effect in this pathology is insufficient.

At the moment, the following systems of interspinous dynamic fixation are used in medicine – Coflex (Co-promotes flexion) – a synonym for U-implant, DIAM (Device for Intervertebral Assisted Motion), Wallis (Wall Inter Spinously placed), X-Stop (eXtension Stop) , In-Space and Aperius.

Peculiarities of surgical treatment of stenosis combined with instability

When stenosis of the spinal canal is combined with instability of the spine, the use of only decompression or interspinous dynamic fixation systems is unacceptable, as it will cause an increase in instability and a deterioration in the patient’s well-being.

In case of instability in combination with stenosis of the spinal canal, the method of choice is the use of stabilizing systems (both anterior and posterior)

Peculiarities of surgical treatment of spinal stenosis in combination with intervertebral hernias

Narrowing of the spinal canal leads to the appearance of even a small protrusion of the intervertebral disc, translating the state of subcompensation into decompensation. A sharp increase in clinical manifestations caused by herniated intervertebral discs indicates its combination with a narrowing of the spinal canal.

This combination requires a microdiscectomy, a feature of which is a wide resection of bone structures (intervertebral joint, half-arch of the vertebra) causing narrowing of the spinal canal.

90,000 Postherpetic neuralgia – Medical and Preventive Center on Zanevsky – North-Western State Medical University named after I.I. Mechnikov

Postherpetic neuralgia

Postherpetic neuralgia

The urgency of the problem under consideration is due to an increase in the incidence of herpes zoster (Herpes zoster).This may be due to an aging population and an increase in the number of people with lowered immunity. The level of specific antibodies to the disease-causing Varicella zoster virus decreases with age, which probably makes a significant contribution to the prevalence of herpes zoster in older age groups, as evidenced by the data according to which, if the total indicator in the population is 2 per 1000 people, then in the age group over 75 years old, it is 10.

Development of cellular immunosuppression may result from severe illness or “aggressive” treatment.Thus, the incidence of Herpes zoster is approximately 15 times higher in HIV-infected patients. An increase in the prevalence of Herpes zoster infection is also “promoted” by the achievements of medicine in the field of organ donation, which requires active immunosuppressive therapy, as well as the emergence of new drug and radiation methods for treating tumor processes and an increase in the life expectancy of cancer patients.

Acute Herpes zoster is associated with significant social and economic losses for society, mainly due to the disability of patients, restrictions in daily activity due to severe neuropathic pain, which is long-term, persistent and often resistant to various methods of therapeutic intervention.So, of patients diagnosed with herpes zoster, or shingles, 45% report pain they experience every day, 23% – about pain all day, and 42% – about “terrible”, “excruciating”, “debilitating” pain. which is often the reason for hospitalization.

As mentioned above, herpes zoster is caused by the Varicella zoster virus, which also causes chickenpox in childhood. Both diseases are primarily characterized by a vesicular rash, in the case of herpes zoster associated with neuropathic pain.It has been proven that approximately 90% of the world’s population has positive serological reactions indicating a meeting with this virus, and in this regard, they are susceptible to a relapse of viral activity in the form of herpes zoster. Before the advent of the vaccine against the Varicella zoster virus in the United States, almost all children between the ages of 5 and 10 were infected with the virus, and about 3.5 million cases of chickenpox were reported in the country every year. The introduction of vaccinations has reduced the incidence of diseases by about 85%.An episode of chickenpox in childhood makes it possible to activate the cellular and humoral response, to form specific antiviral antibodies. Relapse of infection in such patients can develop only against the background of a low immune response. After primary infection, the virus spreads through sensory nerves to the spinal or cranial ganglion, where it is latent. During this time, it does not multiply, therefore, it is not pathogenic. Apparently, the latency of the virus is determined by the level of protective antibodies.Reducing it leads to reactivation of the virus, viral replication (reproduction), which at the clinical level is manifested by herpes zoster (Herpes zoster).

Three main stages of clinical manifestations of acute Herpes zoster infection should be distinguished: prodrome, stage of unilateral rash and stage of pain. The prodrome precedes the herpetic rash in 48-72 hours, is not detected in all patients and is characterized by acute pain or itching of the skin. Herpetic rash, in turn, goes through several stages of formation of vesicles, pustules and drying out in the form of a crust.Vesicles usually form within the first 5-7 days; pustules form over the next 4-6 days when the vesicles break open and release pus. Then the pustules become covered with a hard crust and the healing of the skin occurs within 2-4 weeks from the onset of the disease. The rash is usually localized in one or adjacent dermatomes and is accompanied by the development of acute neuropathic pain.

The clinical diagnosis of Herpes zoster is typically fairly straightforward. However, sometimes laboratory diagnostics are required to identify the virus.The fastest and most sensitive method is the polymerase chain reaction.

In the acute period of the disease or after it, complications may develop that affect one or many systems of the body. For example, a herpes rash can be additionally infected with bacteria from the skin, which requires antibiotic treatment. But the most important are neurological complications associated with reactivation of the virus in the spinal and cranial ganglia: postherpetic neuralgia (PHN), motor neuropathy, cranial neuritis, meningoencephalitis, transverse myelitis.It should be noted that complications from the brain and spinal cord are currently rare. In cases of the development of Herpes zoster in the trigeminal nerve, complications from the eyes are often observed – keratitis, iritis, retinitis, ophthalmitis. Previously, in the absence of specific antiherpetic therapy, frequent complications of Herpes zoster included pneumonia, encephalitis or hepatitis, sometimes leading to death.

Let us dwell in more detail on such a neurological complication as PHN.PHN is the most frequent complication of Herpes zoster, observed in 10-20% of patients. This complication is characterized by a direct correlation between the incidence and duration of PHN with age. More than 50% of patients with PHN are over 60 years old and 75% are in the age group over 75 years old. Half of patients with PHN over the age of 60 years experience constant pain for more than 6 months, with 10% in the age group 30-50 years.

More often, postherpetic pain is defined as persisting for more than 3-4 months. Other researchers use this concept in the earlier stages of the disease.Hence the inconsistency of information about the frequency of development of PHN. In cases where PHN is defined as pain persisting 3-4 weeks after the rash has healed, its prevalence is 8%. When pain persists for 2 months, the frequency is 4.5%. Up to 15% of untreated patients experience persistent pain for 1 month after the rash, and about 25% (4% of the total) of patients note persistence of pain for a year.

The main risk factors for PHN include age, female sex, the presence of pain during the prodrome, the severity of acute skin rashes, and the severity of pain in the acute period.

All these factors are interrelated, so most patients aged 50 years and older experience severe, intolerable pain and have significant skin rashes from acute Herpes zoster, which more often leads to PHN.

The mechanism of development of PHN is not fully understood, but it is clear that the nerve damage is caused by inflammation in acute Herpes zoster. The appearance of neuropathic pain is due to a violation of the interaction of nociceptive and antinociceptive systems, mechanisms for controlling the excitability of nociceptive neurons in the central nervous system.
PHN ranks third in frequency among all types of neuropathic pain and is second only to pain in the lower back and diabetic neuropathy.
This complication is usually accompanied by a variety of somatosensory disorders, including dysesthesia (unpleasant pathological sensations that can be spontaneous or induced), allodynia (pain caused by a usually harmless stimulus such as light contact), and hyperalgesia (exaggerated pain in response to common painful stimulation).

PHN has a direct impact on different aspects of the life of patients, especially the elderly:

1. physical condition – chronic fatigue, weight loss, physical activity, insomnia;
2. mental state – anxiety, anxiety, depression, difficulty concentrating;
3. social status – a decrease in social activity, a change in social role;
4. daily operation – dressing, showering, eating, etc.

One study found that 59% of patients with PHN experienced limitations in daily activity for more than 16 years
Therapeutic tactics for Herpes zoster include two main areas: antiviral therapy and relief of neuropathic pain. This applies to both the acute period of the disease and the stage of PHN.

Treatment of postherpetic neuralgia is successfully carried out by specialists of the neurological department of the medical-prophylactic center of the N.N.I.I. Mechnikov.

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90,000 Free flap operations, skin grafting

Free flap operations

Operation – Transfer of tissue from the donor site using microvascular anastomosis to the remote recipient site

Time – Varies depending on the operation. 4 hours minimum, often 6-8 hours or more

Pain – +++

Position – Variable.Usually on the back. Position change may be required during operation

Blood loss – Often 4-6 units

Practical recommendations – ET + mechanical ventilation, artery and CVP catheters, urinary catheter, epidural catheter for lower extremity flaps.

Before surgery

The free flap is most often used to provide tissue cover after trauma or resection of malignant tumors. This is a common reconstructive technique.An understanding of the task of the operation and the goals of the surgeon is essential.

Typical operations include:

• Free musculocutaneous flap from the transverse rectus abdominis muscle for breast reconstruction after mastectomy;
• Free flap of fine fibrous muscle of the thigh to cover the areas of the lower limbs after trauma with loss of tissue;
• Free fascial-cutaneous flap from the radial surface of the forearm to the oropharynx after tumor excision.

The goal of anesthesia is to provide hyperdynamic circulation with high cardiac output, adequate vasodilation and wide pulse pressure. Patients with lower limb injuries are often young and healthy. Patients after head and neck cancer are often smokers with coronary artery disease. Advanced age and limited cardiorespiratory reserve may be grounds for refusal and surgery in such patients.

During operation

You need to be prepared for a long operation.All patients require balanced OA. Regional anesthesia alone is rarely acceptable for such lengthy operations. Isoflurane is the inhalation anesthetic of choice for its beneficial effects on systemic vascular resistance.

Maintenance with propofol is also ideal, as it lowers systemic vascular resistance, is rapidly metabolized, has antimetallic properties, and helps to avoid postoperative chills, in particular, associated with the use of inhaled anesthetics (there is some in vitro evidence that propofol can be preferable for microvascular blood flow due to the absence of the effect of compaction of the erythrocyte wall, in contrast to inhalation anesthetics).

Regional block is useful as an adjunct to anesthesia. The sympathetic block and dense analgesia create excellent conditions for graft engraftment. Operations on the lower extremities are especially convenient for this. Operations in multiple zones may not be overlapped by a single block. A skin graft is often taken from the leg to cover the muscle flap.

Anesthetic management requires a good working knowledge of circulatory physiology.The blood flow in the microvascular circulation must be optimal to ensure graft engraftment. Blood flow is primarily affected by changes in perfusion pressure, vessel diameter, and blood viscosity [Hagan-Poiseuille formula]. We have only a superficial understanding of the physiology of microcirculation. Much of our anesthetic management is based on experience rather than randomized controlled trials.

Monitor internal (eg rectal or esophageal) and peripheral temperature.Isolate the temperature sensor from any external heat sources (heating blanket). The goal is to maintain a normal or even supranormal temperature and the difference between internal and peripheral less than 2 ° C. This must be achieved prior to completion of the microvascular anastomosis. An increase in the difference between indoor and outdoor temperatures can provoke vasoconstriction. Local vascular spasm can compromise the outcome of the surgery.

Any preoperative fluid deficit should be corrected and fluid loading initiated.Maintenance is continued with crystalloids, adding colloids bolus of 10 ml / kg (for example, gelofusin or hetastarch) as needed to increase the intravascular volume. Objectives – to maintain CVP – 12 mm Hg. Art. (or 2-4 mm Hg. Art. above the baseline), urine output – 2 ml / kg / h, expanded pulse pressure and low systemic vascular resistance. Colloids will increase intravascular volume more effectively than crystalloids. In the transplanted tissues, lymphatic drainage is insufficient and an excessive amount of crystalloids can become one of the causes of flap edema.Excessive volemic load should be carefully avoided in the elderly who are prone to developing pulmonary edema.

Mild hypotension and hemodilution early in the dissection may help reduce blood loss. Further, systolic blood pressure is maintained> 100 mm Hg. Art. or higher, depending on the level of blood pressure recorded before the operation.

Viscosity is closely related to hematocrit (Hct). Above 40% hematocrit, the viscosity rises dramatically. The goal is to maintain a hematocrit of about 30%, which theoretically provides the best balance between blood viscosity, oxygen content in arterial blood, and oxygen delivery to tissues.

Dextran reduces platelet adhesion and factor VIII concentration. This can improve the reliability of the graft. Depending on the preference of the surgeon, you can give 500 ml of dextran 40 during the operation or prescribe 500 ml in a complex daily intravenous infusion for 2-3 days.

Potent vasodilators (eg nitroprusside, hydralazine, and phenoxybenzamine) are not needed. Significant vasodilation can be achieved with anesthetics, provided that the patient is warmed, the volume of fluid is replenished, anesthesia is adequate, and the carbon dioxide level is within normal limits.

Nifedipine 10 mg, given as a premedication and then given three times daily to high-risk patients such as smokers with diabetes and arteriopathies, may improve graft engraftment. Chlorpromazine 1-2 mg IV (contained in an ampoule of 50 mg is diluted, preparing a solution for injection of 1 mg / ml) will help reduce the internal-external temperature difference if all other factors are corrected. To prevent local spasm, the surgeon may apply papaverine directly to the vessels.

Antibiotic prophylaxis is performed upon induction, sometimes repeated during surgery.

Post-operation

• The goal is a smooth awakening.

• Scrupulously careful management continues in the postoperative period. Surveillance of a flap requires specialized nursing experience and is often best done in a plastic surgery department. The need for an ICU / BVZ may be dictated by patient factors.

• Vasoconstriction due to cooling, pain, low circulating volume, hypotension, or hypocapnia is very dangerous for the graft and should be corrected as soon as possible.

• Chills are treated with pethidine 25 mg IV. The use of the warming blanket is continued in the awakening room.

• The condition of the flap is monitored clinically. Hourly observation includes temperature, color and arterial pulsation (if possible with a Doppler sensor), the data about which are recorded in the “flap map”.Pale skin color of the flap, absence of pulse, and delayed capillary filling may indicate problems with arterial blood supply. An edematous, dark flap, whitening easily with rapid capillary recovery, indicates venous drainage problems. The question of the expediency of a second operation should be resolved urgently.

• Long-term epidural analgesia is ideal for lower limb flaps. A catheter to the axillary brachial plexus (eg, infusion of 0.25% bupivacaine 5 ml / h for 2–3 days) may be useful for shoulder and hand surgery.

• Careful consideration should be given to whether more invasive upper trunk analgesia (eg, thoracic epidural block or interpleural analgesia) is warranted. The potential hazards may outweigh the potential benefits. These patients often use IV ACP very well. After operations on the head and neck, ACP is the best solution.

• Perioperative NSAID use is treated differently, but generally cautious.NSAIDs are valuable analgesics that reduce platelet adhesion. They can cause bleeding after long and extensive surgery. It is preferable to prescribe them after surgery, when the clots have already been organized.

Features

• Operations for reimplantation of severed fingers or limbs are performed in the same way as operations with a free flap.

• During the formation of a pedicle flap, arteriovenous connections are preserved, and the mobilized part of the flap is moved to cover a nearby defect.An example is displacement of the rectus abdominis muscle to close chest wounds, displacement of the pectoralis major muscle to reconstruct a defect in the lateral surface of the neck after tumor excision, or reconstruction of the mammary gland by moving the latissimus dorsi muscle on the leg. While surgery may be technically easier than moving a free flap, anesthesia requires the same close attention to detail.

• In general, free flap engraftment occurs in more than 95% of cases.Flap failure entails new reconstructive operations. Patients with a general unsatisfactory condition and concomitant diseases have a greater risk of flap rejection.

Skin graft

Operation – Closure of the surgically “refreshed” surface with a free skin graft after removal of nonviable tissue or granulating wound

Time – Varies 30 min-2 h

Pain – ++ / +++ (especially donor area)

Position – Variable.Depends on the area to be closed. Usually on the back

Blood loss – None with simple transplants. Extensive debridement of non-viable tissue and burn closure may require 6-8 units

Practical recommendations – OA / LM on spontaneous breathing (with a block of the lateral cutaneous nerve of the thigh or a femoral block 3: 1 – if the donor area is on the thigh). Spinal anesthesia for lower limb surgery.

Before surgery

Patient assessment is influenced by indications for skin grafting.

• Patients for simple excision and transplantation in isolated lesions are usually reasonably well preserved.

• Elderly patients for skin excision / grafting for lesions or pretibial tears may be generally very weakened. Local or regional techniques may be preferred over general anesthesia.

• Burn patients who are scheduled for surgical debridement and skin grafting require careful evaluation.In extreme cases, full intensive care may be required.

• Skin grafting can be a component of larger operations, such as skin preparation for a free muscle flap.

In patients with burns, the volemic status should be carefully assessed, and attention should be paid to urine output and commonly prescribed fluids. Check hematocrit, CBC, clotting, urea and electrolytes, arterial blood gases, chest X-rays.

During operation

Full thickness skin graft. Consists of epidermis and dermis. It is used on small areas where the thickness, appearance and texture of the skin are important. Usually cut with a scalpel. Usually the donor area should be in the immediate vicinity of:

• posterior skin for facial grafts.
• groin or cubital fossa on the arm for the treatment of flexion contractures.

Split skin graft.Consists of the epidermis and the varying severity of the dermis layer. It is used much more extensively than a full thickness graft. Usually cut with a special skin graft knife or an electrically powered dermatome. Donor areas heal on their own within 2 weeks. Donor zones are selected in accordance with the required amount of skin, the coincidence of its color and texture, and ease of localization. To stretch the graft in order to increase the size of the covered area, its multiple perforations are used.

Typical donor sites are:

• thigh;
• flexor surface of the forearm, upper arm;
• anterior abdominal wall.

A full thickness skin graft may be cut using a subcutaneous infiltration of local anesthetic with a 27 G needle. The addition of hyaluronidase promotes diffusion (eg, 1500 U to 100 ml of local anesthetic solution).

A split skin graft can be cut using a local anesthetic cream (eg EMLA).It should be applied at least 2 hours before the procedure and covered with an insulating dressing. Anesthesia does not extend into the deeper layers of the dermis, therefore the technique is not suitable for taking a full thickness graft. A lateral femoral cutaneous nerve block or a 3: 1 femoral block will provide beneficial anesthesia to the donor area at the thigh.

Surplus cut skin can be stored at 4 ° C for 2-3 weeks.

Post-operation

• Donor site after taking a split graft, potentially painful wound.Top up with local anesthesia (femoral cutaneous lateral nerve block or 3: 1 femoral block) where possible.

• The type of dressing is important for the comfort of the donor area. The most commonly used anesthetic dressing is Kalostat impregnated with MA (for example, 40 ml bupivacaine 0.25%). The bandage is difficult to fix on the hip and often slips off when the patient moves. Some surgeons use a thin, adhesive cloth bandage (eg sterile “Mefix”), which can improve the fixation and comfort of the donor area.The bandage is soaked after 2 weeks.

• NSAIDs and simple analgesics are usually needed within 3-4 days. After the pain has subsided and healing has begun, itching is often felt.

Peculiarities of management of patients with burns

Extensive surgical debridement and skin grafting on burned surfaces is a major operation. It should be performed using balanced OA. The goal of direct management is to surgically debride the burned tissue and close the area with a full-thickness graft as early as possible (often within 48 hours).This turns the burn surface into a healthy surgical wound. A potential source of sepsis is eliminated, fluid loss is reduced, and intensive care is less stressful.

Two anesthetists may be required. Two surgical teams will significantly speed up the operation, this will help and minimize complications.

Blood loss . 6-8 units should be prepared. Surgically sanitized tissues are very bleeding. Blood loss can be difficult to measure, especially in young children.Monitor hematocrit regularly and maintain it at approximately 30%.

Temperature control . Large areas of the exposed surface of the body will rapidly lose heat through radiation and evaporation. Measure the internal temperature. Use all available heat preservation methods. Only a small part of the body surface may be accessible for a warming blanket. The operating room temperature is maintained at 25 ° C.

Monitoring .The placement of non-invasive monitoring devices can be difficult. An arterial catheter makes it easier to measure blood pressure and collect blood samples. A central venous catheter provides reliable venous access for this and subsequent procedures and helps control intravascular volume. During installation, strictly observe asepsis. The cannula may need to be sewn on. You should try to place it on intact skin. A urinary catheter is very important.

Suxamethonium is contraindicated, except for the first 24 hours after the burn.A massive release of K + can cause cardiac arrest.

Post-operative care . They are returned to the burn department. For large burns (for example, more than 40%) or additional injuries (for example, smoke inhalation), ventilation in the ICU may be required before rewarming and stabilization.

Analgesia is best provided with IV opioids, either as ACP or continuous infusion. Early involvement of the on-call service should be envisaged before the onset of acute pain.Dressing changes can be facilitated with entonox or ketamine / midazolam sedation.

Antibiotics and adequate nutrition are important to improve engraftment.

90,000 Pain. Pain classification – fast and slow pain – Mega-training

Thalamus function in somatic sensations. Cortical sensitivity control

With the destruction of somatosensory cortex, a person loses mainly the ability to subtly distinguish tactile signals, but to a small extent, coarse tactile sensitivity is eventually restored.Therefore, it can be assumed that at the level of the thalamus (as well as other underlying centers) there is little ability to distinguish tactile sensations, although usually the thalamus functions mainly as a station for transmitting this type of information to the cortex.

Conversely, loss of the somatosensory cortex has only a minor effect on the perception of pain sensation and a moderate effect on the perception of temperature. In this regard, there are strong reasons to believe that the brainstem, thalamus and other associated basal regions of the brain play a dominant role in distinguishing between these types of sensitivity.

Interestingly, these types of sensitivity appeared at very early stages of phylogenetic development in animals, while fine tactile sensations and the somatosensory cortex appeared only at later stages of development.

In addition to somatosensory signals , transmitted from the periphery to the brain, the cortex sends so-called corticofugal signals in the opposite direction to the lower sensory relay centers of the thalamus, medulla oblongata and spinal cord.These signals adjust the sensitivity level of the touch input.

Corticofugal signals are almost completely inhibitory, so if the activity of the sensory input becomes too high, they automatically reduce transmission in the switching nuclei. As a result, the following happens. First, the lateral spread of sensory signals to neighboring neurons decreases and, consequently, the contrast increases during signal transmission.

Secondly, the sensor system is kept within the sensitivity range required for its normal functioning, i.e.That is, the sensitivity should be neither so low that the signals become ineffective, nor so high that the system is overexcited, going beyond its ability to differentiate the features of sensory signals. This principle of corticofugal regulation of sensory input is used by all sensory systems, not just the somatic system.

Each spinal nerve innervates a segmental field of the skin called the dermatome. In the figure, various dermatomes are shown as if there are distinct boundaries between adjacent dermatomes, which is far from the truth, as there is significant overlap of one segment with another.

The figure shows that the anal region of the body is located in the dermatome of the most distal segment of the spinal cord – dermatome S5. In the embryo, this is the tail region and the most distal part of the body. According to the dermatome map, the legs are embryologically derived from the lumbar and upper sacral segments (L2 to S3) and not from the distal sacral segments.

Dermatome map shown in the figure can be used to determine the level of spinal cord injury from the resulting sensory impairment in the periphery.

Pain. Pain classification – fast and slow pain

Many diseases are accompanied by pain . Moreover, the ability to diagnose various diseases depends to a large extent on the doctor’s knowledge of the qualities of pain. The first part of this chapter is devoted primarily to pain and the physiological underpinnings of some of the clinical phenomena associated with it.

Pain – defense mechanism .Pain occurs whenever any tissue is damaged, and this prompts the person to take actions that help remove the pain stimulus. Even if a person just sits for a long time, this can cause tissue destruction due to impaired blood flow in the skin, where it is compressed under the weight of the body. When the skin is sore as a result of ischemia, the person usually subconsciously changes the position of the body. But with a loss of pain sensitivity, for example, after damage to the spinal cord, the person will not feel pain and, therefore, will not change position.Soon, this will lead to complete destruction and rejection of the skin in the areas of pressure.

Pain is classified into two main types: rapid pain and slow pain. The sensation of rapid pain occurs approximately 0.1 seconds after the onset of the pain stimulus, while slow pain begins only after 1 second or more, then slowly increases over many seconds, and sometimes even minutes. In this chapter, we will see that for these two types of pain, the pathways are different, and each of them has specific characteristics.

There are many alternative names for rapid pain , such as piercing pain, stabbing pain, sharp pain, electrical pain. This type of pain is felt when the skin is punctured with a needle, cut with a knife, or severely burned. Rapid pain is also felt with electrical injury to the skin. In most cases, the sensation of rapid, piercing pain does not occur when the deeper tissues of the body are damaged.

Slow pain also has many names, such as burning pain, aching pain, throbbing pain, nauseous pain, and chronic pain.This type of pain is usually associated with tissue destruction and can lead to long-term, unbearable suffering. Such pain can occur both in the skin and in almost any deeply located tissue or organ.

Pain receptors – free nerve endings. All pain receptors in the skin and other tissues are free nerve endings. They are widespread in the surface layers of the skin, as well as in some internal tissues, for example, in the periosteum, arterial walls, articular surfaces, sickle and the tentorium of the cranial vault.Painful endings are rare in other deep tissues; however, in most of these areas, any widespread tissue damage can cause slow (chronic) pain.

Three types of stimuli excite pain receptors : mechanical, thermal and chemical. Pain can be triggered by a variety of stimuli – mechanical, thermal, and chemical. Usually, fast (acute) pain is caused by mechanical and thermal stimuli, while slow pain can be caused by all three types of stimuli.Pain-causing chemicals include bradykinin, serotonin, histamine, potassium ions, acids, acetylcholine, and proteolytic enzymes. In addition, prostaglandins and substance P, without directly stimulating pain receptors, increase their sensitivity to pain stimuli. Chemicals play a particularly important role in the development of the slow, excruciating pain that occurs after tissue damage.

Pain receptors do not adapt . Unlike most other sensory receptors, pain receptors hardly adapt.On the contrary, under certain conditions, against the background of a long-acting pain stimulus, the excitation of pain fibers progressively increases; this is especially true for slow, aching pain with nausea. This increase in sensitivity is called hyperalgesia. It is easy to understand the importance of the lack of adaptation of pain receptors, since this allows a person to be informed about the presence of a tissue-damaging stimulus throughout the entire period of its action.

Heading “Conversation with a specialist” Vertebrogenic radiculopathy (this is osteochondrosis)

Lumbosacral radiculopathy (LRS) is one of the most severe variants of vertebral pain syndromes, which is characterized by particularly intense and persistent pain, usually accompanied by a sharp limitation of mobility.Although radiculopathy accounts for about 5% of back pain cases, it is the most common cause of permanent disability. While in 90% of patients with acute back pain (with all its variants included) it resolves on its own within 6 weeks, in at least 30% of people with radiculopathy the pain persists longer.

Epidemiology
RCC occurs in about 35% of people worldwide. The incidence of men and women is approximately equal, but its peak in men is at the age of 4050 years, in women –5060 years.The risk of developing vertebrogenic radiculopathy is increased in persons who are engaged in heavy physical labor, with smoking, with a family history. Regular physical activity may reduce the risk of radiculopathy, but those who start it after an episode of discogenic back pain may be at increased risk.

Causes
The most common cause of RCC is a herniated disc. At a young age, in view of the higher intradiscal pressure, the nucleus pulposus more easily penetrates between the damaged fibers of the annulus fibrosus, which causes more frequent development of discogenic radiculopathy.Herniated intervertebral discs capable of compressing the root are conventionally divided into three types: lateral (displaced towards the intervertebral foramen), paramedian (mediolateral), and median.

In elderly people, radiculopathy is more often caused by compression of the root in the lateral pocket or intervertebral foramen due to the formation of osteophytes, hypertrophy of the articular facets, ligaments, or other reasons. More rare causes – tumors, infections, dysmetabolic spondylopathies – together explain no more than 1% of cases of radiculopathy.

Pathogenesis of pain in radiculopathy
Although mechanical compression of the root and / or spinal ganglion plays a decisive role in the initiation of pain in a herniated disc, persistent maintenance of an intense pain syndrome may be associated not so much with mechanical factors as with secondary toxic, dysimmune and dysmetabolic processes, which are triggered by the insertion of a disc into the epidural space and exposure to material released from the nucleus pulposus.

Pain syndrome in vertebral radiculopathy is mixed. The nociceptive mechanism is associated with irritation of nociceptors in the outer layers of the damaged disc and surrounding tissues, including the dura mater, as well as in spasmodic muscles. The neuropathic component of pain syndrome is associated with damage and irritation of the nerve fibers of the root due to its compression, inflammation, edema, ischemia, demyelination and axonal degeneration.

Clinical presentation
Clinically, RCC is characterized by acutely or subacutely developing paroxysmal (shooting or piercing) or constant intense pain, which at least occasionally radiates to the distal zone of the dermatome (for example, when taking Lasegue).Leg pain is usually associated with lower back pain, but in young people it may only be in the leg. Pain can develop suddenly – after a sudden unprepared movement, lifting or falling. In the history of such patients, there are often indications of repeated episodes of lumbodynia and lumbar ischialgia. At first, the pain may be dull, aching, but it gradually increases, less often it immediately reaches its maximum intensity. If radiculopathy is caused by a herniated disc, the pain usually increases with movement, straining, lifting weights, sitting in a deep chair, prolonged stay in one position, coughing and sneezing, pressing on the jugular veins and weakening at rest, especially if the patient lies on healthy side, bending the sore leg at the knee and hip joints.

Acute bilateral radicular syndrome (cauda equina syndrome) occurs rarely, usually due to a massive median (central hernia of the lower lumbar disc. The syndrome is manifested by rapidly increasing bilateral asymmetric leg pain, numbness and hypoesthesia of the perineum, lower flaccid paraparesis, urinary retention, incontinence). the situation requires urgent consultation with a neurosurgeon.

Diagnosis
The diagnosis of radiculopathy is primarily established on the basis of characteristic clinical signs.The presence of a disc herniation, stenosis of the radicular canal at an appropriate level, or another cause of root compression can be ascertained using computed tomography (CT) or magnetic resonance imaging (MRI). However, when interpreting imaging data, it is important to take into account that in about 2/3 of people who have never experienced back pain, these research methods reveal certain changes in the lumbosacral spine, often at several levels. In half of the patients from these individuals, a uniform symmetric protrusion of the disc is revealed, in a quarter – focal or asymmetric protrusion, often also stenosis of the spinal canal and arthropathy of the facet joints are found.Radiculopathy clearly correlates only with the extrusion of the disc, which is understood as the extreme degree of its protrusion, when the protrusion length exceeds the width of its base.

According to indications, X-ray of the lungs, ultrasound examination of the abdominal cavity and small pelvis, retroperitoneal space, excretory urography, sigmoidoscopy are performed. For women, a gynecologist’s examination is also required. The complex of examination may also include a clinical blood test and a general urine analysis, determination of the content of sugar, electrolytes, urea nitrogen, creatinine, calcium, phosphorus, uric acid, and serum protein electrophoresis.In men, a prostate-specific antigen test is performed.

Course
Over time, in most cases, the size of the disc herniation and signs of root compression spontaneously decrease, regardless of the method of conservative treatment used and age. The vast majority of patients with RCC recover within 3 months. Nevertheless, in a certain proportion of patients, recovery occurs over a longer period (36 months). If an exacerbation lasts more than 6 months (about 15% of patients), the persistence of clinical manifestations can be predicted for at least the next 2 years.The prognosis is worse when the root is compressed in the radicular canal. Prognostically favorable factors are the absence of pronounced symptoms of tension, stenosis of the spinal canal on CT or MRI, the patient’s active participation in rehabilitation programs, the absence of pronounced psychoemotional disorders and rental installation.

General principles of treatment
In the majority of people with discogenic radiculopathy on the background of conservative therapy, it is possible to achieve a significant reduction and regression of pain syndrome.The basis of conservative treatment of radiculopathy, like other variants of back pain, is non-steroidal anti-inflammatory drugs, which should be used from the first hours of the development of the disease, preferably their parenteral administration. With intense pain, it is possible to use tramadol at a dose of up to 300 mg / day. The obligatory component of treatment should be a short (7-14 days) course of muscle relaxants (eg tizanidine or tolperazone).

In recent years, along with traditional discectomy, more gentle surgical techniques have been used: microdiscectomy, laser decompression (vaporization) of the intervertebral disc, high-frequency disc ablation, etc.For example, laser vaporization is potentially effective in radiculopathy associated with a herniated disc while maintaining the integrity of the annulus fibrosus, bulging it by no more than a third of the sagittal size of the spinal canal (about 6 mm), and in the absence of movement disorders or symptoms of root compression in the patient. horse tail. The minimally invasiveness of the intervention expands the range of indications for it. Nevertheless, the principle remains unchanged: surgical intervention should be preceded by optimal conservative therapy for at least 6 weeks.

The use of a complex of high doses of B vitamins in the treatment of RCC
The results obtained indicate that a complex of high doses of B vitamins (as part of the milgamma preparation) can potentiate the analgesic effect of non-steroidal anti-inflammatory drugs and contribute to a more rapid regression of pain in vertebral radiculopathy, effectively affecting neuropathic component of pain. At the same time, the addition of a 14-day course of oral administration of milgamma compositum to the 10-day course of intramuscular injection of milgamma preparation can contribute to a more complete manifestation of the therapeutic potential of the drug, not only in the short-term, but also in the medium-term.Thus, the inclusion of a complex of high doses of B vitamins in the form of milgamma can increase the effectiveness of conservative therapy for radiculopathy.