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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6042_Библиотеки_им_академика_М_И_Перельмана.pdf
145
Case Report
A 20-year-old man with sickle-cell disease (SS) who was followed for severe
recurrent vaso-occlusive crisis with repeated hospital admissions presented with
ascending motor and sensitive neurological defi cits that were later associated with
bladder dysfunction. He was fi rst considered to develop Guillain-Barre syndrome.
However, persisting neurological signs despite adequate treatment lately led to
diagnose subacute combined medullar degeneration due to abnormal cobalamin
(vitamin B12) metabolism induced by repeated use of nitrous oxide during painful
episodes of sickle-cell disease. Inhaled nitric oxide is widely used in the treatment
of vaso- occlusive crisis. Clinicians should be aware of possible severe neurologic
side effects.
Reference
Chaugny C, Simon J, Collin-masson H, et al. Vitamin B12 defi ciency due to nitrous
oxide use: unrecognized cause of combined spinal cord degeneration. Rev Med
Interne. 2014;35(5):328–32.
2015
Pugliese et al.
Recreational Use of Nitrous Oxide
A case of subacute combined degeneration (SCD) of the spinal cord manifesting as
severe ataxia and urinary retention in a patient with a history of heavy nitrous oxide
abuse and self-supplementation with cyanocobalamin is reported.
Case Report
A 27-year-old woman was treated in the emergency department for complaints of
abdominal pain and inability to urinate for about 12 h. The patient also complained
of worsening lower-extremity weakness for 10 days and a “pins and needles” sensation in the lower extremities for approximately 1 year. She reported nitrous oxide
abuse over 3 years (an average of 100–200 “whippit” cartridges daily on 3 or 4
days per week), as well as long-term self-medication with oral and i.m. cyanocobalamin for the purpose of preventing nitrous oxide-induced neurologic symptoms.
Results of magnetic resonance imaging (MRI) were highly suggestive of SCD,
which is typically seen in primary vitamin B12 defi ciency but has been reported in
the context of chronic nitrous oxide exposure. Treatment was initiated with cyanocobalamin 1000 μg i.m. daily, to be continued for 5 days and followed by a fourweek regimen of 1000 μg i.m. weekly. The patient was discharged after 3 days,
despite continued symptoms, with instructions to obtain ongoing care but was lost
to follow-up.
Updates
146
Reference
Pugliese RS, Slagle EJ, Oettinger GR, Neuburger KJ, Ambrose TM. Subacute combined degeneration of the spinal cord in a patient abusing nitrous oxide and selfmedicating with cyanocobalamin. Am J Health Syst Pharm. 2015;72(11):952–7.
Reference
Ahn SC, Brown AW. Cobalamin defi ciency and subacute combined degeneration after nitrous
oxide anesthesia: a case report. Arch Phys Med Rehabil. 2005;86(1):150–3.
47 Subacute Combined Degeneration Provoked by Nitrous Oxide
147
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_48
4 8
Myelopathy due to Cervical Spine Flexion for Pediatric Tracheal Resection
48.1 Definition
This is a paraplegic condition resulting from cervical spine fl exion after tracheal
resection for tracheal stenosis.
48.2 Incidence
After Silver, who made a literature review of paraplegia due to cervical spine fl exion
found 4 case reports.
48.3 Etiology
The cause is not fully understood:
• in children there is undue hypermobility of the cervical spine, which may result
in cord damage without bony injury
• the presence of Schuerman’s disease may cause stretching the cord across
kyphotic spine
• in the elderly with spondylotic cervical spine acute fl exion may cause transient
dislocation, which results in tetraplegia. In the elderly, also vascular damage may
cause cord infarction with resultant ischemic myelopathy. However, this does not
apply to children.
Abstracted from Silver ( 2007 )
148
48.4 Pathology
According to Vaget et al:
According to the distinctive anatomical and physiologic features of children and
adolescents along with growth and development are responsible for the unique
manifestations and complications of SCI in the pediatric population.
SCI without radiologic abnormalities (SCIWORA) and the delayed onset of neurologic defi cits are relatively unique to that population. The unique anatomic and
biomechanical characteristics of the youthful spine are responsible for the higher
incidence of SCIWORA. These characteristics include:
• increased elasticity of the spine
• less fl exibility of the spinal cord
• shallow and horizontally oriented facet joints
• anterior wedging of the vertebral body
• vulnerability of the growth zone of the vertebral end plates
• poorly developed uncinate processes
Pathology of spinal cord:
• minor hemorrhage
• traumatic edema
• severe hemorrhage
• incomplete cord injury
• traction on the cord and extremities
48.5 Clinical Picture
Silver’s case was a child born with tracheal stenosis and had repeated resections
until he was 17-years-old when the stenosis recurred causing shortness of breath
and tracheal resection was done and his neck was fl exed and his chin was sutured to
his chest, to avoid tension on the tracheoplasty and was kept under light anesthesia
for 48 h. When anesthesia was discontinued, he woke up with weakness of the left
upper limb and complete paraplegia with sensory level at T8. MRI showed small
annular disc herniation at C6-C7. Gadolinium showed no enhancement. Upper
extremity weakness improved, but paraplegia persisted.
48.6 Management
Prevention of prolonged fl exion and resorting to some other procedures of
tracheoplasty.
48 Myelopathy due to Cervical Spine Flexion for Pediatric Tracheal Resection
149
In the early phase, steroid therapy may be useful.
In persistent defi cit full rehab program is needed
Reference
Silver JR. Paraplegia as a result of tracheal resection in a 17-year-old male. Spinal Cord.
2007;45(8):576–8.
Reference
151
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_49
4 9
Spinal Cord Stimulator Scar Tissue
49.1 Definition
This is an iatrogenic complication resulting and compression myelopathy due to a
foreign body reaction to spinal cord stimulation for chronic refractory pain.
49.2 Incidence
This is the fi rst case of this nature.
49.3 Etiology
For the last 30 years spinal cord stimulation (SCS) has been used for:
• Failed spinal surgery syndrome
• Radicular pain syndrome
• Epidural fi brosis
• Arachnoiditis
• Complex regional pain syndrome
• Refl ex sympathetic dystrophy
Abstracted from Guzzi et al. ( 2015 )
152
SCS is used after all conservative measures have been tried. The complications
SCS are:
• Pre- and post- OP complications viz.: puncture of the dura, CSF leak, injury of
the cord, hematoma, and in the spinal cord.
• Delayed complications: malfunction, fi brosis and the equipment and manipula-
tion of the spinal cord electrode. A foreign body giant – cell granuloma.
Foreign body reaction to this cord stimulator forming a mass as in the case presented, which has not been reported previously.
49.4 Pathology
A foreign body mass as a reaction to this stimulator occurs with giant cells and
macrophage as a chronic infl ammation response due to invasive procedure and
chronic infl ammatory response with poorly absorbed substance in the tissue.
49.5 Case Report
Fifty nine year old woman with history of back and all extremities pain and was
placed on SCS says the painless refractory to standard measures. The stimulator
was replaced due to fracture of the electrode wire. The system was fully exploited
do to its fracture it was replaced by a simulator to C3 – C5 and can (see details in
the article). There was a staph wound infection necessitating removal of the electrode. Recurrence of pain was worse than before. She also had loss of balance, she
had upper extremity weakness 4/5. She had numbness and tingling and the stocking
and glove distribution and exaggerated deep tendon refl exes. MRI: severe cervical
stenosis secondary to intraspinal mass compressing of the cord at the site of the
previous stimulator.
49.6 Management
Decompression laminectomy and removal of the mass, which gave her recovery.
Pathology of the mass showed fi brous tissue with giant cell reaction to foreign body.
Reference
Guzzi G, Volpentesta G, Chirchiglia D, Della torre A, Lavano F, Lavano A. Cervical spinal cord
compression from delayed epidural scar tissue formation around plate lead for SCS. Case
report and literature review. J Neurosurg Sci. 2015 (in Pubmed: 26430719).
49 Spinal Cord Stimulator Scar Tissue
153
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_50
5 0
Neonatal Paraplegia Through Umbilical Catheterization
50.1 Definition
This is a condition of spinal cord infarction through umbilical artery catheterization
(UAC) for therapeutic purposes.
50.2 Introduction
A brief abstract of the fetal circulation is presented from Gray’s Anatomy
The fetal blood is returned to the fetus from the placenta (with nutrition) through the
umbilical vein, which passes under the liver at the edge of the falciform liga-
ment, gives off 2 or 3 branches, the larger one goes into the left lobe of the liver
and the other two to the quadrate and caudate lobes.
At the porta hepatis it divides into two branches, the larger is joined by the portal vein
to enter the right lobe, the smaller continues upwards to join the inferior vena cava
(and is called the ductus venosus). The blood reaching the inferior vena cava (IVC)
through the hepatic veins and the ductus venosus is admixed with the blood return-
ing from the liver extremities and the abdominal wall. All IVC blood reaches the
right atrium and is directed by IVC valve into the foramen ovale to the left atrium
where it mixes with a small amount returning from the lungs. Then it is distributed
after passing through the left ventricle and the ascending aorta to head and neck
and upper extremities, a small portion goes to the lower extremities.
From the head and neck and upper limbs blood is returned via the superior vena
cava to the right atrium, it goes into the right ventricle and from there to the pul-
monary artery to the lungs, it returns to the left atrium, the greater part passes
through the ductus arterious into the aorta where it is mixed with a small portion
Abstracted from Brown and Phibbs ( 1988 )
154
coming from the left ventricle. Part of the aortic blood is distributed to the
abdominal and pelvic viscera and lower limbs; the greater part is conveyed
through the umbilical arteries to the placenta.
50.3 Incidence
In 1988, Brown and Phibbs reported two cases of spinal cord infarction through catheterization. The collected and reviewed the previous six cases. In our extensive literature search 2 additional cases were found: Munoz et al in 1993 and in 1996, Lemke
et al., reported a case of UAC after switch operation for great vessels transposition.
50.4 Etiology
Catheterization is used for infusion of blood and sometimes hypertrophic solutions.
The cause of the infarct is either the tip of the catheter reaching the arterial blood
supply of the spinal cord, principally the artery of Adamkiewicz leading to thrombosis. Also could be due to embolism (see entry under embolism). Catheters are
also used for blood samples, administration of fl uids or medications. Another causative factor is vasospasm. These newborns are very sick usually in shock, which
together with the use of hypertonic solutions are predisposed for thrombosis. There
is a possibility that blood transfusion may be causative. High insertion of the tip of
the catheter may impinge on the opening of the artery of Adamkiewicz.
Etiology of neonatal paraplegia after UAC, according to Aziz et al., the complications of UAC are thrombosis in 95 % of infants, embolism, vascular perforation,
vasospasm, damage from hypertonic solutions, hemorrhage, infection, and cardiac
arrhythmias. As a result of vascular complications an infarct develops in the spinal
cord especially in the lower thoracic region, the territory of the artery of Adamkiewicz.
50.5 Pathology
The autopsy of the case reported by Brown and Phibbs showed gliosis of the anterior part of the spinal cord demyelination with focal necrosis of the anterior segment
due to infarction. A picture of anterior spinal artery occlusion (Spiller’s syndrome)
spinal infarct has been demonstrated by MRI (Lemke et al.) which demonstrated
hemorrhagic infarct, possibly due to trauma by the catheter tip.
50.6 Clinical Picture
The cases recorded were infants less than 1 week of age and half of them were preterm. They were sick, needing emergency care including UAC e.g. hyperbilirubinemia secondary to ABO, hemolytic disease, respiratory failure due to hyaline
50 Neonatal Paraplegia Through Umbilical Catheterization
155
membrane disease, respiratory failure due to cardiac arrest shortly after birth, Rh
hemolytic disease, and congenital heart disease.
Emergency intensive care is required and UAC is life saving, especially for transfusions or exchange transfusions, medications injected and lab tests. Cord infarction
is manifested by motor and sensory and sometimes mottling of the lower extremities without vascular occlusion as in the case of Brown and Phibbs. MRI shows cord
swelling in the thoracic region and increased signal intensity indicating infarction.
Later atrophy of the cord is manifested on MRI.
50.7 Diagnosis
Diagnosis is based on:
• Neurological fi ndings: fl accid paralysis of the lower extremities, loss of sensa-
tion especially to pain, mottling of the skin.
• MRI: shows swollen edematous spinal cord usually in lower thoracic and lumbar
regions (the zone of artery of Adamkiewicz).
50.8 Management
Survivors are followed up in pediatric rehabilitation. The infant who lived and followed by Brown and Phibbs paraplegia was permanent but sensation was intact.
50.9 Preventative Management
Brown and Phibbs favor having the catheter tip either low i.e. at or below the third
lumbar vertebra or higher above the tenth thoracic vertebra confi rmed radiologically. Transfusions and hypertonic solutions should be limited to necessity.
Transfusions should be carefully administered, diluted with normal saline, slow and
careful infusion with port-fi lters. According to Aziz et al., it is better to direct the tip
of the catheter towards the aortic bifurcation far below the artery of Adamkiewicz.
Reference
Brown MS, Phibbs RH. Spinal cord injury in newborns from use of umbilical artery catheters:
report of two cases and a review of the literature. J Perinatol. 1988;8(2):105–10.
Reference