Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4407_Библиотеки_им_академика_М_И_Перельмана
.pdf
366
https://t.me/med1917
Figure 65.1. Laryngeal foreign bodies. (1) Safety pin. (2) An all pin.
(3, 4) A twisted wire. (5) A fruit seed.
SECTION V — Diseases of Larynx and Trachea
and sometimes even the radiolucent foreign bodies in
the larynx and trachea (Figures 65.3 to 65.5). A coin or
a flat foreign body in trachea lies edge on in PA view
and flat on lateral view.
2. Plain X-ray chest in posteroanterior and lateral views
(Figure 65.6).
(a) It may show the radio-opaque foreign body—its
size, shape and location.
(b) Lobar or segmental atelectasis (complete obstruc-
tion by foreign body).
(c) Unilateral hyperinflation of lobe or segment or
entire lung (if ball valve obstruction). Mediastinal shift to opposite side is seen in hyperinflation.
Fluoroscopy or X-rays taken during inspiration and
expiration are helpful.
Figure 65.2. Types of bronchial obstruction by a foreign body. (A)
Partial obstruction. Air can pass in and out, causing only wheeze. (B)
One way obstruction. Air can go in (during inspiration) but not out,
causing emphysema of lungs. (C) Total obstruction. Air can neither go
in nor out, causing obstructive atelectasis. (D) One way obstruction
(reverse of B). Air can only go out, causing atelectasis. Dark pink shows
normal size of lung while lighter pink indicates effect of obstruction.
one side to the other causing change in the physical signs.
A retained foreign body in the lung may later give rise to
pneumonitis, bronchiectasis or lung abscess.
DIAGNOSIS
It can be made by detailed history of the foreign body
“ingestion”, physical examination of the neck and chest.
A history of sudden onset of coughing, wheezing and diminished entry of air into the lungs on auscultation forms
a classical triad. There should be a high index of suspicion
in children with wheezing, stridor, cough or asthma and
those with recurrent chest infections being treated with
steroids and antibiotics. Radiology is very helpful.
1. Soft tissue posteroanterior and lateral view of the neck
in its extended position. This can show radio-opaque
Figure 65.3. A radiolucent fruit seed (chiku) seen in subglottic region
of larynx (arrow). Patient has a tracheostomy (dashed arrows).
Figure 65.4. PA view chest showing a nail in the right bronchus.
Figure 65.5. PA view chest showing a broken piece of Fuller’s trache-
https://t.me/med1917
ostomy tube in the left bronchus.
Figure 65.6. X-ray chest showing a spring from a ball pen in the
right bronchus.
(d) Pneumomediastinum or pneumothorax.
(e) A normal X-ray chest. In early cases within 24 h or
a foreign body causing partial obstruction with full
ingress and egress of air does not produce any sign.
(f) Pneumonitis/bronchiectasis. Prolonged stay of for-
eign body may cause atelectasis, pneumonitis or
bronchiectasis.
3. X-ray chest at the end of inspiration and expiration.
Atelectasis and obstructive emphysema can be seen.
They are indirect evidence of radiolucent foreign bodies.
4. Fluoroscopy/videofluoroscopy. Evaluation during inspiration and expiration can be made.
5. CT chest.
MANAGEMENT
Laryngeal foreign body. A large bolus of food obstructed
above the cords may make the patient totally aphonic,
unable to cry for help. He may die of asphyxia unless immediate first aid measures are taken. The measures con-
Chapter 65 — Foreign Bodies of Air Passages
Figure 65.7. Heimlich manoeuvre. Sudden thrust directed upwards
and backwards, below the epigastrium, squeezes the air from the
lungs, sufficient to dislodge a foreign body.
367
sist of pounding on the back, turning the patient upside
down and following Heimlich manoeuvre. These measures should not be done if patient is only partially obstructed, for fear of causing total obstruction.
Heimlich manoeuvre. Stand behind the person and place
your arms around his lower chest and give four abdominal thrusts. The residual air in the lungs may dislodge the
foreign body providing some airway (Figure 65.7).
Cricothyrotomy or emergency tracheostomy should
be done if Heimlich manoeuvre fails. Once acute respiratory emergency is over, foreign body can be removed by
direct laryngoscopy or by laryngofissure, if impacted.
Tracheal and bronchial foreign bodies can be removed by bronchoscopy with full preparation and under
general anaesthesia. Emergency removal of these foreign
bodies is not indicated unless there is airway obstruction
or they are of the vegetable nature (e.g. seeds) and likely
to swell up.
Methods to remove tracheobronchial foreign body:
1. Conventional rigid bronchoscopy.
2. Rigid bronchoscopy with telescopic aid.
3. Bronchoscopy with C-arm fluoroscopy.
4. Use of Dormia basket or Fogarty’s balloon for rounded
objects.
5. Tracheostomy first and then bronchoscopy through
the tracheostome.
6. Thoracotomy and bronchotomy for peripheral foreign
bodies.
7. Flexible fibreoptic bronchoscopy in selected adult pa-
tients.
Equipment for foreign body removal include:
1. Bronchoscope, appropriate for the age of patient and a
size smaller and the other a size larger (see p. 523).
2. Telescope or optical forceps.
3. Two laryngoscopes.
4. Foreign body forceps, Dormia basket, Fogarty’s cath-
eter and a syringe to inflate it.
Page left intentionally blank
https://t.me/med1917
SECTION VI
https://t.me/med1917
Thyroid Gland and
Its Disorders
S e c t i o n o u t l i n e
66 Thyroid Gland and Its Disorders, 371
Page left intentionally blank
https://t.me/med1917
https://t.me/med1917
372
https://t.me/med1917
SECTION VI — Thyroid Gland and Its Disorders
Figure 66.1. Anatomy of thyroid gland. (Modified with permission from Becker and Stucchi, Essentials of Surgery, 1st ed, Elsevier, 2005).
Figure 66.2. Lymphatic drainage of thyroid gland.
II, III and IV nodes. Nodes are important when treating
thyroid malignancies (Figure 66.2).
PARATHYROID GLANDS
usually lies anterior to RLN. However inferior parathyroid
may be located anywhere from the hyoid bone above to
the superior mediastinum below. It descends along the
thymus gland.
During thyroid surgery, these glands should be identified and preserved in benign disease. Superior parathyroids are more constant in location than inferior. Superior
parathyroid is located above the inferior thyroid artery,
posterior to RLN and close to cricoid cartilage along the
posterior border of thyroid gland. Inferior parathyroid
is located below the level of inferior thyroid artery and
STRAP MUSCLES AND THEIR NERVE SUPPLY
Sternohyoid, sternothyroid and omohyoid muscles receive their motor nerve supply from the ansa hypoglossi,
which supplies them in their lower half. If strap muscles
need division for exposure of large goitres, they are transected in their upper part to preserve their innervation.
Figure 66.3. A 15-year-old female with a lingual thyroid (arrow) (A); CT scan sagittal view of the same (B).
https://t.me/med1917
RLN TRIANGLE (OF LORE)
It is bounded medially by trachea and oesophagus, laterally by retracted strap muscles, and superiorly by the
lower pole of thyroid. Its apex is directed interiorly at thoracic inlet. RLN runs through this triangle from lateral to
medial side on the right and straight up along tracheoesophageal groove on the left.
Chapter 66 — Thyroid Gland and Its Disorders
373
LINGUAL THYROID (FIGURE 66.3)
It is seen in 1:3000 to 1:4000 patients of thyroid disease.
It may be the only thyroid tissue or be present in addition to normal thyroid or an ectopic thyroid. When large
it causes airway obstruction or difficulty to swallow. It is
seen as a mass at the base of tongue on indirect laryngoscopy. It should be differentiated from other masses occurring at the base of tongue, i.e. lymphoma, squamous cell
carcinoma, minor salivary gland tumour, lingual tonsil or
rarely thyroglossal cyst. Surgical removal should be done,
if lingual thyroid causes symptoms of airway obstruction
or dysphagia by suprahyoid transpharyngeal approach.
It requires lifelong replacement of thyroid hormone, if it
was the only thyroid tissue.
PHYSIOLOGY OF THYROID
Thyroid gland contains two types of cells:
(i) follicular cells which synthesize and liberate T4 (thyroxine) and T3 (tri-iodothyronine) and (ii) parafollicular
’C’ cells which liberate calcitonin which has a calcium
lowering effect (Figure 66.4).
Synthesis and release of thyroid hormones take place
through five steps:
1. Active uptake of iodide.
2. Oxidation of iodide to iodine and binding of iodine to
tyrosine molecule to form diiodotyrosine or monoio-
dotyrosine. The enzyme responsible for oxidation and
binding is thyroid peroxidase.
3. Coupling of iodotyrosines to form T4 and T3. Two mol-
ecules of di-iodotyrosines (DIT) form T4 and coupling
one molecule of monoiodotyrosine (MIT) with one
molecule of di-iodotyrosine form T3. Again thyroid
Figure 66.4. Structure of thyroid.
peroxidase is responsible for coupling and iodination.
DIT, MIT, T4, T3 and thyroglobulin are bound together
and form the colloid which is stored in the follicles of
the thyroid gland.
4. At the time of secretion, colloid is taken up by thyroid
cells and the peptide bonds between thyroglobulin
and iodinated residues are broken by proteases to release T4, T3, DIT and MIT.
5. Uncoupled iodinated tyrosines (MIT and DIT) are deiodinated by enzyme iodotyrosine deiodinase and the iodine thus liberated is recycled. However, the enzyme
does not act on coupled iodinated tyrosine(s). Thus T4
and T3 are not affected.
In the congenital absence of this iodotyrosine deiodi-
nase enzyme, MIT and DIT are not deiodinated and appear in urine with loss of iodine causing iodine deficiency. T3 is the active thyroid hormone but thyroid gland
provides only 20% if it. Rest of the 80% of T3 is formed
in the peripheral tissues by deiodination of T4. T3 is three
times more potent than T4. Synthesis and release of thyroid hormone is under the control of hypothalamus-pituitary-thyroid axis (Figure 66.5 ).
Hypothalamus secretes thyrotropin releasing hormone
(TRH), which stimulates pituitary to release thyroid stimulating hormone (TSH). TSH acts on thyroid gland for
synthesis and releases T4 and T3. In the feedback mechanism, T4 and T3 hormones inhibit formation and release
of TRH and TSH.
374
https://t.me/med1917
Figure 66.5. Hypothalamus-pituitary-thyroid axis. TRH, thyrotropin releasing hormone; TSH, thyroid stimulating hormone (aka thyrotropin);
T4, thyroxine; T3, tri-iodothyronine.
SECTION VI — Thyroid Gland and Its Disorders
Scan to play Physiology of Thyroid Gland.
Important terms used in thyroid disease are discussed
in Box 66.1.
BENIGN DISORDERS OF THYROID
HASHIMOTO THYROIDITIS (Syn. Chronic
Lymphocytic Thyroiditis)
Hashimoto disease is an autoimmune disorder. Antibodies develop against thyroglobulin and thyroid peroxidase
and lead to hypothyroidism and raised TSH. The thyroid
parenchyma is diffusely infiltrated with lymphocytes and
fibrotic septae extend into the parenchyma. Thyroid size
may be normal, enlarged or small. Multiple or a single
regenerative nodules may form. Disease is more common
in females and diagnosis can be made by measuring the
level of antibodies against thyroglobulin and thyroid
peroxidase. Nodules in Hashimoto disease may develop
into a lymphoma or sometimes papillary cell carcinoma.
Treatment of Hashimoto disease is thyroxine therapy to
combat hypothyroidism.
BOX 66.1 Important Terms Used in Thyroid
Disease
1. Thyrotropin releasing hormone (TRH). It is secreted
by hypothalamus and acts on anterior pituitary to release
TSH.
2. Thyrotropin, also called thyroid stimulating hormone
(TSH), acts on TSH receptors of the follicular cells which
then synthesize and liberate thyroid hormones and thyroglobulin.
3. Thyroglobulin (Tg). A glycoprotein produced only by
follicular cells of thyroid. It is present as colloid in the lumen
of thyroid follicles. After total thyroidectomy or radioactive
iodine ablation Tg levels should be zero; presence of Tg
indicates recurrence of disease.
4. Calcitonin. It is secreted by parafollicular C-cells of the
thyroid. It reduces the number and activity of osteoclasts
and thus the bone resorption. High levels of this hormone
are seen in medullary carcinoma.
5. TSH-receptor antibodies. They are seen in Graves’
disease-an autoimmune disorder. Antibodies develop
against TSH receptors on follicular cells. When these antibodies bind to TSH receptors, the latter are stimulated and
produce T4 and T3 hormones and symptoms of hyperthyroidism.
6. Thyroglobulin antibodies. Antibodies develop against
thyroglobulin in autoimmune disorders of thyroid gland
causing hypothyroidism, e.g. Hashimoto disease. Antibodies to thyroglobulin alone are uncommon. They are usually
associated with thyroid peroxidase (TPO) antibodies.
7. Thyroid peroxidase. It is an enzyme which is responsi-
ble for (i) conversion of iodide to iodine, (ii) iodination of
tyrosine to monoiodotyrosine and (iii) coupling of di-iodotyrosines to form T4.
8. Antimicrosomal antibodies. Ever since the introduc-
tion of immunoassay techniques, the term antiperoxidase
antibodies is used interchangeably with antimicrosomal
antibodies.
9. Antiperoxidase (or TPO) antibodies. They are seen
in patients of autoimmune disorders of thyroid. They are
present in nearly 100% of the cases of Hashimoto disease
and 80% of patients of Graves’ disease.
10. Propylthiouracil and methimazole impair organi-
fication of iodine and thus cause fall in T4 and T3 levels.
They are used in hyperthyroidism. Propylthiouracil is preferred in pregnancy as it does not cross placental barrier to
affect the foetus.
11. Excess iodine inhibits release of thyroid hormones
from the thyroid glands with fall in T4 and T3 (Wolff–
Chaikoff effect) levels. Thus Lugol iodine or potassium
iodine has been used in preparation of hyperthyroid
patients before surgery.
Autoantibodies (TPO and Tg antibodies)
Thyroid inflammation with destruction of thyroid tis-
Multiple micronodules or a large nodule (can change
to lymphoma or papillary cancer)
Responds to exogenous thyroid
↓
sue and fibrosis
↓
Raised TSH level
↓
↓
HYPOTHYROIDISM
It is due to low levels of thyroid hormones. Iodine deficiency is the most common cause. Other causes include
Hashimoto disease, total or subtotal thyroidectomy, radiation to neck as for lymphoma or head and neck cancers
or radioactive iodine for Graves’ disease. Certain drugs
can induce hypothyroidism, e.g. amiodarone, lithium,
para-aminosalicylic acid or antithyroid drugs or goitrogenic substances in diet.
Symptoms and signs of hypothyroidism are listed in
Table 66.1.
Chapter 66 — Thyroid Gland and Its Disorders
https://t.me/med1917
375
TABLE 66.1 SYMPTOMS AND SIGNS OF
HYPOTHYROIDISM
Symptoms Signs
• Fatigueandweakness
• Intolerancetocold
• Dryskin
• Coarseandsparsehair
• Hoarseness
• Poormemoryandlackof
concentration
• Weightgain
• Excessivemenstrualbleeding
followed later by oligomenorrhoea
or amenorrhoea
• Constipation
• Hearingloss
• Dryandcoarseskin
• Puffyface
• Pufnessofhands
and feet
• Lossofhair
• Bradycardia
It can be treated by giving exogenous thyroid hor-
mone.
Hypothyroidism can also occur in neonates (1:5000)
and thus there is need to test them after birth. Cretinism manifests after several months of extrauterine life. It
causes lethargy, stunted growth, mental retardation and
hearing loss.
Neonatal hypothyroidism or cretinism can arise from
inadequate iodine in mother’s diet, administration of antithyroid drugs or radioactive iodine to mother to treat
her thyrotoxicosis or agenesis of thyroid in the infant. It
is therefore essential for all pregnant mothers to maintain
a euthyroid state.
GRAVES’ DISEASE
It is an autoimmune disorder presenting clinically with
feature of hyperthyroidism, goitre, ophthalmopathy and
uncommonly dermopathy. Women are affected much
more than men (5:1 to 10:1). Both genetic and environmental factors play their role in the causation of disease.
It is caused by antibodies against TSH receptors. When
antibodies react with their receptors, thyroid cells are
stimulated to form excess thyroid hormone. Diagnosis is
made on clinical features of hyperthyroidism (Table 66.2)
and laboratory tests. TSH is suppressed and T4 (free and
bound) is raised. Causes of hyperthyroidism are listed in
Table 66.3.
TABLE 66.2 SYMPTOMS AND SIGNS OF
HYPERTHYROIDISM
Symptoms Signs
• Nervousness
• Irritability
• Hyperactivity
• Heatintolerance
and sweating
• Weightlossin
spite of increased
appetite
• Diarrhoea
• Palpitations
• Fatigueand
weakness (due to
myopathy)
• Oligomenorrhoea
• Tremors
• Warmandmoistskin
• Tachycardia,atrial
fibrillations
• Highpulsepressure
• Proximalmyopathy
• Diffusealopecia
• Goitre(diffuseor
nodular)
• Lidretraction
• Exophthalmos
• Periorbitaloedema
• Thyroiddermopathy
(localized myxoedema)
in Graves’
disease
only
TABLE 66.3 CAUSES OF HYPERTHYROIDISM AND
THYROTOXICOSIS
• Graves’disease(autoimmunedisorder)
• Toxicmultinodulargoitre
• Autonomousnodule
• TSH-secretorypituitarytumour
• Functioningthyroidcancer/metastases
• Exogenousintakeofthyroidhormone(thyrotoxicosisfactitia)
• Thyroiditis
TABLE 66.4 MALIGNANT NEOPLASM OF THYROID
Per cent of all
Type
• Well-differentiated (from follicular
cells)
• Papillary carcinoma 65–70%
• Follicular carcinoma 10–15%
• Hurthle cell carcinoma
• Undifferentiated (from follicular cells).
Anaplastic carcinoma
• Medullary(fromparafollicularCcells) 5%
• Sporadic 80%
• Familial
- MEN-type II a
- MEN type II b
• Lymphoma 5%
• Otherneoplasms(metastasesto
thyroid)
thyroid malignancies
<5%
5%
20%
MALIGNANT DISORDERS OF THYROID
Thyroid cancer constitutes 2-3 new cases per 100,000 every year. It is two to four times more common in females
than males. Genetic factors also play a part in their development. Various malignant neoplasms of the thyroid are
listed in Table 66.4.
PAPILLARY THYROID CARCINOMA
It is the most common cancer constituting 65-70% of
all thyroid cancers. Majority of them are seen in third
and fourth decade with two to three times preponderance in females. It is also seen in children even with
cervical and distant metastases but has a favourable
prognosis. It arises from follicular cells of thyroid and
consists of fibrovascular stalk with cancerous follicular cells forming a papilla hence the name. Cells have
abundant pale cytoplasm with typical nuclei. The latter are folded or grooved with intranuclear cytoplasm.
Nucleoli are prominent and give typical Orphan Annie
eye appearance. These features help to diagnose the
tumour at fine needle aspiration cytology (FNAC). Papillary carcinoma may undergo cystic change and also
present laminated calcium bodies called psammoma
bodies.
Соседние файлы в папке Библиотека им академика М.И. Перельмана