25. 1 Acute pancreatitis

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Содержание Gastric ulcer H. pylori Clinical Features X-ray Study FibreoptIc Gastroscopy Surgical Treatment Highly selective vagotomy and ulcer excision Vagotomy and pyloroplasty Nicholas dudley

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GASTRIC ULCER

It may be simpler to differentiate between two types of gastric ulcers: (1) the common variety, where gastric acid secretion is normal or low and the ulcer is situated on the lesser curve near the incisura angularis, and (11) the less common variety, where it occurs in association with duodenal ulcer, is located close to the pylorus and the gastric acid secretion is similar to that of duodenal ulcer.

The following description mainly applies to the first, i.e. the common variety of gastric ulcer.

Gastric ulcer is far less common than duodenal ulcer. Males suffer much more commonly than females both for gastric and duodenal ulcers. Gastric ulcer is found in patients who are about 10 years older than those suffering from duodenal ulcer.

Aetiology

Acid secretion is normal or even low In gastric ulcer patients, and defective mucosal resistance is an Important factor in the pathogenesis. The mucosal resistance is determined by a number of factors.

1. Antral gastritis is generally present being most severe near the pylorus and gradually dimi­nishing. H. pylori is present on the luminal surface beneath the mucus layer, and gastric ulcer is probably the result of infection with this organism.

2. Vascular There is evidence that the arteries crossing the muscularis mucosa into the mucosa, in the lesser curve, and first part of the duodenum are end arteries. Contraction of the stomach wall could lead to local ischaemia in those areas of the stomach and duodenum which are most prone to ulceration.

3. Though mucus secretion is not disturbed, but there may be deficiency in the lipoprotein cell fraction which may allow digestion of mucus by bile or acid.

4. Prostaglandlns increase mucosal blood flow and

bicarbonate secretion, and abnormality of pro-

staglandin production may explain pathogenesis

of gastric ulcer.

When the gastric mucosal resistance is com­promised, it is more prone to attack from the following.

1. Drugs like aspirin and indomethacine.

2. Duodenogastric reflux due to a defect in antroduodenal motility. Bile and pancreatic juices may reflux into stomach and produce gastritis and ulceration.

3. Cigarette smoking There is a constant asso­ciation of cigarette smoking and gastric ulcer.

Pathology

Gastric ulcer is larger in size than a duodenal ulcer. It is round or ovoid in shape with sharply defined edges. Ninety five per cent of the gastric, ulcers are on the lesser curve. The ulcer invades the muscular coat and a posterior wall ulcer tends to invade the pancreas. The microscopic picture of a chronic gastric ulcer is similar to that of a chronic duodenal ulcer. A chronic gastric ulcer. may become malignant, but the incidence does not exceed 0.5 per cent.

Clinical Features

Pain is the most common presenting symptom which is felt in the epigastrium. It starts almost immediately after taking food. There is no pain on empty stomach. Antacids have little or no effect on pain. There is some periodicity of pain as long as the ulcer remains uncomplicated. An ulcer in the posterior wall of the stomach may burrow into the pancreas when the pain becomes a boring, cons­tant one felt in the back.

Vomiting is an important symptom. The vomitus is slimy and tends to be alkaline. Vomiting frequently follows a meal and may occasionally be self-induced as it relieves the pain.

There is loss of appetite initially, because the patient is afraid of eating but later, because of the associated chronic gastritis. Hence, by the time the patient presents, there is loss of weight and anaemia.

Haematemesis is more common than melaena. Sometimes haematemesis is the first symptom.

The abdominal examination may reveal tender­ness in the epigastrium on deep pressure. The usual point of maximum tenderness is 1 cm to 2.5 cm to the left of the midline just above the umbilicus.

Complications

Bleeding, perforation and obstruction are the principal complications of gastric ulcer.

Investigations

Gastric Analysis

Gastric ulcer is not associated with high level of gastric acid secretion. Gastric analysis has fallen in disfavour because it lacks precise correlation with , disease. However, it is indicated in a patient with gastric ulcer to determine whether the patient has achlorhydria which would strongly point to carcinoma.

X-ray Study

Barium meal shows an ulcer usually on the lesser curvature or in the pyloric area. A niche with smooth outline projecting from the lesser curvature is the typical finding. Niche and notch appearance is fairly characteristic. The suggestion of malignancy is based on: (i) the presence of meniscus sign, i.e. a prominent rim of translucency surrounding the ulcer, caused by heaped up edges of tumour; and (ii) cancer is more common in ulcers greater than 2 cm in diameter. Differentiation between the benign and malignant ulcers can be difficult and gastroscopy is more accurate.

FibreoptIc Gastroscopy Fibreoptic gastroscopy allows a direct look of the gastric ulcer, to take a picture of it, and to obtain with a biopsy forceps small fragments of the edges of the ulcer for histological examination. The rolled -up margins of the malignant ulcer (that produce the meniscus sign on X-ray), can be distinguished from the flat edges characteristic of a benign ulcer. Multiple (preferably 6) biopsies and brush biopsy should be routinely obtained from the edges of the lesion.

Treatment

It used to be taught that whereas duodenal ulcer was primarily a medical condition, gastric ulceration was primarily surgical. This was because medical treatment often failed to secure healing of the ulcer permanently. The pathologic process continued to extend, leading to haemorrhage and perforation. Another cause of mortality amongst patients treated medically was that the presence of an ulcer or cancer was sometimes missed.

That the gastric ulcer may be malignant must never be forgotten. All gastric ulcers should be assumed to be malignant until they have been proved to be benign, and such proof must rest on the evidence obtained by endoscopy and the taking of multiple biopsies.

Medical management of gastric ulcer is the same as duodenal ulcer. H₂ receptor antagonists, or omeprazole can bring the condition under control, and treatment of H. pylori infection (by colloidal bismuth subcitrate, amoxycillin and metronidazole) can almost eliminate the problem of recurrence. The success of therapy in this regard can be checked by serologic testing for H. pylori antibodies. Repeat endoscopy should be obtained to document the rate of healing.

Intractibillty to medical therapy is an indication for surgery.

Surgical Treatment

Billroth I partial gastrectomy This has been widely used in the treatment of gastric ulceration in the past and the results are good. There is, however, a certain mortality associated with the major procedure, and there may be long-term sequelae of dumping, vomiting and abdominal discomfort.

The stomach is mobilised by division of the main arterial supply. The distal part including the ulcer is resected. The cut edge of the remnant is partially closed, leaving a stoma at the lower end which matches the lumen of the duodenum. The duodenum is mobilised by Kocher's method and it allows gastroduodenal anastomosis without tension. The resected ulcer is subjected to histological examination to confirm that it is benign.

Highly selective vagotomy and ulcer excision This secures the biopsy evidence of the benign nature of the ulcer and has the advantage of disturbing the gastric physiology least. All late postgastrectomy problems are thus avoided. This method is, however, still under full evaluation.

Vagotomy and pyloroplasty This has been advocated for benign gastric ulcer. Biopsy of the ulper, with frozen section histology is essential to establish the benign nature of the ulcer. This is a controversial approach and cancer may still be missed.

Managemem of Complications of Peptic ulcer

These have been separately discussed under separate headings.


11.1 The thyroid gland


NICHOLAS DUDLEY


SURGICAL ANATOMY

General orientations

The thyroid gland is situated in the anterior triangle of the neck, weighs approximately 20 g and consists of two lateral lobes (right and left), joined together by a midline isthmus. The small pyramidal lobe of Lalouette, of variable size, commonly joins the isthmus at its junction with the left lateral lobe by a fibrous band or strand of muscle fibres known as the levator glandulae thyroideae. The lobes measure approximately 5 × 3 × 1.5 cm (slightly larger in women) and extend from the middle of the thyroid cartilage above to the sixth tracheal ring below. Each lobe fills the space between the trachea and oesophagus medially and the carotid sheath laterally. A strong condensation of vascular connective tissue, known as the suspensory ligament of Berry, binds the gland firmly to each side of the cricoid cartilage and it is this ligament, together with the pretracheal fascia which splits to invest the gland, which makes the thyroid move up and down on swallowing. The fascia (false or surgical capsule) sends fibrous septa into the gland substance, dividing it into numerous lobules. Each lobule consists of 30 to 40 follicles that contain colloid; these are the main secretory and storage elements.


Development of the thyroid

The thyroid gland develops from two distinct embryological structures: the primitive pharynx and the neural crest. A median pharyngeal downgrowth migrates between the first and the second arch components of the tongue and descends in a caudal direction along a line extending from the foramen caecum at the back of the tongue to the pyramidal lobe of the thyroid. In doing so, the track passes ventral to the hyoid bone and then loops behind it (Fig. 1) 739. The track usually becomes obliterated but part occasionally persists, giving rise to a thyroglossal cyst or fistula. Rarely the thyroid bud fails to descend but develops in situ at the back of the tongue (lingual thyroid). Conversely, it may descend too far, causing a primary mediastinal or retrosternal goitre. Even less commonly the thyroid bud may fail to divide in two and appear as one lateral lobe, the left usually being absent. The parafollicular or C cells scattered between the cuboidal epithelial cells that line the thyroid follicles, are derived from the neural crest. They first migrate to the ultimobranchial bodies of the fourth and fifth branchial pouches and then to the thyroid (Fig. 2) 740. These are the cells which in later life have the potential to undergo hyperplastic and malignant change, resulting in calcitonin-producing medullary carcinoma of the thyroid.


Blood supply (Fig. 3) 741

The vascular supply of the gland is impressive and becomes more so in hyperactive thyroid states. The main supply is via two paired arteries; a third vessel occasionally supplies the lower pole of one or other lobe. The superior thyroid artery, the first branch of the external carotid, runs downward on the inferior constrictor to reach the apex of the lateral lobe, where it divides into a large anterior branch and a usually smaller, but important, posterior branch. Occasionally a tributary leaves high on the left to supply the pyramidal lobe near the midline. The inferior thyroid artery is generally much larger than the superior thyroid artery but is less constant, being absent or duplicated on one side or the other in 10 per cent of individuals. It arises from the thyrocervical trunk and passes upwards for a variable distance before looping down, running medially behind the carotid sheath to reach the posterolateral aspect of the gland at the junction of the middle and lower thirds. Numerous unnamed accessory arteries arise from the oesophagus and trachea, but the most frequently encountered is the thyroidea ima (Neubauer's artery), which courses up anteriorly on the trachea to reach the isthmus or one of the lower poles and originates from the aorta or brachiocephalic artery. In the absence of the inferior thyroid artery on one side, the thyroidea ima may be the principal source of blood supply to the lobe and therefore substantial. The named thyroid veins, although three in number like the arteries, are subject to greater variation. The superior thyroid vein, formed by a confluence of vessels from the upper pole, crosses the common carotid artery high in the neck to drain into the internal jugular. The middle thyroid vein, which overlies the inferior thyroid artery, also ends in the internal jugular vein after crossing the common carotid artery. The inferior thyroid veins descend from the isthmus and inferior poles of the lateral lobes to join the internal jugular or brachiocephalic veins in the anterior mediastinum and are intimately associated with the thyrothymic ligaments, which expand inferiorly as the lobes of the thymus.


Lymphatic drainage

The thyroid is generously supplied with lymphatics and a rich network ramifies throughout the gland. They drain primarily into mediastinal nodes inferiorly, tracheo-oesophageal nodes laterally, and the midline delphian nodes superiorly. Studies performed following injection of dye suggest that the majority of lymph from the thyroid returns to the thoracic duct without passing through the deep cervical lymph node chain or the nodes of the posterior triangle, although these pathways may open up secondarily (Fig. 4) 742. This has implications for the assessment of patients with carcinoma of the thyroid, who may develop lymph node deposits outside the primary drainage areas, even on the contralateral side.


Important anatomical relationships

Recurrent laryngeal nerves (Fig. 5) 743

There are several structures closely related to the gland with which a surgeon must be familiar. The most important of these is the recurrent laryngeal nerve on each side, which is a branch of the vagus. The latter, having entered the mediastinum, gives off the recurrent nerve, which returns to the neck having circled around the arch of the aorta on the left and the right subclavian artery on the right. It ascends in the tracheo-oesophageal groove and has a variable relationship with the inferior thyroid artery on each side (Fig. 6) 744. Occasionally the nerve itself divides early and branches around the artery (10 per cent of individuals). In approximately 0.25 per cent of individuals the recurrent laryngeal nerve on the right is non-recurrent but passes directly from the vagus to the cricothyroid muscles. As it takes the same course as the inferior thyroid artery, it is particularly vulnerable if its presence is unrecognized when this vessel is routinely ligated laterally. Whichever course the nerve takes, it ultimately enters the larynx posterior to the cricothyroid articulation passing under or through Berry's ligament. The nerve supplies all the intrinsic muscles of the larynx together with some sensory supply to the mucosa below the vocal cords. The principal effect of division of this nerve is paralysis of the vocal cord on that side.


The superior laryngeal nerve

This also arises from the vagus (inferior ganglion) and divides at the level of the hyoid bone into a large internal laryngeal nerve and a smaller external laryngeal nerve. The latter runs close to the superior thyroid artery but at a deeper plane, immediately above the superior pole of the thyroid. It terminates as the nerve supply to the cricothyroid muscle which acts as a tensor of the vocal cords on the same side.


The cervical sympathetic chain

This underlies the carotid sheath just medial to the vagus on the prevertebral fascia and is in close proximity to the inferior thyroid artery as it arches around medially.


Parathyroid glands

There are normally four parathyroid glands, the upper pair of which lie in close proximity to the dorsal aspect of the thyroid. They are usually found just above and medial to where the recurrent laryngeal nerve crosses the inferior thyroid artery, frequently tucked round behind its branches (Fig. 7) 745. The lower parathyroid gland on each side is situated within a 2-cm radius of the lower pole of the thyroid typically on its surface anterolaterally and at a level below and medial to where the recurrent laryngeal nerve crosses the inferior thyroid artery (Fig. 8) 746.


PHYSIOLOGY

The thyroid, the largest endocrine gland in the body, produces three hormones, thyroxine (T&sub4;), tri-iodothyronine (T&sub3;) and calcitonin. T&sub4; and T&sub3; are both stored in the colloid, consisting primarily of thyroglobulin which is an iodinated glycoprotein. Thyroglobulin stores are dependent on adequate dietary iodine intake, which is essential for T&sub3; and T&sub4; synthesis. Iodine is derived mainly from milk and dairy products with a smaller proportion from salt water fish and iodized salt. An average diet in the United Kingdom gives an intake of 100 to 150 &mgr;g of iodide daily—this is higher in North America, where iodine is added to a wider range of foodstuffs. Plasma levels therefore vary widely, depending on geographical locality. Iodides are absorbed in the stomach and upper gastrointestinal tract; approximately two-thirds is excreted via the kidneys, and one-third is trapped in the thyroid, where 95 per cent of the body stores of iodine are found. Hormone synthesis takes place only after the iodide has been oxidized to an active form by a peroxidase enzyme system, which is in turn generated by one of the cytochrome reductase systems. The activated iodine is bound covalently to tyrosine or monoiodotyrosine. The peroxidase system is also responsible for the coupling of iodotyrosines to produce iodothyronines. Antithyroid drugs, notably carbimazole, are rapidly converted to methimazole, which specifically prevents iodine becoming trapped by inhibiting the peroxidase system within the thyroid.


The release of thyroid hormones from the colloid begins when microvilli on the surface of the thyroid cell engulf droplets of colloid by pinocytosis; these then fuse with lysosomes containing proteolytic enzymes, which hydrolyse the colloid. The iodotyrosines are rapidly converted to iodide and thyroxine, which enters the blood stream via the thyroid capillaries (Fig. 9) 747. A small quantity of unhydrolysed thyroglobulin returns to the circulation via the thyroid lymphatic system. The iodide released from the thyroid contributes to a much larger circulating iodide pool than the quite separate dietary iodide pool which delivers the element to the gland. Turnover is also slower.


Thyroid stimulating hormone (TSH) produced by the thyrotrophic cells of the anterior pituitary control the complex enzymatic reactions that trap iodine, convert it to T&sub3; and T&sub4; and release them into the circulation. When T&sub3; and T&sub4; levels rise above the normal range TSH production is shut down by a negative biofeedback loop (Fig. 10) 748. Release of TSH is regulated by thyrotrophin releasing hormone (TRH), which is produced in the hypothalamus. TRH enters the capillary bed of the stalk median eminence passing via the portal veins and sinusoids to bathe the anterior pituitary cells. TSH biosynthesis shows a circadian rhythm, its secretion being maximal in the evening before the onset of sleep, remaining high overnight and falling to a low around midday. The pineal gland may be responsible for this rhythm.


The role of calcitonin in normal thyroid physiology has not been established in man, but it may be involved in the regulation of plasma calcium and phosphate concentration. However thyroidectomy which removes nearly all the parafollicular C cells causes no disturbance of calcium homeostasis. Medullary thyroid carcinoma, a tumour of the C cells which frequently results in gross hypercalcitoninaemia also rarely disturbs calcium levels in the plasma. The rise in plasma calcitonin which occurs during pregnancy and lactation appears to have no effect on the maternal skeleton, but calcium resorption may be prevented by a concommitant increase in the level of circulating cholecalciferol.


PATHOPHYSIOLOGY

Nearly all disorders of the thyroid result in some swelling of the gland itself and the non-specific term ‘goitre’ embraces them all. In clinical practice a working classification based on whether the gland is toxic or not and the nature of the enlargement is helpful. This enables a diagnosis to be made and appropriate action taken in the majority of patients (Fig. 11) 749.


Non-toxic goitre

Diffuse/simple goitre

Physiological goitre

Enlargement of the thyroid is common during puberty and pregnancy, and at the menopause. This may be the result of increased physiological demand for thyroid hormone or as a response to growth hormone and variation in oestrogen levels. Increased levels of TSH are believed to be involved in the process but are not readily detectable in euthyroid patients.


Primary iodine deficiency/endemic goitre

The majority of ‘endemic’ goitres are due to low dietary intake of iodine (less than 100 &mgr;g a day). The worldwide geographical distribution of endemic goitre corresponds closely to alpine areas where glacial action has leached iodine from the soil and carried it away to the sea: endemic goitres are rarely seen in coastal areas. The response of high-risk populations to the addition of iodine to table salt or drinking water or to a depot injection of intramuscular lipiodol suggests that some patients with endemic goitres also have a metabolic defect in thyroxine synthesis which only declares itself when iodine is scarce.