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• de Quervain’s thyroiditis. Self-limiting and probably caused by viral infection. The gland enlarges diffusely and flu-like symptoms are prominent. Mild hyperthyroidism occurs initially, followed by slight hypothyroidism. Isotope scanning reveals low uptake. Treatment is symptomatic.

• Postpartum thyroiditis. Affects 5% of women. An autoimmune condition causing thyroid dyfunction within a year of delivery, there is a modest, firm goitre and hyperthyroidism or hypothyroidism may occur. Antithyroid drugs, radioiodine and surgery are contraindicated and the condition resolves spontaneously.

• Silent thyroiditis. A painless, diffuse goitre with mild hyperthyroidism, but none of the features of Graves’ disease. It occurs at any age and affects males more frequently than other varieties. Usually self-limiting, but may recur.

3.Chronic thyroiditis.

• Riedel’s thyroiditis. Dense fibrosis of the gland occurs which is of normal or reduced size. The thyroid remains non-tender but becomes very hard (‘woody’). Patients are usually middle-aged and euthyroid. Malignancy must be excluded.

• Hashimoto’s thyroiditis is characterized by a large, rubbery goitre with hyperthyroidism progressing to hypothyroidism as the immune process destroys the gland. Antithyroid drugs or thyroxine maybe necessary, but steroids are unhelpful. Surgery may be required if the gland is unresponsive to thyroxine and if malignancy is suspected. • Atrophic thyroiditis. The end result of autoimmune thyroiditis, leaving a fibrotic,

shrunken gland, usually with hypothyroisism. Thyroxine is the only treatment required.

Thyroid adenoma See Thyroid neoplasms (p. 324).

Malignant thyroid neoplasms See Thyroid neoplasms (p. 324).

Investigation of goitre

Morphological and functional aspects are important. Ultrasound scanning demonstrates single or multiple solid or ‘cystic’ lesions. Standard CXR views will indicate retrosternal extension and tracheal deviation. CT scanning shows tumour transgression of the thyroid capsule or retrosternal extension. Scintiscanning using123_{iodine or technetium}99m _{is rarely}

justified. FNAC is very accurate (in experienced hands) in the diagnosis of goitres and is easily performed in the clinic. The technique will not distinguish between follicular adenoma and follicular carcinoma.

Thyroid function is assessed by TSH, T3 and T4. Total T4 may be misleading because

hyperthyroidism may be caused by raised T3; TBG may be increased during pregnancy or

oestrogen therapy—e.g. oral contraceptives (low T4); TBG may fall during liver disease

or nephrotic syndrome (high T4). Thyroid autoantibody titres should be measured if

thyroiditis is suspected.

Treatment for goitre

Endemic goitre can be treated with thyroxine, but older patients with established goitre rarely benefit from thyroxine. Thyroxine is commonly given to suppress multinodular goitre and may be effective in the early stages, but frequently does not reduce the size of an established, nodular goitre(c)_{. It is usually effective in suppressing dyshormogenetic}

goitres.

Propylthiouracil and carbimazole are used to treat hyperthyroidism. These drugs are usually given for 14–24 months and more than 50% of patients relapse after cessation of treatment. Agranulocytosis may occur on treatment and regular FBC is necessary. Beta- blockers are used to control tachycardia, sweating and tremor.

Radioiodine as133_{I can be offered to patients beyond reproductive age. The choice}

between radioiodine and surgery should rest with the patient when the pros and cons of each treatment have been explained.

Surgery is appropriate in the following circumstances: • Discomfort;

• Unacceptable appearance of goiter;

• Dyspnoea, dysphagia or retrosternal extension; • Failure of thyroxine to suppress goiter;

• Possible malignancy- solitary cold nodule (p. 326); • Thyrotoxicosis (p. 173).

Further reading

Young AE. The thyroid gland. In: Burnand KG, Young AE (eds) The New Aird’s Companion in

Surgical Studies (2nd Edn). London: Churchill Livingstone, 1998; 459–483.

Related topics of interest

Hyperparathyroidism (p. 170); Hyperthyroidism—treatment (p. 173); Thyroglossal tract anomalies (p. 322); Thyroid neoplasms (p. 324).

HAEMORRHOIDS

Deya Marzouk Aetiology and pathogenesis

The anal canal submucosa forms a series of ‘cushions’. The three main cushions are found in the left lateral, right posterior and right anterior positions (3, 7 and 11 o’clock). They consist of venous dilatations surrounded by a network of smooth muscle, elastic and fibrous tissue, as well as the overlying mucosa. The submucosal smooth muscles are anchored to the internal sphincter and the longitudinal muscle passing through the internal sphincter fasciculi. This network of muscle supports the anal canal lining during defecation. It returns the anal canal lining to its initial position after the temporary downward displacement in defecation.

Haemorrhoids are prolapsed anal cushions. They are caused primarily by deterioration and disruption of the fibromuscular supporting framework of the cushions from the 3rd decade onwards, allowing them to slide downwards and allowing the submucosal vessels to engorge as they prolapse. This is especially liable to occur as a result of constipation and straining. In some patients this is aggravated by a tight internal anal sphincter. Heredity may play a role either environmentally (same family having similar dietary or bowel habits) or through inheritance of weakened fibrocollagenous supporting tissue.

Increased intra-abdominal pressure as a result of pregnancy or pelvic tumours may increase venous engorgement leading to development of secondary haemorrhoids.

Clinical features and diagnosis

Haemorrhoids are commoner in males. They are rare below 20. Common symptoms include:

• Bleeding per rectum, during or after defecation, which is bright red in colour and separate from stools (on surface, not mixed within). It is often slight and noted on the toilet paper. Sometimes it is more pronounced and drips into the pan, but is rarely massive.

• Prolapsed haemorrhoids

• Slight mucus discharge which may lead to pruritis ani may occur in patients with prolapsed haemorrhoids.

• Mild anal discomfort. Acute or severe pain is not a symptom of haemorrhoids unless there is complication such as thrombosis or the patient is suffering from another condition (e.g. anal fissure or abscess).

• Mild obstructive defecatory symptoms occur in patients with bulky prolapsed haemorrhoids.

Digital rectal examination and proctoscopy confirms the diagnosis. Haemorrhoids are classified according to their location in the anal canal into:

• Internal: above the dentate line (their vessels arise from the superior haemorrhoidal plexus), they are covered with pink rectal mucosa.

• External: below the dentate line (their vessels arise from the inferior haemorrhoidal plexus), they are covered with violet anal mucosa or skin.

• Internal-external: mixture of the above two types, usually with a groove between them.

Haemorrhoids are further classified by the degree of prolapse and for purposes of treatment into:

First degree: Project into the lumen during straining, but don’t prolapse

Second degree: Prolapse during defecation, then is reduced spontaneously into the anal canal Third degree: Prolapse during defecation, require manual reduction

Fourth degree: Prolapsed irreducible haemorrhoids

All patients should have at least rigid sigmoidoscopy to exclude colorectal cancer (flexible sigmoidoscopy is desirable in most patients above 40 years). Barium enemas and/or colonoscopy are needed if bleeding is mixed with stools or there is change in bowel habits.

Bleeding haemorrhoids needs differentiation from colorectal cancer and proctocolitis. Prolapsing haemorrhoids needs differentiation from mucosal rectal prolapse, anal warts, anal carcinomas, prolapsed rectal polyps or skin tags associated with anal fissures. Finally, they should be distinguished from rectal varices in patients with portal hypertension.

Treatment