Sacramentos, fiestas e imágenes religiosas

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• Constipation: faecal retention can also reduce bladder volume and cause bladder neck dysfunction.

• Low levels of antidiuretic hormone: children who wet the bed may have a lower level of this hormone, which suppresses the rate of urine production.

• Polyuria: this often leads to enuresis in children, so diseases such as diabetes mellitus, diabetes insipidus and chronic renal failure must be considered.

• Delayed growth and development: some children’s nervous systems are not mature enough to be able to sense when the bladder is full.

• Diet: dairy products, citrus fruits, chocolate and foods containing high levels of artificial colours and sweeteners have been connected with bed-wetting.

• Psychological and social factors: emotional problems can be a cause of bed-wetting. Secondary enuresis is common following family break-up or bereavement, and it is important to note that child sexual abuse may also present in this way.

The most common organic disease to lead to enuresis is urinary tract infection, especially in girls: enuretic girls have a fourfold increased likelihood of having a urinary tract infection compared with those without enuresis.

Secondary enuresis (having previously been reliably continent) should be considered suspicious of a urinary tract infection, especially when associated with other symptoms such as urinary frequency, abdominal pain, dysuria and wetting in the daytime.

Secondary enuresis can also be caused by neurological problems such as neurogenic bladder (associated with spina bifida or other cord lesions, such as tumours).

Dribbling urinary incontinence may be the presenting sign of an ectopic ureter draining below the sphincter, or overflow from an obstructed bladder.

EPIPHORA Reginald Daniel

Epiphora is the overflow of tears onto the cheek, and may be due either to increased production of tears or inade-quate drainage of tears through the nasolacrimal drainage system (Box E.3).

Increased production of tears

Psychic lacrimation is normally associated with pain or emotional upset. Reflex stimulation of lacrimation causing epiphora is commonly associated with irritative conditions or corneal disease. Corneal injury, a blast of air

or a foreign body on the surface of the eye causes irritation of the trigeminal nerve that excites lacrimation. Even strong light, yawning, vomiting and laughing are associ-ated with reflex lacrimation.

Inadequate drainage of tears

This may be due to malposition of the lacrimal puncta, which should normally be closely applied to the eye in order to attract tears by capillary action. Such malposition may occur in ectropion associated with laxity of the lids, which may occur with age, or paralysis of the eyelid muscles that are responsible for blinking in facial palsy, or cicatricial lid disease, which pulls the punctum out of its correct position. Obstruction of the lacrimal drainage apparatus (canaliculus and nasolacrimal duct) will also cause epiphora, which is in fact the most common cause of this problem.

EPISTAXIS Michael Gleeson

It is important to realize that epistaxis (bleeding from the nose) is a sign, not a disease. Possible causes of the condi-tion are shown in Box E.4.

Epistaxis often arises from the anterior part of the nasal septum (Little’s area). It is usually of a minor nature, and self-limiting. Bleeding from other parts of the nose may be extremely serious and, on occasion, life-threatening.

The nose receives its blood supply from branches of both the internal and external carotid arteries. The upper part of the nose is supplied by the anterior and posterior ethmoid arteries, branches of the ophthalmic artery (derived from the internal carotid), which enter it through the medial wall of the orbit. The rest of the nose receives

Box E.3 Causes of epiphora Increased tear secretion Corneal foreign bodies Corneal irritation Corneal inflammation Nasal irritation

Inadequate drainage of tears Obstructions in lacrimal pathway Strictures in lacrimal pathway Tumours in lacrimal pathway Punctal or eyelid malpositions

Weakness of orbicularis muscle – ectropion Nasal obstruction with normal lacrimal pathway

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its blood supply through the sphenopalatine branch of the maxillary artery and septal branches of the facial artery.

Very often, epistaxis can be controlled by simple measures, for example, compression of the nostrils and application of cold packs. In childhood, when bleeding is almost always from Little’s area, these measures are usually effective. If this fails and the site of haemorrhage can be seen, bleeding can often be arrested by cauteriza-tion. Otherwise, the nose has to be packed with nasal tampons that expand when irrigated with water. When packing with tampons is ineffective, 1  cm ribbon gauze impregnated with an antiseptic such as bismuth-iodoform paraffin paste may be used instead. All nasal packs should be carefully secured lest they fall backwards into the airway.

Continued bleeding despite local measures may require surgical or radiological intervention. Nowadays, endonasal endoscopic ligation of the sphenopalatine artery is possible, and often effective. Other more radical approaches include intra-arterial embolization, or ligation of the external carotid artery in the neck, maxillary artery behind the maxillary antrum, and ethmoid arteries in the orbit.

Once the bleeding has been stopped and the patient’s condition is stable, attention must be devoted to identifica-tion of the cause. This is particularly indicated in patients with severe or recurrent minor bleeds. A number of

patients will be taking non-steroidal anti-inflammatory drugs, and these need to be stopped. Others may be antico-agulated, and this may need temporary adjustment. Blood film indices and coagulation studies should be carefully examined, to eliminate blood dyscrasias and coagulopa-thies. Hypertension alone rarely causes nose bleeds, but it is often an accompanying and exacerbating feature and should be controlled in the recovery phase.

It should be remembered that recurrent unilateral nose bleeds may be the first sign of a nasal tumour, and if seen in an adolescent boy should alert one to the possibil-ity of a juvenile angiofibroma (Figs E.3–E.5).

Box E.4 Causes of epistaxis Local causes

Trauma to Little’s area Dryness of nasal mucosa

Abnormal anatomy (e.g. septal deviations, spurs) Ulceration and excoriation

Nasal fracture Nasal infections

Tumours of the nose and sinuses (e.g. juvenile angiofibroma, squamous cell carcinoma)

Septal granulomas and perforations Foreign bodies

Systemic causes

Drugs, anticoagulants, non-steroidal anti-inflammatory drugs, cytotoxic drugs

Hypertension Atherosclerosis

Coagulopathies: haemophilia, Christmas disease, von Willebrand’s disease

Dyscrasias: purpura, leukaemia Hereditary haemorrhagic telangiectasis Vitamin deficiency – vitamin C, vitamin K Renal dialysis

Figure E.3 Magnetic resonance scan of a juvenile angioma (arrow).

The patient, an adolescent male, presented with progressive, left-sided, nasal obstruction and torrential epistaxes.

Figure E.4 At operation, the anterior end of the tumour is visible in the left nasal aperture.

Figure E.5 The operative specimen. The tumour has been completely removed, albeit in two pieces.

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A B C D E F G H I J K L M N O P Q R S T U V W X Y Z ERYTHEMA

Barry Monk

Erythema – redness of the skin – is, along with swelling, heat and pain, one of the four cardinal signs of inflamma-tion, and is the result of vasodilatation caused by release of inflammatory mediators. There are many causes, both local and general (Box E.5).

Box E.5 Causes of erythema Localized erythema

Internal

● Boil, herpes simplex, herpes zoster, impetigo, erysipelas, gout, thrombophlebitis, lymphangitis

External

● Irritant (thermal, caustic, traumatic)

● Allergic (allergic contact dermatitis)

● Fixed drug eruption

Localized patterns of erythema (Figs E.6–E.10) Rosacea

Palmar erythema Psoriasis Contact dermatitis Erythema ab igne Livedo reticularis

Erythema annulare centrifugum (Lyme disease) Erythema induratum (Bazin’s disease) Generalized erythema (Figs E.11–E.13) Toxic erythema

Exanthems

● Measles, rubella, scarlet fever, erythema infectiosum

● HIV infection Erythema multiforme Erythema nodosum Lupus erythematosus Dermatomyositis

Figure E.6 Psoriasis.

Figure E.7 Contact dermatitis.

Figure E.8 Rosacea.

Figure E.9 Erythema chronicum migrans in a case of Lyme disease.

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Local erythema

A localized area of tender erythema may be the initial manifestation of an infection, such as a boil, or of celluli-tis. The diagnosis usually becomes evident over the following hours, as the skin becomes rapidly hotter and more tender. Local infections in a limb may be associated with an ascending lymphangitis, manifested with a line streak of erythema moving towards the regional lymph nodes. Occasionally, malignant infiltration of the cutane-ous lymphatics may present with linear erythematcutane-ous streaks mimicking an infective lymphangitis, so-called lymphangitis carcinomatosa. In herpetic infections, the initial presentation may be with a local patch of erythema, the hallmark vesicles only becoming evident some hours later. Local erythema over a joint may suggest the diagno-sis of gout. Erythema associated with swelling of the skin and intense itching occurs in an acute eczema, whether irritant or allergic in cause. Fixed drug eruption is an unusual disorder in which exposure to a causative drug (e.g. phenolphthalein, codeine or sulphonamides) gives a violent local erythema that rapidly darkens to a magenta colour, and usually blisters. It recurs at the same skin sites at each drug exposure.

Selected localized patterns of erythema Rosacea

The characteristic feature of rosacea is a symmetrical erythema over the cheeks and nose, spreading onto the forehead and chin. The affected area is red and swollen, and surmounted by sterile pustules and papules. The papules and pustules resolve with oral oxytetracycline, but the erythema tends to persist.

Palmar erythema

As an isolated phenomenon, this is best known in pregnancy, but it is also seen in chronic liver disease,

thyrotoxicosis, rheumatoid arthritis and high-output cardiac states. It may also occur as a familial trait.

Erythema ab igne

This is a reticulate erythema that progresses to persistent haemosiderin pigmentation due to long-continued exposure to heat (infrared radiation). It used to be seen on the legs of elderly ladies with long-standing neglected hypothyroidism who sat close to open fires, but is now most commonly encountered on the abdomen in patients with chronic pancreatitis and other painful disorders who have used local heat as a form of analgesia.

Erythema chronicum migrans (Lyme disease)

The slowly spreading annular erythematous margin arising at the site of a tick bite is an important manifesta-tion of Lyme disease. This disorder is now known to be a zoonosis, caused by the spirochaete Borrelia burgdorferi.

The reservoir of infection is in deer, and the vector is the tick Ixodes ricinus. The condition is so named because of an outbreak of the disorder around the town of Lyme in the north-east of the USA. A rising specific IgA titre aids clinical diagnosis. Adequate treatment with penicillin or tetracycline is very important, as a proportion of untreated patients progress to serious central nervous system, cardiac or rheumatological problems, sometimes after the erythema has resolved.

Some very rare migratory erythemas can be cutane-ous markers of underlying neoplasia; examples include necrolytic migratory erythema (glucagon-secreting pancreatic tumour) and erythema gyratum repens (carci-noma or lymphoma).

Erythema induratum (Bazin’s disease)

This is a rare manifestation of tuberculosis that is seen in middle-aged women. The site affected is the posterior aspect of the legs, and the condition begins as a symme-trical eruption of deep-seated, painless red nodules. The surface becomes purple, and deep cold ulcers form, which have undermined borders. The patients show extreme sensitivity to tuberculin on skin testing.

Generalized erythema Erythema nodosum

In this distinctive disorder, there is an acute eruption of hot, tender, erythematous nodules, usually over the extensor aspects of the lower legs, but the thighs, buttocks and extensor surfaces of the arms may also be involved.

The nodules are hard and deep, with shiny red overlying skin, but they gradually soften and their colour changes to Figure E.10 Tinea manuum.

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A B C D E F G H I J K L M N O P Q R S T U V W X Y Z violet and finally yellow; however, they never suppurate or

ulcerate. An accompanying arthralgia is common, and there may be fever and malaise, whatever the underlying cause. Some cases are apparently idiopathic, but an assid-uous search must be made for an underlying cause. The relative frequency of different causes will vary in different parts of the world. In Britain, the most common cause (among women) is sarcoidosis, but in patients of South Asian origin, tuberculosis should be suspected. Penicillin, sulphonamides and barbiturates are the most commonly implicated drugs. Rarer causes include ulcerative colitis, Crohn’s disease, histoplasmosis, coccidioidomycosis, blastomycosis, chlamydial infections and Behçet’s syndr-ome. A leprosy conversion reaction may manifest itself as an erythema nodosum-like phenomenon.

Erythema multiforme

This disorder is characterized by a sudden eruption of erythematous lesions arising especially over the hands, feet, buttocks and genitalia, often accompanied by lesions on the oral or genital mucosa and the conjunctiva (Fig. E.11). The skin lesions are classically polycyclic, giving the appearance of an archery target (‘target lesions’). In severe cases, the centre of the lesion may blister or become necrotic. When the mucosal lesions are severe, the condition is termed ‘Stevens–Johnson syndrome’. In some cases, no specific cause is found, but it may be triggered by an infection (herpes simplex, orf or Mycoplasma), a drug or radiotherapy. Spontaneous resolution occurs, but recurrent episodes may arise.

many causes such as viral infections (especially glandular fever) and also drug hypersensitivity, especially to ampicillin, amoxycillin (Fig. E.12), sulphonamides and non-steroidal anti-inflammatory drugs. Often, no cause is found. Spontaneous resolution, which usually occurs within 10–15 days, is often followed by desquamation.

Figure E.11 Erythema multiforme.

Toxic erythema

This is a widespread, symmetrical, blotchy erythema that tends to affect the trunk more than the extremities, and is often accompanied by malaise, fever and lymphadenopa-thy. This cutaneous reaction pattern may be provoked by

Figure E.12 Drug reaction (amoxycillin).

Exanthems

In measles, the rash usually develops on the fourth day, behind the ears. It spreads to the face and downwards to the trunk and extremities on the fifth to seventh days.

The eruption is usually preceded by 1–7 days of prodro-mal coryza, nasal discharge and conjunctival injection, on the second or third day of which Koplik’s spots appear, as white specks surrounded by redness, on the buccal mucosa opposite the molar teeth. Koplik’s spots may be lentil-sized and few in number, or salt grain-sized and very numerous. The fever, which may have been high during the prodromal stage, persists while the rash appears and usually decreases as it fades. Cough, facial puffiness and photophobia are also diagnostic pointers.

Rubella usually affects an older child or young adult, and is typically accompanied by posterior cervical and postauricular lymph node enlargement. The rash, which also begins on the face and spreads downwards to trunk and extremities, is composed of faint pink macules, and fades in 3 days. Constitutional symptoms are mild, but joint pain may be prominent in adults.

Scarlet fever usually affects children under 10 years of age, who become acutely ill with high fever and vomiting.

The throat is red and oedematous, and there is character-istically a ‘strawberry tongue’. The rash is lobster-red with punctate deeper red lesions (likened to small spots of red ink on red blotting paper), and appears on the second and third days behind the ears, spreading rapidly to the face, upper chest and flexor surfaces of the limbs. Purpura may

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develop in the skin creases. The fever persists with the rash from 2 to 5 days, and is followed by desquamation in large flakes from the palms and soles.

Erythema infectiosum (fifth disease) affects children between 2 and 10 years of age. It begins with a ‘slapped-face’ erythema on the cheeks in an otherwise well child.

Over the next few days, a maculopapular eruption spreads, sometimes in a gyrate pattern over the limbs and trunk. The illness is due to a parvovirus, and heals in 1–2 weeks, although successive bouts may occur.

A macular erythematous rash accompanies the seroconversion illness of primary infection with HIV in some 50 per cent of patients. Between 10 and 14 days after exposure, fever, systemic toxicity and lymphadenopathy may occur. From 5 to 8 days later, oval macular erythema-tous lesions may appear on the trunk and limbs, extend-ing beyond the usual T-shirt distribution of pityriasis rosea onto the palms and soles. The oral mucosa can be affected with superficial erosions. The whole illness most closely resembles secondary syphilis or glandular fever with rash. Lymphopenia and thrombocytopenia may occur. HIV seroconversion occurs at 4–8 weeks.

Lupus erythematosus

This is an important cause of erythema. It is more common in women than men, and is usually classified into two varieties: systemic and discoid. The systemic form affects joints, kidneys and the haemopoietic, cardio-vascular, respiratory and central nervous systems, as well as the skin, and occurs in a younger age group than the discoid form, which is a dermatological disorder. In the skin, both types of lupus erythematosus cause perifollicu-lar inflammation that is followed by scarring. The classic lesion of lupus erythematosus is an atrophic, red, scaly plaque with follicular plugging. The histopathology is characteristic, showing epidermal thinning and basal cell liquefaction. Direct immunofluorescence microscopy demonstrates linear staining at the basement membrane in the lesions of both types.

Systemic lupus erythematosus (SLE) should be suspected in young women presenting with weakness, fever, weight loss, arthralgia and proteinuria, as well as a persistent erythematous rash on the face or areas exposed to sunlight. The so-called ‘butterfly rash’ over the face, although well known, occurs in only a minority of patients with cutaneous manifestations of SLE. Although typical lupus erythematosus plaques may be found – particularly over the dorsa of the hands and fingers – they are less common than other erythematous rashes seen

in SLE, such as urticaria, urticated plaques, livedo reticu-laris, photosensitivity and nailfold erythema. A diffuse telogen effluvium is not infrequent. Established cases often have tell-tale signs on the hands; as well as nailfold erythema and telangiectasia, there may be infarcts of the cuticles, finger nodules and pulp atrophy. Some 80–90 per cent of such patients will have circulating antinuclear antibodies in high titre, and raised DNA-binding proteins. Different varieties of antinuclear antibody exist and relate to differing clinical presentations, and this is the subject of current clinical research. The antinuclear antibodies can often be demonstrated throughout the skin (e.g. by taking a biopsy of non-light-exposed normal skin). This test is negative in the discoid variety. A systemic pattern, but without renal mortality, can be induced by certain drugs, such as hydralazine, procaina-mide, griseofulvin and phenytoin.

Chronic discoid lupus erythematosus lesions largely occur on sun-exposed sites such as the cheeks, forehead, nose and perioral skin, although the scalp is not infre-quently affected. Lesions persist for many months, extending slowly, and leaving depigmented, central atrophic and hairless scars. Close examination of the erythematous active edge shows telangiectasia and follic-ular plugging (which can be demonstrated by detaching an adherent scale and observing downward-projecting

‘tin-tack’ plugs). Although the direct immunofluores-cence test of such lesions will be positive, in 80 per cent of patients no circulating antinuclear antibodies are found.

Less than 5 per cent of patients progress to the systemic form.

Dermatomyositis

The principal cutaneous signs of dermatomyositis are erythema and oedema (Fig. E.13). The proximal myopathy is described in detail elsewhere. There is often marked discordance between the severity of skin and muscle disease in any individual patient. The dermato-logical hallmark is a particular periorbital bluish-red

The principal cutaneous signs of dermatomyositis are erythema and oedema (Fig. E.13). The proximal myopathy is described in detail elsewhere. There is often marked discordance between the severity of skin and muscle disease in any individual patient. The dermato-logical hallmark is a particular periorbital bluish-red

In document LA MISIÓN CAPUCHINA EN EL CAQUETÁ Y EL PUTUMAYO 1893-1929 (página 55-58)