The clinical term whitlow is applied to an acute infection, usually followed by suppuration, commonly met with in the fingers, less frequently in the toes. The point of infection is often trivial—a pin-prick, a puncture caused by a splinter of wood, a scratch, or even an imperceptible lesion of the skin.
Several varieties of whitlow are recognised, but while it is convenient to describe them separately, it is to be clearly understood that clinically they merge one into another, and it is not always possible to determine in which connective-tissue plane a given infection has originated.
Initial Stage.—Attention is usually first attracted to the condition by a sensation of tightness in the finger and tenderness when the part is squeezed or knocked against anything. In the course of a few hours the part becomes red and swollen; there is continuous pain, which soon assumes a throbbing character, particularly when the hand is dependent, and may be so severe as to prevent sleep, and the patient may feel generally out of sorts.
If a constricting band is applied at this stage, the infection can usually be checked and the occurrence of suppuration prevented. If this fails, or if the condition is allowed to go untreated, the inflammatory reaction increases and terminates in suppuration, giving rise to one or other of the forms of whitlow to be described.
The Purulent Blister.—In the most superficial variety, pus forms between the rete Malpighii and the stratum corneum of the skin, the latter being raised as a blister in which fluctuation can be detected (Fig. 9,a). This is commonly met with in the palm of the hand of labouring men who have recently resumed work after a spell of idleness. When the blister forms near the tip of the finger, the pus burrows under the nail—which corresponds to the stratum corneum—raising it from its bed.
There is some local heat and discoloration, and considerable pain and tenderness, but little or no constitutional disturbance. Superficial lymphangitis may extend a short distance up the forearm. By clipping away the raised epidermis, and if necessary the nail, the pus is allowed to escape, and healing speedily takes place.
Whitlow at the Nail Fold.—This variety, which is met with among those who handle septic material, occurs in the sulcus between the nail and the skin, and is due to the introduction of infective matter at the root of the nail (Fig. 9,b). A small focus of suppuration forms under the nail, with swelling and redness of the nail fold, causing intense pain and discomfort, interfering with sleep, and producing a constitutional reaction out of all proportion to the local lesion.
To allow the pus to escape, it is necessary, under local anæsthesia, to cut away the nail fold as well as the portion of nail in the infected area, or, it may be, to remove the nail entirely. If only a small opening is made in the nail it is apt to be blocked by granulations.
Fig. 9.—Diagram of various forms of Whitlow. a = Purulent blister. b = Suppuration at nail fold. c = Subcutaneous whitlow. d = Whitlow in sheath of flexor tendon (e).Fig. 9.—Diagram of various forms of Whitlow.a= Purulent blister.b= Suppuration at nail fold.c= Subcutaneous whitlow.d= Whitlow in sheath of flexor tendon (e).
Fig. 9.—Diagram of various forms of Whitlow.
Subcutaneous Whitlow.—In this variety the infection manifests itself as a cellulitis of the pulp of the finger (Fig. 9,c), which sometimes spreads towards the palm of the hand. The finger becomes red, swollen, and tense; there is severe throbbing pain, which is usually worst at night and prevents sleep, and the part is extremely tender on pressure. When the palm is invaded there may be marked œdema of the back of the hand, the dense integument of the palm preventing the swelling from appearing on the front. The pus may be under such tension that fluctuation cannot be detected. The patient is usually able to flex the finger to a certain extent without increasing the pain—a point which indicates that the tendon sheaths have not been invaded.The suppurative process may, however, spread to the tendon sheaths, or even to the bone. Sometimes the excessive tension and virulent toxins induce actual gangrene of the distal part, or even of the whole finger. There is considerable constitutional disturbance, the temperature often reaching 101° or 102° F.
The treatment consists in applying a constriction band and making an incision over the centre of the most tender area, care being taken to avoid opening the tendon sheath lest the infection be conveyed to it. Moist dressings should be employed while the suppuration lasts. Carbolic fomentations, however, are to be avoided on account of the risk of inducing gangrene.
Whitlow of the Tendon Sheaths.—In this form the main incidence of the infection is on the sheaths of the flexor tendons, but it is not always possible to determine whether it started there or spread thither from the subcutaneous cellular tissue (Fig. 9,d). In some cases both connective tissue planes are involved. The affected finger becomes red, painful, and swollen, the swelling spreading to the dorsum. The involvement of the tendon sheath is usually indicated by the patient being unable to flex the finger, and by the pain being increased when he attempts to do so. On account of the anatomical arrangement of the tendon sheaths, the process may spread into the forearm—directly in the case of the thumb and little finger, and after invading the palm in the case of the other fingers—and there give rise to a diffuse cellulitis which may result in sloughing of fasciæ and tendons. When the infection spreads into the common flexor sheath under the transverse carpal (anterior annular) ligament, it is not uncommon for the intercarpal and wrist joints to become implicated. Impaired movement of tendons and joints is, therefore, a common sequel to this variety of whitlow.
Thetreatmentconsists in inducing passive hyperæmia by Bier's method, and, if this is done early, suppuration may be avoided. If pus forms, small incisions are made, under local anæsthesia, to relieve the tension in the sheath and to diminish the risk of the tendons sloughing. No form of drain should be inserted. In the fingers the incisions should be made in the middle line, and in the palm they should be made over the metacarpal bones to avoid the digital vessels and nerves. If pus has spread under the transverse carpal ligament, the incision must be made above the wrist. Passive movements and massage must be commenced as early as possible and be perseveringly employed to diminish the formation of adhesions and resulting stiffness.
Subperiosteal Whitlow.—This form is usually an extension of the subcutaneous or of the thecal variety, but in some cases the inflammation begins in the periosteum—usually of the terminal phalanx. It may lead to necrosis of a portion or even of the entire phalanx. This is usually recognised by the persistence of suppuration long after the acute symptoms have passed off, and by feeling bare bone with the probe. In such cases one or more of the joints are usually implicated also, and lateral mobility and grating may be elicited. Recovery does not take place until the dead bone is removed, and the usefulness of the finger is often seriously impaired by fibrous or bony ankylosis of the interphalangeal joints. This may render amputation advisable when a stiff finger is likely to interfere with the patient's occupation.
Cellulitis of the forearmis usually a sequel to one of the deeper varieties of whitlow.
In theregion of the elbow-joint, cellulitis is common around the olecranon. It may originate as an inflammation of the olecranon bursa, or may invade the bursa secondarily. In exceptional cases the elbow-joint is also involved.
Cellulitis of theaxillamay originate in suppuration in the lymph glands, following an infected wound of the hand, or it may spread from a septic wound on the chest wall or in the neck. In some cases it is impossible to discover the primary seat of infection. A firm, brawny swelling forms in the armpit and extends on to the chest wall. It is attended with great pain, which is increased on moving the arm, and there is marked constitutional disturbance. When suppuration occurs, its spread is limited by the attachments of the axillary fascia, and the pus tends to burrow on to the chest wall beneath the pectoral muscles, and upwards towards the shoulder-joint, which may become infected. When the pus forms in the axillary space, the treatment consists in making free incisions, which should be placed on the thoracic side of the axilla to avoid the axillary vessels and nerves. If the pus spreads on to the chest wall, the abscess should be opened below the clavicle by Hilton's method, and a counter opening may be made in the axilla.
Cellulitis of thesole of the footmay follow whitlow of the toes.
In theregion of the anklecellulitis is not common; butaround the kneeit frequently occurs in relation to the prepatellar bursa and to the popliteal lymph glands, and may endanger theknee-joint. It is also met with in thegroinfollowing on inflammation and suppuration of the inguinal glands, and cases are recorded in which the sloughing process has implicated the femoral vessels and led to secondary hæmorrhage.
Cellulitis of the scalp, orbit, neck, pelvis, and perineum will be considered with the diseases of these regions.
While it is true that a chronic pyogenic abscess is sometimes met with—for example, in the breast and in the marrow of long bones—in the great majority of instances the formation of a chronic or cold abscess is the result of the action of the tubercle bacillus. It is therefore more convenient to study this form of suppuration with tuberculosis (p. 139).
Sinus.—A sinus is a track leading from a focus of suppuration to a cutaneous or mucous surface. It usually represents the path by which the discharge escapes from an abscess cavity that has been prevented from closing completely, either from mechanical causes or from the persistent formation of discharge which must find an exit. A sinus is lined by granulation tissue, and when it is of long standing the opening may be dragged below the level of the surrounding skin by contraction of the scar tissue around it. As a sinus will persist until the obstacle to closure of the original abscess is removed, it is necessary that this should be sought for. It may be a foreign body, such as a piece of dead bone, an infected ligature, or a bullet, acting mechanically or by keeping up discharge, and if the body is removed the sinus usually heals. The presence of a foreign body is often suggested by a mass of redundant granulations at the mouth of the sinus. If a sinus passes through a muscle, the repeated contractions tend to prevent healing until the muscle is kept at rest by a splint, or put out of action by division of its fibres. The sinuses associated with empyema are prevented from healing by the rigidity of the chest wall, and will only close after an operation which admits of the cavity being obliterated. In any case it is necessary to disinfect the track, and, it may be, to remove the unhealthy granulations lining it, by means of the sharp spoon, or to excise it bodily. To encourage healing from the bottom the cavity should be packed with bismuth or iodoform gauze. The healing of longand tortuous sinuses is often hastened by the injection of Beck's bismuth paste (p. 145). If disfigurement is likely to follow from cicatricial contraction—for example, in a sinus over the lower jaw associated with a carious tooth—the sinus should be excised and the raw surfaces approximated with stitches.
Thetuberculous sinusis described under Tuberculosis.
Afistulais an abnormal canal passing from a mucous surface to the skin or to another mucous surface. Fistulæ resulting from suppuration usually occur near the natural openings of mucous canals—for example, on the cheek, as a salivary fistula; beside the inner angle of the eye, as a lacrymal fistula; near the ear, as a mastoid fistula; or close to the anus, as a fistula-in-ano. Intestinal fistulæ are sometimes met with in the abdominal wall after strangulated hernia, operations for appendicitis, tuberculous peritonitis, and other conditions. In the perineum, fistulæ frequently complicate stricture of the urethra.
Fistulæ also occur between the bladder and vagina (vesico-vaginal fistula), or between the bladder and the rectum (recto-vesical fistula).
Thetreatmentof these various forms of fistula will be described in the sections dealing with the regions in which they occur.
Congenital fistulæ, such as occur in the neck from imperfect closure of branchial clefts, or in the abdomen from unobliterated fœtal ducts such as the urachus or Meckel's diverticulum, will be described in their proper places.
We have here to consider under the terms Sapræmia, Septicæmia, and Pyæmia certain general effects of pyogenic infection, which, although their clinical manifestations may vary, are all associated with the action of the same forms of bacteria. They may occur separately or in combination, or one may follow on and merge into another.
Sapræmia, or septic intoxication, is the name applied to a form of poisoning resulting from the absorption into the blood of the toxic products of pyogenic bacteria. These products, which are of the nature of alkaloids, act immediately on their entrance into the circulation, and produce effects in direct proportion to the amount absorbed. As the toxins are gradually eliminated from the body the symptoms abate, and if no more are introduced they disappear. Sapræmia in these respects, therefore,is comparable to poisoning by any other form of alkaloid, such as strychnin or morphin.
Clinical Features.—The symptoms of sapræmia seldom manifest themselves within twenty-four hours of an operation or injury, because it takes some time for the bacteria to produce a sufficient dose of their poisons. The onset of the condition is marked by a feeling of chilliness, sometimes amounting to a rigor, and a rise of temperature to 102°, 103°, or 104° F., with morning remissions (Fig. 10). The heart's action is markedly depressed, and the pulse is soft and compressible. The appetite is lost, the tongue dry and covered with a thin brownish-red fur, so that it has the appearance of “dried beef.” The urine is scanty and loaded with urates. In severe cases diarrhœa and vomiting of dark coffee-ground material are often prominent features. Death is usually impending when the skin becomes cold and clammy, the mucous membranes livid, the pulse feeble and fluttering, the discharges involuntary, and when a low form of muttering delirium is present.
Fig. 10.—Charts of Acute sapræmia from (a) case of crushed foot, and (b) case of incomplete abortion.Fig. 10.—Charts of Acute sapræmia from (a) case of crushed foot, and (b) case of incomplete abortion.
Fig. 10.—Charts of Acute sapræmia from (a) case of crushed foot, and (b) case of incomplete abortion.
A local form of septic infection is always present—it may be an abscess, an infected compound fracture, or an infection of the cavity of the uterus, for example, from a retained portion of placenta.
Treatment.—The first indication is the immediate and complete removal of the infected material. The wound must be freely opened, all blood-clot, discharge, or necrosed tissue removed, and the area disinfected by washing with sterilised salt solution, peroxide of hydrogen, or eusol. Stronger lotions are to be avoided as being likely to depress the tissues, and so interfere with protective phagocytosis. On account of its power of neutralising toxins, iodoform is useful in these cases, and is best employed by packing the wound with iodoform gauze, and treating it by the open method, if this is possible.
The general treatment is carried out on the same lines as for other infective conditions.
Chronic sapræmia or Hectic Fever.—Hectic fever differs from acute sapræmia merely in degree. It usually occurs in connection with tuberculous conditions, such as bone or joint disease, psoas abscess, or empyema, which have opened externally, and have thereby become infected with pyogenic organisms. It is gradual in its development, and is of a mild type throughout.
Fig. 11.—Chart of Hectic Fever.Fig. 11.—Chart of Hectic Fever.
Fig. 11.—Chart of Hectic Fever.
The pulse is small, feeble, and compressible, and the temperature rises in the afternoon or evening to 102° or 103° F. (Fig. 11), the cheeks becoming characteristically flushed. In the early morning the temperature falls to normal or below it, and the patient breaks into a profuse perspiration, which leaves him pale, weak, and exhausted. He becomes rapidly and markedly emaciated, even although in some cases the appetite remains good and is even voracious.
The poisons circulating in the blood producewaxy degenerationin certain viscera, notably the liver, spleen, kidneys, and intestines. The process begins in the arterial walls, and spreadsthence to the connective-tissue structures, causing marked enlargement of the affected organs. Albuminuria, ascites, œdema of the lower limbs, clubbing of the fingers, and diarrhœa are among the most prominent symptoms of this condition.
Theprognosisin hectic fever depends on the completeness with which the further absorption of toxins can be prevented. In many cases this can only be effected by an operation which provides for free drainage, and, if possible, the removal of infected tissues. The resulting wound is best treated by the open method. Even advanced waxy degeneration does not contra-indicate this line of treatment, as the diseased organs usually recover if the focus from which absorption of toxic material is taking place is completely eradicated.
Fig. 12.—Chart of case of Septicæmia followed by Pyæmia.Fig. 12.—Chart of case of Septicæmia followed by Pyæmia.
Fig. 12.—Chart of case of Septicæmia followed by Pyæmia.
Septicæmia.—This form of blood-poisoning is the result of the action of pyogenic bacteria, which not only produce their toxins at the primary seat of infection, but themselves enter the blood-stream and are carried to other parts, where they settle and produce further effects.
Clinical Features.—There may be an incubation period of some hours between the infection and the first manifestation of acute septicæmia. In such conditions as acute osteomyelitis or acute peritonitis, we see the most typical clinical pictures of this condition. The onset is marked by a chill, or a rigor, which may be repeated, while the temperature rises to 103° or 104° F., although in very severe cases the temperature may remain subnormal throughout, the virulence of the toxins preventing reaction. It is in the general appearance of thepatient and in the condition of the pulse that we have our best guides as to the severity of the condition. If the pulse remains firm, full, and regular, and does not exceed 110 or even 120, while the temperature is moderately raised, the outlook is hopeful; but when the pulse becomes small and compressible, and reaches 130 or more, especially if at the same time the temperature is low, a grave prognosis is indicated. The tongue is often dry and coated with a black crust down the centre, while the sides are red. It is a good omen when the tongue becomes moist again. Thirst is most distressing, especially in septicæmia of intestinal origin. Persistent vomiting of dark-brown material is often present, and diarrhœa with blood-stained stools is not uncommon. The urine is small in amount, and contains a large proportion of urates. As the poisons accumulate, the respiration becomes shallow and laboured, the face of a dull ashy grey, the nose pinched, and the skin cold and clammy. Capillary hæmorrhages sometimes take place in the skin or mucous membranes; and in a certain proportion of cases cutaneous eruptions simulating those of scarlet fever or measles appear, and are apt to lead to errors in diagnosis. In other cases there is slight jaundice. The mental state is often one of complete apathy, the patient failing to realise the gravity of his condition; sometimes there is delirium.
Theprognosisis always grave, and depends on the possibility of completely eradicating the focus of infection, and on the reserve force the patient has to carry him over the period during which he is eliminating the poison already circulating in his blood.
Thetreatmentis carried out on the same lines as in sapræmia, but it is less likely to be successful owing to the organisms having entered the circulation. When possible, the primary focus of infection should be dealt with.
Pyæmiais a form of blood-poisoning characterised by the development of secondary foci of suppuration in different parts of the body. Toxins are thus introduced into the blood, not only at the primary seat of infection, but also from each of these metastatic collections. Like septicæmia, this condition is due to pyogenic bacteria, thestreptococcus pyogenesbeing the commonest organism found. The primary infection is usually in a wound—for example, a compound fracture—but cases occur in which the point of entrance of the bacteria is not discoverable. The dissemination of the organisms takes place through the medium of infected emboli which form in a thrombosed vein in the vicinity of the original lesion, and, breaking loose, are carriedthence in the blood-stream. These emboli lodge in the minute vessels of the lungs, spleen, liver, kidneys, pleura, brain, synovial membranes, or cellular tissue, and the bacteria they contain give rise to secondary foci of suppuration. Secondary abscesses are thus formed in those parts, and these in turn may be the starting-point of new emboli which give rise to fresh areas of pus formation. The organs above named are the commonest situations of pyæmic abscesses, but these may also occur in the bone marrow, the substance of muscles, the heart and pericardium, lymph glands, subcutaneous tissue, or, in fact, in any tissue of the body. Organisms circulating in the blood are prone to lodge on the valves of the heart and give rise to endocarditis.
Fig. 13.—Chart of Pyæmia following on Acute Osteomyelitis.Fig. 13.—Chart of Pyæmia following on Acute Osteomyelitis.
Fig. 13.—Chart of Pyæmia following on Acute Osteomyelitis.
Clinical Features.—Before antiseptic surgery was practised, pyæmia was a common complication of wounds. In the present day it is not only infinitely less common, but appears also to be of a less severe type. Its rarity and its mildness may be related as cause and effect, because it was formerly found that pyæmia contracted from a pyæmic patient was more virulent than that from other sources.
In contrast with sapræmia and septicæmia, pyæmia is late of developing, and it seldom begins within a week of the primary infection. The first sign is a feeling of chilliness, or a violent rigor lasting for perhaps half an hour, during which time the temperature rises to 103°, 104°, or 105° F. In the course of an hour it begins to fall again, and the patient breaks into aprofuse sweat. The temperature may fall several degrees, but seldom reaches the normal. In a few days there is a second rigor with rise of temperature, and another remission, and such attacks may be repeated at diminishing intervals during the course of the illness (Figs. 12and13). The pulse is soft, and tends to remain abnormally rapid even when the temperature falls nearly to normal.
The face is flushed, and wears a drawn, anxious expression, and the eyes are bright. A characteristic sweetish odour, which has been compared to that of new-mown hay, can be detected in the breath and may pervade the patient. The appetite is lost; there may be sickness and vomiting and profuse diarrhœa; and the patient emaciates rapidly. The skin is continuously hot, and has often a peculiar pungent feel. Patches of erythema sometimes appear scattered over the body. The skin may assume a dull sallow or earthy hue, or a bright yellow icteric tint may appear. The conjunctivæ also may be yellow. In the latter stages of the disease the pulse becomes small and fluttering; the tongue becomes dry and brown; sordes collect on the teeth; and a low muttering form of delirium supervenes.
Secondary infection of the parotid gland frequently occurs, and gives rise to a suppurative parotitis. This condition is associated with severe pain, gradually extending from behind the angle of the jaw on to the face. There is also swelling over the gland, and eventually suppuration and sloughing of the gland tissue and overlying skin.
Secondary abscesses in the lymph glands, subcutaneous tissue, or joints are often so insidious and painless in their development that they are only discovered accidentally. When the abscess is evacuated, healing often takes place with remarkable rapidity, and with little impairment of function.
The general symptoms may be simulated by an attack of malaria.
Prognosis.—The prognosis in acute pyæmia is much less hopeless than it once was, a considerable proportion of the patients recovering. In acute cases the disease proves fatal in ten days or a fortnight, death being due to toxæmia. Chronic cases often run a long course, lasting for weeks or even months, and prove fatal from exhaustion and waxy disease following on prolonged suppuration.
Treatment.—In such conditions as compound fractures and severe lacerated wounds, much can be done to avert the conditions which lead to pyæmia, by applying a Bier's constrictingbandage as soon as there is evidence of infection having taken place, or even if there is reason to suspect that the wound is not aseptic.
If sepsis is already established, and evidence of general infection is present, the wound should be opened up sufficiently to admit of thorough disinfection and drainage, and the constricting bandage applied to aid the defensive processes going on in the tissues. If these measures fail, amputation of the limb may be the only means of preventing further dissemination of infective material from the primary source of infection.
Attempts have been made to interrupt the channel along which the infective emboli spread, by ligating or resecting the main vein of the affected part, but this is seldom feasible except in the case of the internal jugular vein for infection of the transverse sinus.
Secondary abscesses must be aspirated or opened and drained whenever possible.
The general treatment is conducted on the same lines as on other forms of pyogenic infection.
The process ofulcerationmay be defined as the molecular or cellular death of tissue taking place on a free surface. It is essentially of the same nature as the process of suppuration, only that the purulent discharge, instead of collecting in a closed cavity and forming an abscess, at once escapes on the surface.
Anulceris an open wound or sore in which there are present certain conditions tending to prevent it undergoing the natural process of repair. Of these, one of the most important is the presence of pathogenic bacteria, which by their action not only prevent healing, but so irritate and destroy the tissues as to lead to an actual increase in the size of the sore. Interference with the nutrition of a part by œdema or chronic venous congestion may impede healing; as may also induration of the surrounding area, by preventing the contraction which is such an important factor in repair. Defective innervation, such as occurs in injuries and diseases of the spinal cord, also plays an important part in delaying repair. In certain constitutional conditions, too—for example, Bright's disease, diabetes, or syphilis—the vitiated state of the tissues is an impediment to repair. Mechanical causes, such as unsuitable dressings or ill-fitting appliances, may also act in the same direction.
Clinical Examination of an Ulcer.—In examining any ulcer, we observe—(1) Itsbaseorfloor, noting the presence or absence of granulations, their disposition, size, colour, vascularity, and whether they are depressed or elevated in relation to the surrounding parts. (2) Thedischargeas to quantity, consistence, colour, composition, and odour. (3) Theedges, noting particularly whether or not the marginal epithelium isattempting to grow over the surface; also their shape, regularity, thickness, and whether undermined or overlapping, everted or depressed. (4) Thesurrounding tissues, as to whether they are congested, œdematous, inflamed, indurated, or otherwise. (5) Whether or not there ispainor tenderness in the raw surface or its surroundings. (6) Thepart of the bodyon which it occurs, because certain ulcers have special seats of election—for example, the varicose ulcer in the lower third of the leg, the perforating ulcer on the sole of the foot, and so on.
The Healing Sore.—If a portion of skin be excised aseptically, and no attempt made to close the wound, the raw surface left is soon covered over with a layer of coagulated blood and lymph. In the course of a few days this is replaced by the growth ofgranulations, which are of uniform size, of a pinkish-red colour, and moist with a slight serous exudate containing a few dead leucocytes. They grow until they reach the level of the surrounding skin, and so fill the gap with a fine velvety mass of granulation tissue. At the edges, the young epithelium may be seen spreading in over the granulations as a fine bluish-white pellicle, which gradually covers the sore, becoming paler in colour as it thickens, and eventually forming the smooth, non-vascular covering of the cicatrix. There is no pain, and the surrounding parts are healthy.
This may be used as a type with which to compare the ulcers seen at the bedside, so that we may determine how far, and in what particulars, these differ from the type; and that we may in addition recognise the conditions that have to be counteracted before the characters of the typical healing sore are assumed.
For purposes of contrast we may indicate the characters of an open sore in which bacterial infection with pathogenic bacteria has taken place. The layer of coagulated blood and lymph becomes liquefied and is thrown off, and instead of granulations being formed, the tissues exposed on the floor of the ulcer are destroyed by the bacterial toxins, with the formation of minute sloughs and a quantity of pus.
The discharge is profuse, thin, acrid, and offensive, and consists of pus, broken-down blood-clot, and sloughs. The edges are inflamed, irregular, and ragged, showing no sign of growing epithelium—on the contrary, the sore may be actually increasing in area by the breaking-down of the tissues at its margins. The surrounding parts are hot, red, swollen, and œdematous; and there is pain and tenderness both in the sore itself and in the parts around.
Classification of Ulcers.—The nomenclature of ulcers is much involved and gives rise to great confusion, chiefly for the reason that no one basis of classification has been adopted. Thus some ulcers are named according to the causes at work in producing or maintaining them—for example, the traumatic, the septic, and the varicose ulcer; some from the constitutional element present, as the gouty and the diabetic ulcer; and others according to the condition in which they happen to be when seen by the surgeon, such as the weak, the inflamed, and the callous ulcer.
So long as we retain these names it will be impossible to find a single basis for classification; and yet many of the terms are so descriptive and so generally understood that it is undesirable to abolish them. We must therefore remain content with a clinical arrangement of ulcers,—it cannot be called a classification,—considering any given ulcer from two points of view: first itscause, and second itspresent condition. This method of studying ulcers has the practical advantage that it furnishes us with the main indications for treatment as well as for diagnosis: the cause must be removed, and the condition so modified as to convert the ulcer into an aseptic healing sore.
A.Arrangement of Ulcers according to their Cause.—Although any given ulcer may be due to a combination of causes, it is convenient to describe the following groups:
Ulcers due to Traumatism.—Traumatism in the form of acrushorbruiseis a frequent cause of ulcer formation, acting either by directly destroying the skin, or by so diminishing its vitality that it is rendered a suitable soil for bacteria. If these gain access, in the course of a few days the damaged area of skin becomes of a greyish colour, blebs form on it, and it undergoes necrosis, leaving an unhealthy raw surface when the slough separates.
Heatandprolonged exposure to the Röntgen raysorto radium emanationsact in a similar way.
Thepressureof improperly padded splints or other appliances may so far interfere with the circulation of the part pressed upon, that the skin sloughs, leaving an open sore. This is most liable to occur in patients who suffer from some nerve lesion—such as anterior poliomyelitis, or injury of the spinal cord or nerve-trunks. Splint-pressure sores are usually situated over bony prominences, such as the malleoli, the condyles of the femur or humerus, the head of the fibula, the dorsum of the foot, or the base of the fifth metatarsal bone. On removing the splint, the skin of the part pressed upon is found to be of a red or pinkcolour, with a pale grey patch in the centre, which eventually sloughs and leaves an ulcer. Certain forms ofbed-soreare also due to prolonged pressure.
Pressure sores are also known to have been produced artificially by malingerers and hysterical subjects.
Fig. 14.—Leg Ulcers associated with Varicose Veins and Pigmentation of the Skin.Fig. 14.—Leg Ulcers associated with Varicose Veins and Pigmentation of the Skin.
Fig. 14.—Leg Ulcers associated with Varicose Veins and Pigmentation of the Skin.
Ulcers due to Imperfect Circulation.—Imperfect circulation is an important causative factor in ulceration, especially when it isthevenous returnthat is defective. This is best illustrated in the so-calledleg ulcer, which occurs most frequently on the front and medial aspect of the lower third of the leg. At this point the anastomosis between the superficial and deep veins of the leg is less free than elsewhere, so that the extra stress thrown upon the surface veins interferes with the nutrition of the skin (Hilton). The importance of imperfect venous return in the causation of such ulcers is evidenced by the fact that as soon as the condition of the circulation is improved by confining the patient to bed and elevating the limb, the ulcer begins to heal, even although all methods of local treatment have hitherto proved ineffectual. In a considerable number of cases, but by no means in all, this form of ulcer is associated with the presence of varicose veins, and in such cases it is spoken of as thevaricose ulcer(Fig. 14). The presence of varicose veins is frequently associated with a diffuse brownish or bluish pigmentation of the skin of the lower third of the leg, or with an obstinate form of dermatitis (varicose eczema), and the scratching or rubbing of the part is liable to cause a breach of the surface and permit of infection which leads to ulceration. Varicose ulcers may also originate from the bursting of a small peri-phlebitic abscess.
Varicose veins in immediate relation to the base of a large chronic ulcer usually become thrombosed, and in time are reduced to fibrous cords, and therefore in such cases hæmorrhage is not a common complication. In smaller and more superficial ulcers, however, the destructive process is liable to implicate the wall of the vessel before the occurrence of thrombosis, and to lead to profuse and it may be dangerous bleeding.
These ulcers are at first small and superficial, but from want of care, from continued standing or walking, or from injudicious treatment, they gradually become larger and deeper. They are not infrequently multiple, and this, together with their depth, may lead to their being mistaken for ulcers due to syphilis. The base of the ulcer is covered with imperfectly formed, soft, œdematous granulations, which give off a thin sero-purulent discharge. The edges are slightly inflamed, and show no evidence of healing. The parts around are usually pigmented and slightly œdematous, and as a rule there is little pain. This variety of ulcer is particularly prone to pass into the condition known as callous.
Inanæmicpatients, especially young girls, ulcers are occasionally met with which have many of the clinical characters of those associated with imperfect venous return. They are slow to heal, and tend to pass into the condition known as weak.
Ulcers due to Interference with Nerve-Supply.—Any interference with the nerve-supply of the superficial tissues predisposes to ulceration. For example,trophiculcers are liable to occur in injuries or diseases of the spinal cord, in cerebral paralysis, in limbs weakened by poliomyelitis, in ascending or peripheral neuritis, or after injuries of nerve-trunks.
Theacute bed-soreis a rapidly progressing form of ulceration, often amounting to gangrene, of portions of skin exposed to pressure when their trophic nerve-supply has been interfered with.
Fig. 15.—Perforating Ulcers of Sole of Foot. (From Photograph lent by Sir Montagu Cotterill.)Fig. 15.—Perforating Ulcers of Sole of Foot.(From Photograph lent by Sir Montagu Cotterill.)
Fig. 15.—Perforating Ulcers of Sole of Foot.
(From Photograph lent by Sir Montagu Cotterill.)
Theperforating ulcer of the footis a peculiar type of sore which occurs in association with the different forms of peripheral neuritis, and with various lesions of the brain and spinal cord, such as general paralysis, locomotor ataxia, or syringo-myelia (Fig. 15). It also occurs in patients suffering from glycosuria, and is usually associated with arterio-sclerosis—local or general. Perforating ulcer is met with most frequently under the head of the metatarsal bone of the great toe. A callosity forms and suppuration occurs under it, the pus escaping through a small hole in the centre. The process slowly and gradually spreads deeper and deeper, till eventually the bone or joint is reached, and becomes implicated in the destructive process—hence the term “perforating ulcer.” The flexor tendons are sometimes destroyed, the toe being dorsiflexed by the unopposed extensors. The depth of the track being so disproportionate to its superficial area, the condition closely simulates a tuberculous sinus, for which it is liable to be mistaken. The raw surface is absolutely insensitive, so that the probe can be freely employed without the patient even being aware of it or suffering the least discomfort—a significant fact in diagnosis. The cavity is filled with effete and decomposing epidermis, which has a most offensive odour. The chronic and intractable character of the ulcer is due to interference with the trophic nerve-supply of the parts, and to the fact that the epithelium of the skin grows in and lines the track leading down to the deepest part of the ulcer and so prevents closure. While they are commonest on the sole of the foot and other parts subjected to pressure, perforating ulcers are met with on the sides and dorsum of the foot and toes, on the hands, and on other parts where no pressure has been exerted.
Thetuberculous ulcer, so often seen in the neck, in the vicinity of joints, or over the ribs and sternum, usually results from the bursting through the skin of a tuberculous abscess.The base is soft, pale, and covered with feeble granulations and grey shreddy sloughs. The edges are of a dull blue or purple colour, and gradually thin out towards their free margins, and in addition are characteristically undermined, so that a probe can be passed for some distance between the floor of the ulcer and the thinned-out edges. Thin, devitalised tags of skin often stretch from side to side of the ulcer. The outline is irregular; small perforations often occur through the skin, and a thin, watery discharge, containing grey shreds of tuberculous debris, escapes.
Bazin's Disease.—This term is applied to an affection of the skin and subcutaneous tissue which bears certain resemblances to tuberculosis. It is met with almost exclusively between the knee and the ankle, and it usually affects both legs. It is commonest in girls of delicate constitution, in whose family history there is evidence of a tuberculous taint. The patient often presents other lesions of a tuberculous character, notably enlarged cervical glands, and phlyctenular ophthalmia.The tubercle bacillus has rarely been found, but we have always observed characteristic epithelioid cells and giant cells in sections made from the edge or floor of the ulcer.