Fig. 22.—Gangrene of Terminal Phalanx of Index-Finger, following cellulitis of hand resulting from a scratch on the palm of the hand.Fig. 22.—Gangrene of Terminal Phalanx of Index-Finger, following cellulitis of hand resulting from a scratch on the palm of the hand.
Fig. 22.—Gangrene of Terminal Phalanx of Index-Finger, following cellulitis of hand resulting from a scratch on the palm of the hand.
Rigors may occur, but the temperature is not necessarily raised—indeed, it is sometimes subnormal. The pulse is small, feeble, rapid, and irregular. Unless amputation is promptly performed, death usually follows within thirty-six or forty-eight hours. Even early operation does not always avert the fatal issue, because the quantity of toxin absorbed and its extreme virulence are often more than even a robust subject can outlive.
Treatment.—Every effort must be made to purify all such wounds as are contaminated by earth, street dust, stable refuse, or other forms of gross dirt. Devitalised and contaminated tissue is removed with the knife or scissors and the wound purified with antiseptics of the chlorine group or with hydrogen peroxide. If there is a reasonable prospect that infection has been overcome, the wound may be at once sutured, but if this is doubtful it is left open and packed or irrigated.
When acute gangrene has set in no treatment short of amputation is of any avail, and the sooner this is done, the greater is the hope of saving the patient. The limb must be amputated well beyond the apparent limits of the infected area, and stringent precautions must be taken to avoid discharge from the already gangrenous area reaching the operation wound. An assistant or nurse, who is to take no other part in the operation, is told off to carry out the preliminary purification, and to hold the limb during the operation.
Malignant Œdema.—This form of acute gangrene has been defined as “a spreading inflammatory œdema attended with emphysema, and ultimately followed by gangrene of the skin and adjacent parts.” The predominant organism is thebacillus of malignant œdemaorvibrion septiqueof Pasteur, which is found in garden soil, dung, and various putrefying substances. It is anaërobic, and occurs as long, thick rods with somewhat rounded ends and several laterally placed flagella. Spores, which have a high power of resistance, form in the centre of the rods, and bulge out the sides so as to give the organisms a spindle-shaped outline. Other pathogenic organisms are also present and aid the specific bacillus in its action.
At the bedside it is difficult, if not impossible, to distinguish it from acute infective gangrene. Both follow on the same kinds of injury and run an exceedingly rapid course. In malignant œdema, however, the incidence of the disease is mainly on the superficial parts, which become œdematous and emphysematous, and acquire a marbled appearance with the veins clearly outlined. Early disappearance of sensation is a particularly grave symptom. Bullæ form on the skin, and thetissues have “a peculiar heavy but not putrid odour.” The constitutional effects are extremely severe, and death may ensue within a few hours.
Acute EmphysematousorGas Gangrenewas prevalent in certain areas at various periods during the European War. It follows infection of lacerated wounds with thebacillus ærogenes capsulatus, usually in combination with other anaërobes, and its main incidence is on the muscles, which rapidly become infiltrated with gas that spreads throughout the whole extent of the muscle, disintegrating its fibres and leading to necrosis. The gangrenous process spreads with appalling rapidity, the limb becoming enormously swollen, painful, and crepitant or even tympanitic. Patches of coppery or purple colour appear on the skin, and bullæ containing blood-stained serum form on the surface. The toxæmia is profound, and the face and lips assume a characteristic cyanosis. The condition is attended with a high mortality. Only in the early stages and when the infection is limited are local measures successful in arresting the spread; in more severe cases amputation is the only means of saving life.
Cancrum OrisorNoma.—This disease is believed to be due to a specific bacillus, which occurs in long delicate rods, and is chiefly found at the margin of the gangrenous area. It is prone to attack unhealthy children from two to five years of age, especially during their convalescence from such diseases as measles, scarlet fever, or typhoid, but may attack adults when they are debilitated. It is most common in the mouth, but sometimes occurs on the vulva. In the mouth it begins as an ulcerative stomatitis, more especially affecting the gums or inner aspect of the cheek. The child lies prostrated, and from the open mouth foul-smelling saliva, streaked with blood, escapes; the face is of an ashy-grey colour, the lips dark and swollen. On the inner aspect of the cheek is a deeply ulcerated surface, with sloughy shreds of dark-brown or black tissue covering its base; the edges are irregular, firm, and swollen, and the surrounding mucous membrane is infiltrated and œdematous. In the course of a few hours a dark spot appears on the outer aspect of the cheek, and rapidly increases in size; towards the centre it is black, shading off through blue and grey into a dark-red area which extends over the cheek (Fig. 23). The tissue implicated is at first firm and indurated, but as it loses its vitality it becomes doughy and sodden. Finally a slough forms, and, when it separates, the cheek is perforated.
Meanwhile the process spreads inside the mouth, and thegums, the floor of the mouth, or even the jaws, may become gangrenous and the teeth fall out. The constitutional disturbance is severe, the temperature raised, and the pulse feeble and rapid.
Fig. 23.—Cancrum oris. (From a photograph lent by Sir George T. Beatson.)Fig. 23.—Cancrum oris.(From a photograph lent by Sir George T. Beatson.)
Fig. 23.—Cancrum oris.
(From a photograph lent by Sir George T. Beatson.)
The extremely fœtid odour which pervades the room or even the house the patient occupies, is usually sufficient to suggest the diagnosis of cancrum oris. The odour must not be mistaken for that due to decomposition of sordes on the teeth and gums of a debilitated patient.
Theprognosisis always grave in the extreme, the main risks being general toxæmia and septic pneumonia. When recovery takes place there is serious deformity, and considerable portions of the jaws may be lost by necrosis.
Treatment.—The only satisfactory treatment is thorough removal under an anæsthetic of all the sloughy tissue, with the surrounding zone in which the organisms are active. This is most efficiently accomplished by the knife or scissors, cutting until the tissue bleeds freely, after which the raw surface is painted with undiluted carbolic acid and dressed with iodoform gauze. It may be necessary to remove large pieces of bone when the necrotic process has implicated the jaws. The mouth must be constantly sprayed with peroxide of hydrogen, and washed out with a disinfectant and deodorant lotion, such as Condy's fluid. The patient's general condition calls for free stimulation.
The deformity resulting from these necessarily heroic measures is not so great as might be expected, and can be further diminished by plastic operations, which should be undertaken before cicatricial contraction has occurred.
Bed-sores are most frequently met with in old and debilitated patients, or in those whose tissues are devitalised by acute orchronic diseases associated with stagnation of blood in the peripheral veins. Any interference with the nerve-supply of the skin, whether from injury or disease of the central nervous system or of the peripheral nerves, strongly predisposes to the formation of bed-sores. Prolonged and excessive pressure over a bony prominence, especially if the parts be moist with skin secretions, urine, or wound discharges, determines the formation of a sore. Excoriations, which may develop into true bed-sores, sometimes form where two skin surfaces remain constantly apposed, as in the region of the scrotum or labium, under pendulous mammæ, or between fingers or toes confined in a splint.
Fig. 24.—Acute Bed-Sores over Right Buttock.Fig. 24.—Acute Bed-Sores over Right Buttock.
Fig. 24.—Acute Bed-Sores over Right Buttock.
Clinical Features.—Two clinical varieties are met with—the acute and the chronic bed-sore.
Theacutebed-sore usually occurs over the sacrum or buttock. It develops rapidly after spinal injuries and in the course of certain brain diseases. The part affected becomes red and congested, while the surrounding parts are œdematous and swollen, blisters form, and the skin loses its vitality (Fig. 24).
In advanced cases of general paralysis of the insane, a peculiar form of acute bed-sore beginning as a blister, and passing on tothe formation of a black, dry eschar, which slowly separates, occurs on such parts as the medial side of the knee, the angle of the scapula, and the heel.
Thechronicbed-sore begins as a dusky reddish purple patch, which gradually becomes darker till it is almost black. The parts around are œdematous, and a blister may form. This bursts and exposes the papillæ of the skin, which are of a greenish hue. A tough greyish-black slough forms, and is slowly separated. It is not uncommon for the gangrenous area to continue to spread both in width and in depth till it reaches the periosteum or bone. Bed-sores over the sacrum sometimes implicate the vertebral canal and lead to spinal meningitis, which usually proves fatal.
In old and debilitated patients the septic absorption taking place from a bed-sore often proves a serious complication of other surgical conditions. From this cause, for example, old people may succumb during the treatment of a fractured thigh.
The granulating surface left on the separation of the slough tends to heal comparatively rapidly.
Prevention of Bed-sores.—The first essential in the prevention of bed-sores is the regular changing of the patient's position, so that no one part of the body is continuously pressed upon for any length of time. Ring-pads of wool, air-cushions, or water-beds are necessary to remove pressure from prominent parts. Absolute dryness of the skin is all-important. At least once a day, the sacrum, buttocks, shoulder-blades, heels, elbows, malleoli, or other parts exposed to pressure, must be sponged with soap and water, thoroughly dried, and then rubbed with methylated spirit, which is allowed to dry on the skin. Dusting the part with boracic acid powder not only keeps it dry, but prevents the development of bacteria in the skin secretions.
In operation cases, care must be taken that irritating chemicals used to purify the skin do not collect under the patient and remain in contact with the skin of the sacrum and buttocks during the time he is on the operating-table. There is reason to believe that the so-called “post-operation bed-sore” may be due to such causes. A similar result has been known to follow soiling of the sheets by the escape of a turpentine enema.
Treatment.—Once a bed-sore has formed, every effort must be made to prevent its spread. Alcohol is used to cleanse the broken surface, and dry absorbent dressings are applied and frequently changed. It is sometimes found necessary to employ moist or oily substances, such as boracic poultices, eucalyptus ointment, or balsam of Peru, to facilitate the separation ofsloughs, or to promote the growth of granulations. In patients who are not extremely debilitated the slough may be excised, the raw surface scraped, and then painted with iodine.
Skin-grafting is sometimes useful in covering in the large raw surface left after separation or removal of sloughs.
Erysipelas, popularly known as “rose,” is an acute spreading infective disease of the skin or of a mucous membrane due to the action of a streptococcus. Infection invariably takes place through an abrasion of the surface, although this may be so slight that it escapes observation even when sought for. The streptococci are found most abundantly in the lymph spaces just beyond the swollen margin of the inflammatory area, and in the serous blebs which sometimes form on the surface.
Clinical Features.—Facial erysipelasis the commonest clinical variety, infection usually occurring through some slight abrasion in the region of the mouth or nose, or from an operation wound in this area. From this point of origin the inflammation may spread all over the face and scalp as far back as the nape of the neck. It stops, however, at the chin, and never extends on to the front of the neck. There is great œdema of the face, the eyes becoming closed up, and the features unrecognisable. The inflammation may spread to the meninges, the intracranial venous sinuses, the eye, or the ear. In some cases the erysipelas invades the mucous membrane of the mouth, and spreads to the fauces and larynx, setting up an œdema of the glottis which may prove dangerous to life.
Erysipelas occasionally attacks an operation wound that has become septic; and it may accompany septic infection of the genital tract in puerperal women, or the separation of the umbilical cord in infants (erysipelas neonatorum). After an incubation period, which varies from fifteen to sixty hours, the patient complains of headache, pains in the back and limbs, loss of appetite, nausea, and frequently there is vomiting. He has a chill or slight rigor, initiating a rise of temperature to 103°,104°, or 105° F.; and a full bounding pulse of about 100 (Fig. 25). The tongue is foul, the breath heavy, and, as a rule, the bowels are constipated. There is frequently albuminuria, and occasionally nocturnal delirium. A moderate degree of leucocytosis (15,000 to 20,000) is usually present.
Around the seat of inoculation a diffuse red patch forms, varying in hue from a bright scarlet to a dull brick-red. The edges are slightly raised above the level of the surrounding skin, as may readily be recognised by gently stroking the part from the healthy towards the affected area. The skin is smooth, tense, and glossy, and presents here and there blisters filled with serous fluid. The local temperature is raised, and the part is the seat of a burning sensation and is tender to the touch, the most tender area being the actively spreading zone which lies about half an inch beyond the red margin.
Fig. 25.—Chart of Erysipelas occurring in a wound.Fig. 25.—Chart of Erysipelas occurring in a wound.
Fig. 25.—Chart of Erysipelas occurring in a wound.
The disease tends to spread spasmodically and irregularly, and the direction and extent of its progress may be recognised by mapping out the peripheral zone of tenderness. Red streaks appear along the lines of the superficial lymph vessels, and the deep lymphatics may sometimes be palpated as firm, tender cords. The neighbouring glands, also, are generally enlarged and tender.
The disease lasts for from two or three days to as many weeks, and relapses are frequent. Spontaneous resolution usually takes place, but the disease may prove fatal from absorption of toxins, involvement of the brain or meninges, or from general streptococcal infection.
Complications.—Diffuse suppurative cellulitisis the most serious local complication, and results from a mixed infection with other pyogenic bacteria. Smalllocalised superficial abscessesmay form during the convalescent stage. They are doubtless due to the action of skin bacteria, which attack the tissues devitalised by the erysipelas. A persistent form ofœdemasometimes remains after recurrent attacks of erysipelas, especially when they affect the face or the lower extremity, a condition which is referred to with elephantiasis.
Treatment.—The first indication is to endeavour to arrest the spread of the process. We have found that by painting with linimentum iodi, a ring half an inch broad, about an inch in front of the peripheral tender zone—not the red margin—an artificial leucocytosis is produced, and the advancing streptococci are thereby arrested. Several coats of the iodine are applied, one after the other, and this is repeated daily for several days, even although the erysipelas has not overstepped the ring. Success depends upon using the liniment of iodine (the tincture is not strong enough), and in applying it well in front of the disease. To allay pain the most useful local applications are ichthyol ointment (1 in 6), or lead and opium fomentations.
The general treatment consists in attending to the emunctories, in administrating quinine in small—two-grain—doses every four hours, or salicylate of iron (2–5 gr. every three hours), and in giving plenty of fluid nourishment. It is worthy of note that the anti-streptococcic serum has proved of less value in the treatment of erysipelas than might have been expected, probably because the serum is not made from the proper strain of streptococcus.
It is not necessary to isolate cases of erysipelas, provided the usual precautions against carrying infection from one patient to another are rigidly carried out.
Diphtheria is an acute infective disease due to the action of a specific bacterium, thebacillus diphtheriæorKlebs-Löffler bacillus. The disease is usually transmitted from one patient to another, but it may be contracted from cats, fowls, or through the milk of infected cows. Cases have occurred in which the surgeon has carried the infection from one patient to another through neglect of antiseptic precautions. The incubation period varies from two to seven days.
Clinical Features.—Inpharyngeal diphtheria, on the firstor second day of the disease, redness and swelling of the mucous membrane of the pharynx, tonsils, and palate are well marked, and small, circular greenish or grey patches of false membrane, composed of necrosed epithelium, fibrin, leucocytes, and red blood corpuscles, begin to appear. These rapidly increase in area and thickness, till they coalesce and form a complete covering to the parts. In the pharynx the false membrane is less adherent to the surface than it is when the disease affects the air-passages. The diphtheritic process may spread from the pharynx to the nasal cavities, causing blocking of the nares, with a profuse ichorous discharge from the nostrils, and sometimes severe epistaxis. The infection may spread along the nasal duct to the conjunctiva. The middle ear also may become involved by spread along the auditory (Eustachian) tube.
The lymph glands behind the angle of the jaw enlarge and become tender, and may suppurate from superadded infection. There is pain on swallowing, and often earache; and the patient speaks with a nasal accent. He becomes weak and anæmic, and loses his appetite. There is often albuminuria. Leucocytosis is usually well marked before the injection of antitoxin; after the injection there is usually a diminution in the number of leucocytes. The false membrane may separate and be cast off, after which the patient gradually recovers. Death may take place from gradual failure of the heart's action or from syncope during some slight exertion.
Laryngeal Diphtheria.—The disease may arise in the larynx, although, as a rule, it spreads thence from the pharynx. It first manifests itself by a short, dry, croupy cough, and hoarseness of the voice. The first difficulty in breathing usually takes place during the night, and once it begins, it rapidly gets worse. Inspiration becomes noisy, sometimes stridulous or metallic or sibilant, and there is marked indrawing of the epigastrium and lower intercostal spaces. The hoarseness becomes more marked, the cough more severe, and the patient restless. The difficulty of breathing occurs in paroxysms, which gradually increase in frequency and severity, until at length the patient becomes asphyxiated. The duration of the disease varies from a few hours to four or five days.
After the acutesypmtomshave passed off, various localised paralyses may develop, affecting particularly the nerves of the palatal and orbital muscles, less frequently the lower limbs.
Diagnosis.—The finding of the Klebs-Löffler bacillus is the only conclusive evidence of the disease. The bacillusmay be obtained by swabbing the throat with a piece of aseptic—not antiseptic—cotton wool or clean linen rag held in a pair of forceps, and rotated so as to entangle portions of the false membrane or exudate. The swab thus obtained is placed in a test-tube, previously sterilised by having had some water boiled in it, and sent to a laboratory for investigation. To identify the bacillus a piece of the membrane from the swab is rubbed on a cover glass, dried, and stained with methylene blue or other basic stain; or cultures may be made on agar or other suitable medium. When a bacteriological examination is impossible, or when the clinical features do not coincide with the results obtained, the patient should always be treated on the assumption that he suffers from diphtheria. So much doubt exists as to the real nature of membranous croup and its relationship to true diphtheria, that when the diagnosis between the two is uncertain the safest plan is to treat the case as one of diphtheria.
In children, diphtheria may occur on the vulva, vagina, prepuce, or glans penis, and give rise to difficulty in diagnosis, which is only cleared up by demonstration of the bacillus.
Treatment.—An attempt may be made to destroy or to counteract the organisms by swabbing the throat with strong antiseptic solutions, such as 1 in 1000 corrosive sublimate or 1 in 30 carbolic acid, or by spraying with peroxide of hydrogen.
The antitoxic serum is our sheet-anchor in the treatment of diphtheria, and recourse should be had to its use as early as possible.
Difficulty of swallowing may be met by the use of a stomach tube passed either through the mouth or nose. When this is impracticable, nutrient enemata are called for.
In laryngeal diphtheria, the interference with respiration may call for intubation of the larynx, or tracheotomy, but the antitoxin treatment has greatly diminished the number of cases in which it becomes necessary to have recourse to these measures.
Intubation consists in introducing through the mouth into the larynx a tube which allows the patient to breathe freely during the period while the membrane is becoming separated and thrown off. This is best done with the apparatus of O'Dwyer; but when this instrument is not available, a simple gum-elastic catheter with a terminal opening (as suggested by Macewen and Annandale) may be employed.
When intubation is impracticable, the operation of tracheotomy is called for if the patient's life is endangered by embarrassment of respiration. Unless the patient is in hospital with skilled assistance available, tracheotomy is the safer of the two procedures.
Tetanus is a disease resulting from infection of a wound by a specific micro-organism, thebacillus tetani, and characterised by increased reflex excitability, hypertonus, and spasm of one or more groups of voluntary muscles.
Etiology and Morbid Anatomy.—The tetanus bacillus, which is a perfect anaërobe, is widely distributed in nature and can be isolated from garden earth, dung-heaps, and stable refuse. It is a slender rod-shaped bacillus, with a single large spore at one end giving it the shape of a drum-stick (Fig. 26). The spores, which are the active agents in producing tetanus, are highly resistant to chemical agents, retain their vitality in a dry condition, and even survive boiling for five minutes.
The organism does not readily establish itself in the human body, and seems to flourish best when it finds a nidus in necrotic tissue and is accompanied by aërobic organisms, which, by using up the oxygen in the tissues, provide for it a suitable environment. The presence of a foreign body in the wound seems to favour its action. The infection is for all practical purposes a local one, the symptoms of the disease being due to the toxins produced in the wound of infection acting upon the central nervous system.
The toxin acts principally on the nerve centres in the spinal medulla, to which it travels from the focus of infection by way of the nerve fibres supplying the voluntary muscles. Its first effect on the motor ganglia of the cord is to render them hypersensitive, so that they are excited by mild stimuli, which under ordinary conditions would produce no reaction. As the toxin accumulates the reflex arc is affected, with the result that when a stimulus reaches the ganglia a motor discharge takes place, which spreads by ascending and descending collaterals to the reflex apparatus of the whole cord. As the toxin spreads it causes both motor hyper-tonus and hyper-excitability, which accounts for the tonic contraction and the clonic spasms characteristic of tetanus.
Fig. 26.—Bacillus of Tetanus from scraping of a wound of finger, × 1000 diam. Basic fuchsin stain.Fig. 26.—Bacillus of Tetanus from scraping of a wound of finger, × 1000 diam. Basic fuchsin stain.
Fig. 26.—Bacillus of Tetanus from scraping of a wound of finger, × 1000 diam. Basic fuchsin stain.
Clinical Varieties of Tetanus.—AcuteorFulminating Tetanus.—This variety is characterised by the shortness of the incubation period, the rapidity of its progress, the severity of its symptoms, and its all but universally fatal issue in spite oftreatment, death taking place in from one to four days. The characteristic symptoms may appear within three or four days of the infliction of the wound, but the incubation period may extend to three weeks, and the wound may be quite healed before the disease declares itself—delayed tetanus. Usually, however, the wound is inflamed and suppurating, with ragged and sloughy edges. A slight feverish attack may mark the onset of the tetanic condition, or the patient may feel perfectly well until the spasms begin. If careful observations be made, it may be found that the muscles in the immediate neighbourhood of the wound are the first to become contracted; but in the majority of instances the patient's first complaint is of pain and stiffness in the muscles of mastication, notably the masseter, so that he has difficulty in opening the mouth—hence the popular name “lock-jaw.” The muscles of expression soon share in the rigidity, and the face assumes a taut, mask-like aspect. The angles of the mouth may be retracted, producing a grinning expression known as therisus sardonicus.
The next muscles to become stiff and painful are those of the neck, especially the sterno-mastoid and trapezius. The patient is inclined to attribute the pain and stiffness to exposure to cold or rheumatism. At an early stage the diaphragm and the muscles of the anterior abdominal wall become contracted; later the muscles of the back and thorax are involved; and lastly those of the limbs. Although this is the typical order of involvement of the different groups of muscles, it is not always adhered to.
To this permanent tonic contraction of the muscles there are soon added clonic spasms. These spasms are at first slight and transient, with prolonged intervals between the attacks, but rapidly tend to become more frequent, more severe, and of longer duration, until eventually the patient simply passes out of one seizure into another.
The distribution of the spasms varies in different cases: in some it is confined to particular groups of muscles, such as those of the neck, back, abdominal walls, or limbs; in others all these groups are simultaneously involved.
When the muscles of the back become spasmodically contracted, the body is raised from the bed, sometimes to such an extent that the patient rests only on his heels and occiput—the position ofopisthotonos. Lateral arching of the body from excessive action of the muscles on one side—pleurosthotonos—is not uncommon, the arching usually taking place towards the side on which the wound of infection exists. Less frequently the body is bent forward so that the knees and chin almost meet (emprosthotonos). Sometimes all the muscles simultaneously become rigid, so that the body assumes a statuesque attitude (orthotonos). When the thoracic muscles, including the diaphragm, are thrown into spasm, the patient experiences a distressing sensation as if he were gripped in a vice, and has extreme difficulty in getting breath. Between the attacks the limbs are kept rigidly extended. The clonic spasms may be so severe as to rupture muscles or even to fracture one of the long bones.
As time goes on, the clonic exacerbations become more and more frequent, and the slightest external stimulus, such as the feeling of the pulse, a whisper in the room, a noise in the street, a draught of cold air, the effort to swallow, a question addressed to the patient or his attempt to answer, is sufficient to determine an attack. The movements are so forcible and so continuous that the nurse has great difficulty in keeping the bedclothes on the patient, or even in keeping him in bed.
The general condition of the patient is pitiful in the extreme. He is fully conscious of the gravity of the disease, and his mind remains clear to the end. The suffering induced by the cramp-like spasms of the muscles keeps him in a constant state of fearful apprehension of the next seizure, and he is unable to sleep until he becomes utterly exhausted.
The temperature is moderately raised (100° to 102° F.), or may remain normal throughout. Shortly before death very high temperatures (110° F.) have been recorded, and it has been observed that the thermometer sometimes continues to rise after death, and may reach as high as 112° F. or more.
The pulse corresponds with the febrile condition. It is accelerated during the spasms, and may become exceedingly rapid and feeble before death, probably from paralysis of the vagus. Sudden death from cardiac paralysis or from cardiac spasm is not uncommon.
The respiration is affected in so far as the spasms of the respiratory muscles produce dyspnœa, and a feeling of impending suffocation which adds to the horrors of the disease.
One of the most constant symptoms is a copious perspiration, the patient being literally bathed in sweat. The urine is diminished in quantity, but as a rule is normal in composition; as in other acute infective conditions, albumen and blood may be present. Retention of urine may result from spasm of the urethral muscles, and necessitate the use of the catheter.
The fits may cease some time before death, or, on the other hand, death may occur during a paroxysm from fixation of the diaphragm and arrest of respiration.
Differential Diagnosis.—There is little difficulty, as a rule, in diagnosing a case of fulminating tetanus, but there are several conditions with which it may occasionally be confused. Instrychnin poisoning, for example, the spasms come on immediately after the patient has taken a toxic dose of the drug; they are clonic in character, but the muscles are relaxed between the fits. If the dose is not lethal, the spasms soon cease. Inhydrophobiaa history of having been bitten by a rabid animal is usually forthcoming; the spasms, which are clonic in character, affect chiefly the muscles of respiration and deglutition, and pass off entirely in the intervals between attacks. Certain cases ofhæmorrhage into the lateral ventriclesof the brain also simulate tetanus, but an analysis of the symptoms will prevent errors in diagnosis.Cerebro-spinal meningitisandbasal meningitispresent certain superficial resemblances to tetanus, but there is no trismus, and the spasms chiefly affect the muscles of the neck and back.Hysteria and catalepsymay assume characters resembling those of tetanus, but there is little difficulty in distinguishing between these diseases. Lastly, in thetetanyof children, or that following operations on the thyreoid gland, the spasms are of a jerking character, affect chiefly the hands and fingers, and yield to medicinal treatment.
Chronic Tetanus.—The difference between this and acute tetanus is mainly one of degree. Its incubation period is longer, it is more slow and insidious in its progress, and it never reaches the same degree of severity. Trismus is the most marked and constant form of spasm; and while the trunk muscles may be involved, those of respiration as a rule escape. Every additional day the patient lives adds to the probability of his ultimate recovery. When the disease does prove fatal, it is from exhaustion, and not from respiratory or cardiac spasm. The usual duration is from six to ten weeks.
Delayed Tetanus.—During the European War acute tetanus occasionally developed many weeks or even months after a patient had been injured, and when the original wound had completely healed. It usually followed some secondary operation,e.g., for the removal of a foreign body, or the breaking down of adhesions, which aroused latent organisms.
Local Tetanus.—This term is applied to a form of the disease in which the hypertonus and spasms are localised to the muscles in the vicinity of the wound. It usually occurs in patients who have had prophylactic injections of anti-tetanic serum, the toxins entering the blood being probably neutralised by the antibodies in circulation, while those passing along the motor nerves are unaffected.
When it occurs in thelimbs, attention is usually directed to the fact by pain accompanying the spasms; the muscles are found to be hard and there are frequent twitchings of the limb. A characteristic reflex is present in the lower extremity, namely, extension of the foot and leg when the sole is tickled.
Cephalic Tetanusis another localised variety which follows injury in the distribution of the facial nerve. It is characterised by the occurrence on the same side as the injury, of facial spasm, rapidly followed by more or less complete paralysis of the muscles of expression, with unilateral trismus and difficulty in swallowing. Other cranial nerves, particularly the oculomotor and the hypoglossal, may also be implicated. A remarkable feature of this condition is that although the muscles are irresponsive to ordinary physiological stimuli, they are thrown into spasm by the abnormal impulses of tetanus.
Trismus.—This term is used to denote a form of tetanic spasm limited to the muscles of mastication. It is really a mild form of chronic tetanus, and the prognosis is favourable. It must not be confused with the fixation of the jaw sometimes associated with a wisdom-tooth gumboil, with tonsillitis, or with affections of the temporo-mandibular articulation.
Tetanus neonatorumis a form of tetanus occurring in infants of about a week old. Infection takes place through the umbilicus, and manifests itself clinically by spasms of the muscles of mastication. It is almost invariably fatal within a few days.
Prophylaxis.—Experience in the European War has established the fact that the routine injection of anti-tetanic serum to all patients with lacerated and contaminated wounds greatly reduces the frequency of tetanus. The sooner the serum is given after the injury, the more certain is its effect; within twenty-four hours 1500 units injected subcutaneously is sufficient for the initial dose; if a longer period has elapsed, 2000 to 3000 units should be given intra-muscularly, as this ensures more rapid absorption. A second injection is given a week after the first.
The wound must be purified in the usual way, and all instruments and appliances used for operations on tetanic patients must be immediately sterilised by prolonged boiling.
Treatment.—When tetanus has developed the main indications are to prevent the further production of toxins in the wound, and to neutralise those that have been absorbed into the nervous system. Thorough purification with antiseptics, excision of devitalised tissues, and drainage of the wound are first carried out. To arrest the absorption of toxins intra-muscular injections of 10,000 units of serum are given daily into the muscles of the affected limb, or directly into the nerve trunks leading from the focus of infection, in the hope of “blocking” the nerves with antitoxin and so preventing the passage of toxins towards the spinal cord.
To neutralise the toxins that have already reached the spinal cord, 5000 units should be injected intra-thecally daily for four or five days, the foot of the bed being raised to enable the serum to reach the upper parts of the cord.
The quantity of toxin circulating in the blood is so small as to be practically negligible, and the risk of anaphylactic shock attending intra-venous injection outweighs any benefit likely to follow this procedure.
Baccelli recommends the injection of 20 c.c. of a 1 in 100 solution of carbolic acid into the subcutaneous tissues every four hours during the period that the contractions persist. Opinionsvary as to the efficiency of this treatment. The intra-thecal injection of 10 c.c. of a 15 per cent. solution of magnesium sulphate has proved beneficial in alleviating the severity of the spasms, but does not appear to have a curative effect.
To conserve the patient's strength by preventing or diminishing the severity of the spasms, he should be placed in a quiet room, and every form of disturbance avoided. Sedatives, such as bromides, paraldehyde, or opium, must be given in large doses. Chloral is perhaps the best, and the patient should rarely have less than 150 grains in twenty-four hours. When he is unable to swallow, it should be given by the rectum. The administration of chloroform is of value in conserving the strength of the patient, by abolishing the spasms, and enabling the attendants to administer nourishment or drugs either through a stomach tube or by the rectum. Extreme elevation of temperature is met by tepid sponging. It is necessary to use the catheter if retention of urine occurs.
Hydrophobia is an acute infective disease following on the bite of a rabid animal. It most commonly follows the bite or lick of a rabid dog or cat. The virus appears to be communicated through the saliva of the animal, and to show a marked affinity for nerve tissues; and the disease is most likely to develop when the patient is infected on the face or other uncovered part, or in a part richly endowed with nerves.
A dog which has bitten a person should on no account be killed until its condition has been proved one way or the other. Should rabies develop and its destruction become necessary, the head and spinal cord should be retained and forwarded, packed in ice, to a competent observer. Much anxiety to the person bitten and to his friends would be avoided if these rules were observed, because in many cases it will be shown that the animal did not after all suffer from rabies, and that the patient consequently runs no risk. If, on the other hand, rabies is proved to be present, the patient should be submitted to the Pasteur treatment.
Clinical Features.—There is almost always a history of the patient having been bitten or licked by an animal supposed to suffer from rabies. The incubation period averages about forty days, but varies from a fortnight to seven or eight months, and is shorter in young than in old persons. The original wound has long since healed, and beyond a slight itchiness or pain shooting along the nerves of the part, shows no sign of disturbance. A few days of general malaise, with chills and giddiness precede the onset of the acute manifestations, which affect chiefly the muscles of deglutition and respiration. One of the earliest signs is that the patient has periodically a sudden catch in his breathing “resembling what often occurs when a person goes into a cold bath.” This is due to spasm of the diaphragm, and is frequently accompanied by a loud-sounding hiccough, likened by the laity to the barking of a dog. Difficulty in swallowing fluids may be the first symptom.
The spasms rapidly spread to all the muscles of deglutition andrespiration, so that the patient not only has the greatest difficulty in swallowing, but has a constant sense of impending suffocation. To add to his distress, a copious secretion of viscid saliva fills his mouth. Any voluntary effort, as well as all forms of external stimuli, only serve to aggravate the spasms which are always induced by the attempt to swallow fluid, or even by the sound of running water.
The temperature is raised; the pulse is small, rapid, and intermittent; and the urine may contain sugar and albumen.
The mind may remain clear to the end, or the patient may have delusions, supposing himself to be surrounded by terrifying forms. There is always extreme mental agitation and despair, and the sufferer is in constant fear of his impending fate. Happily the inevitable issue is not long delayed, death usually occurring in from two to four days from the onset. The symptoms of the disease are so characteristic that there is no difficulty in diagnosis. The only condition with which it is liable to be confused is the variety of cephalic tetanus in which the muscles of deglutition are specially involved—the so-called tetanus hydrophobicus.
Prophylaxis.—The bite of an animal suspected of being rabid should be cauterised at once by means of the actual or Paquelin cautery, or by a strong chemical escharotic such as pure carbolic acid, after which antiseptic dressings are applied.
It is, however, to Pasteur'spreventive inoculationthat we must look for our best hope of averting the onset of symptoms. “It may now be taken as established that a grave responsibility rests on those concerned if a person bitten by a mad animal is not subjected to the Pasteur treatment” (Muir and Ritchie).
This method is based on the fact that the long incubation period of the disease admits of the patient being inoculated with a modified virus producing a mild attack, which protects him from the natural disease.
Treatment.—When the symptoms have once developed they can only be palliated. The patient must be kept absolutely quiet and free from all sources of irritation. The spasms may be diminished by means of chloral and bromides, or by chloroform inhalation.
Anthrax is a comparatively rare disease, communicable to man from certain of the lower animals, such as sheep, oxen, horses, deer, and other herbivora. In animals it is characterised by symptoms of acute general poisoning, and, from the fact that it produces a marked enlargement of the spleen, is known in veterinary surgery as “splenic fever.”
Thebacillus anthracis(Fig. 27), the largest of the known pathogenic bacteria, occurs in groups or in chains made up of numerous bacilli, each bacillus measuring from 6 to 8 µ in length. The organisms are found in enormous numbers throughout the bodies of animals that have died of anthrax, and are readily recognised and cultivated. Sporulation only takes place outside the body, probably because free oxygen is necessary to theprocess. In the spore-free condition, the organisms are readily destroyed by ordinary germicides, and by the gastric juice. The spores, on the other hand, have a high degree of resistance. Not only do they remain viable in the dry state for long periods, even up to a year, but they survive boiling for five minutes, and must be subjected to dry heat at 140° C. for several hours before they are destroyed.