Angina

ANGINA (from Greek ancho—I strangle, I press), an ancient designation for diseases of the neck region (mouth, pharynx, larynx, and their surroundings) leading to obstructions in the acts of swallowing, breathing, and to a feeling of constriction in the indicated region. Later, the term Angina began to imply two kinds of suffering. Proper Angina (throat Angina)—a term firmly associated with inflammatory diseases of the throat (isthmus faucium) or deep cervical tissue (Ludwig's angina) of various etiologies, entailing more or less significant difficulties in swallowing and breathing. The detailed localization of such Anginas of an inflammatory nature can be different (uvulitis, amygdalitis, or tonsillitis); combinations with pharyngitis are not uncommon; the latter is nevertheless usually separated from Angina as such. The second, no less important category of Angina relates to the well-known symptom complex—Angina pectoris (see Angina pectoris), which lacks an inflammatory substrate and is localized in the neurovascular apparatus of the heart. Subjective sensations of heart constriction and angiospastic phenomena on the part of the heart vessels justify the use of the term Angina here as well. By Angina (throat) or quinsy, one understands an acute or chronic inflammation of the mucous membrane of the throat. Since the latter contains adenoid tissue in the form of clusters in the tonsils with a peculiar complex structure, the clinical picture and course of inflammatory processes are very diverse depending on the share of participation of one or another anatomical section of this lymphoid tissue. Inflammation can spread simultaneously to all parts of the mucosa and be diffuse in nature or can concern individual places and capture primarily the system of lymphoid tissue; thus, the surface of the tonsils or its lacunae can be affected independently; the parenchyma of the tonsils with the follicles embedded in it can be involved in the suffering, and then one can speak of amygdalitis or tonsillitis (A. tonsillaris). Angina can be a purely local suffering of various etiologies, but more often Angina is a symptom of a general, usually infectious disease. The most frequent pathogen is the streptococcus, less often the staphylococcus, pneumococcus, and Friedländer's diplobacillus. People of all ages get Angina; children are especially predisposed to it; it is undoubted that in some, the tendency to the disease is inherited, which can be considered an anomaly of the constitution of the organism. Among the acute forms of anginal diseases, three groups stand out that are most frequently encountered—catarrhal Angina, lacunar, and follicular; certain diseases of the throat during infectious contagious diseases should be assigned to a special group. Catarrhal Angina develops for the most part under the influence of thermal, chemical, and mechanical irritations, especially from a cold and from inhaling dust. The mucous membrane appears reddened, slightly swollen, moderately covered with mucus; with strong inflammation, pinpoint hemorrhages and edema of the uvula and palatine arches are observed, while the tonsils sometimes remain unaffected or only slightly redden. Subjective disorders boil down to a sensation of dryness, soreness, and moderate pain when swallowing; in small children, the temperature is often high. The disease lasts 2–3 days. If catarrhal quinsy is a companion of an infectious disease, it is accompanied by concomitant symptoms: with influenza—runny nose and cough; with scarlet fever—a fine-spotted rash on the body; the redness of the throat occupies the center of the soft palate and is delimited by very sharp edges, whereas with simple quinsy, the redness imperceptibly merges with the normal mucosa; with measles, the redness is observed not as diffuse, but spotted; it appears on the 2nd–3rd day. Acute lacunar Angina (see table to art. 159–160, fig. 1) is a disease of an infectious nature (cyclic course, appearance in the form of a family epidemic). On the reddened surface of the tonsil, whitish or yellowish spots of various sizes are discovered, which in the form of plugs fill the slits of the lacunae and consist of serous-fibrinous exudate with an admixture of epithelium, leukocytes, and microorganisms, most often streptococci. The tonsils become similar to a "starry sky" (Stromeyer), their parenchyma responds to irritation with swelling and an increase in volume. The disease begins and proceeds with high fever, in children up to 40° [Celsius], and is often accompanied by delirium and general malaise, ending in a crisis on the 3rd–4th day. The disease can easily be mistaken for punctate diphtheria, in which, however, the exudate usually first occupies the convex places around the lacunae and has a tendency to spread over the surrounding surface and merge into plaques. Lacunar Angina is accompanied for the most part by catarrhal changes in the throat mucosa. Follicular Angina (see table to art. 159–160, fig. 1), also an infectious disease, proceeds independently or joins lacunar Angina. Due to inflammation and suppuration of the follicles, a significant number of yellowish round, slightly elevated islets, the size of a pinhead, appear on the reddened surface of both tonsils; their eruption never goes beyond the boundaries of the tonsils. These islets are nothing other than suppurated follicular nodules, shining through the thinned mucosa. After 2–3 days, they open; in the contents, one finds for the most part streptococci. The disease often begins suddenly, with a formidable picture with chills and general malaise, pain when swallowing, in the limbs, in the back, headache; the temperature rises to 40° and more; from the swelling of the throat mucosa, the timbre of the voice takes on a special shade. The submandibular glands enlarge and are painful, as with an infectious disease; the spleen is for the most part palpable; the composition of the blood often changes. Sometimes with Angina, a sharp increase in the number of monocytes occurs in the blood (monocytic Angina). Since follicular Angina is a systemic disease, adenoid tissue in other organs is simultaneously affected (appendicitis); patients suffer from constipation or diarrhea; the nasopharyngeal and lingual tonsils become inflamed. The course of follicular Angina is stormy, symptoms increase rapidly, it lasts no more than one week, and the matter ends either in complete recovery or chronic tonsillitis. From severe complications with acute Anginas, manifestations of sepsis can be observed: myositis, synovitis, pleurisy, endocarditis, osteomyelitis, nephritis, otitis, pyemia, meningitis. In adults, the most frequent complication is phlegmonous Angina. Treatment of acute Anginas is limited to quiet confinement in bed and symptomatic means. Local application of compresses, disinfecting, softening, and astringent medicines, as well as swabbing, act only in the sense of alleviating pain and do not affect the course of the painful process itself. Also, anti-streptococcal and polyvalent sera do not have a noticeable abortive effect on purulent infection. With severe pain, narcotics taken internally and locally are useful. Anginal infection does not possess great volatility, but, being transmitted by the droplet method, requires caution against close contact with the sick. Phlegmonous Angina (see table to art. 159–160, fig. 3) develops in those cases when a suppurated follicle does not break through to the surface of the tonsil and the suppuration spreads to the tissue; infection can also get there from the slits and crypts, especially when the local resistance of the tissue is lowered, e.g., with chronic tonsillitis. Upon the end of acute Angina, the phlegmon is discovered by a new rise in temperature and the renewal of pain radiating to the ear, with swelling of the lateral wall of the throat; as the infiltrate increases, the pain grows, swallowing becomes impossible, the patient cannot open his mouth, his speech becomes indistinct, saliva flows from the mouth, the tongue is coated, the general condition is poor. The tonsil is pushed to the midline, the edematous uvula is shifted to the other side. Pathologically-anatomically, the matter boils down to purulent infiltration of the tissue adjacent to the lymphoid tissue of the tonsil, with the gradual formation of a limited abscess. Less often, the abscess develops in the tonsil itself. After 4–5 days, the abscess matures, and after the breakthrough of pus, all symptoms rapidly subside. In rarer cases, the spread of suppuration along the vascular bundle down the neck can occur, with subsequent septicopyemia. A severe complication of phlegmonous Angina is purulent erosion of the wall of the internal carotid artery with usually fatal hemorrhage. Treatment boils down to the timely opening of the abscess by an incision through the soft palate or through the fossa supratonsillaris. To accelerate suppuration, hot gargles and poultices are used. Aspirin improves the general condition. Close to phlegmonous Anginas is erysipelas (see) of the throat, which passes here from the face, with a picture of high fever, swelling of the glands, redness, and edema of the mucosa. Besides the described forms, a number of throat diseases are of great importance, in which a characteristic sign is the formation of ulcers, plaques, and films, usually as a local manifestation of one or another general infectious disease. This includes aphthous Angina (in children) with the formation on the soft palate and tonsils of small round superficial yellowish ulcers with sharp injected edges; it proceeds together with aphthous stomatitis, often with high fever.

Microscopically, in aphthae, one finds the picture of superficial fibrinous inflammation. Herpetic Angina: Groups of closely packed vesicles appear on the tonsil, which soon burst, coalesce, and leave behind an abrasion surrounded by a bright red background. The eruption is preceded by a 2-3 day fever; at the same time, herpes is present on the lips. The disease lasts 3-4 days with symptoms of acute angina. Simultaneously described by two authors—Plaut and Vincent (1894)—ulceromembranous Angina (Angina Vincenti), which in appearance is very similar to diphtheritic angina, is caused by a symbiosis of two types of microbes: specific spirilla and the fusiform bacillus of Vincent (Bacillus fusiformis), which are found in ulcers and plaques on the tonsils and in other places of the mucous membrane of the soft palate, tongue, throat, mouth, and larynx. The ulcers have a tendency to deepen; their edges are uneven and undermined; the base is covered with a whitish plaque, which is easily removed, and ulceration and decay are discovered underneath. The onset of the disease is accompanied by a slight temperature; local symptoms are weak and do not correspond to the objective picture—mild pain upon swallowing, slight swelling of the submandibular glands, and slight tenderness. There is a foul odor from the mouth and increased salivation. The course is chronic—lasting weeks and months; the disease sometimes ceases by itself. It most often affects the age group from 18 to 30 years. Contagiousness is weak. As complications after this form of Angina, eruptions of polymorphic erythema and the appearance of joint pains, and sometimes albuminuria and abscesses, have been observed. According to some authors (A. F. Ivanov), these complications depend on the addition of a streptococcal infection, especially in cases of extensive stomatitis and involvement of the tongue. Treatment is reduced to gargling, dusting with salvarsan, etc. Diphtheritic Angina, observed during diphtheria and caused by the Löffler bacillus, manifests in 4 types: catarrhal form, punctate form, membranous diphtheria, and septic diphtheritic Angina, whereby all forms can be observed sequentially in the same patient (see Diphtheria). For the diagnosis of diphtheritic Angina, a bacteriological examination of the mucus or plaque taken from the surface of the throat for the presence of the diphtheritic Löffler bacillus is necessary. Scarlatinal Angina (see Scarlet Fever). The clinical picture of Angina can be different. In mild cases, catarrhal angina is encountered, often with a good general condition; in others, follicular or lacunar Angina; in severe cases, diphtheritic or gangrenous. Similar acute Anginas are also encountered in other infectious diseases: in smallpox, typhus, and sometimes malignant lesions of the throat of an undefined character are observed. Chronic Angina is a very common disease; it can involve either the entire mucous membrane of the throat and proceed in the form of catarrhal pharyngitis, or manifest in the form of chronic tonsillitis, leading to hypertrophy of the tonsil. From a clinical point of view, it is necessary to distinguish two forms of tonsillar hypertrophy: the first is hypertrophy not accompanied by noticeable inflammatory changes on the surface of the tonsils and, in essence, not related to inflammation; it appears on the basis of a constitutional anomaly and hereditary predisposition, as well as after having suffered from diphtheria and scarlet fever. In this case, it is a matter of hyperplasia of all elements of the tonsillar tissue; the latter are enlarged, soft to the touch, and have a normal color. They often do not cause any painful signs and only cause discomfort due to their size (in children); they often decrease on their own after the removal of adenoids. The other form of hypertrophy—inflammatory—is more common in adults and is the result of repeated acute Angina. Such tonsils are usually of a dense consistency and have a non-smooth surface, pitted due to adhesions and scars, on which elevations alternate with depressions, crypts, and fissures; the tonsils either protrude from behind the palatine arches or are covered by them. Upon pressure, caseous masses—plugs with an unpleasant odor—or purulent secretion emerge from the dilated lacunae. The tonsils have a tendency toward exacerbation of the inflammatory process at the slightest provocation (habitual Angina) and cause a whole series of painful symptoms: an unpleasant taste in the mouth, cough, all kinds of paresthesias, earaches, runny nose, otitis, and enlargement of the cervical glands, which are hard and sensitive. Lacunar plugs lodged deep in the tonsils often serve as the cause of a number of severe diseases (arthritis, endocarditis, lymphadenitis, septicemia, glomerulonephritis, peritonsillar abscesses). Treatment for simple hypertrophy is, for the most part, not required; in the case of inflammatory hypertrophy, as a preventive measure, the plugs are squeezed out with special instruments, the tonsil is partially removed or extirpated entirely, and the crypts are cauterized with a galvanocautery. Syphilitic Angina in the secondary period manifests either in the form of erythema of the throat of a copper-red color (ham color) with sharply defined edges, or in the form of broad condylomata (plaques muqueuses), in the form of whitish spots of small size, representing a clouding of the epithelium and resembling spots from a silver nitrate solution. Angina leptothricia is associated with the keratinization of the lacunar squamous epithelium and the accumulation of a specific fungus, Leptothrix. Hard rods in the form of small hedgehog needles appear on the tonsils. Subjective disorders are absent. Treatment at the present time is unsuccessful. Agranulocytic Angina, first described in 1922, is characterized by a combination of necrotizing angina and the almost complete disappearance of granular leukocytes (granulocytes) from the blood (see Agranulocytosis), whereby the total number of white blood cells can fall to a few hundred per 1 cubic mm. The disease begins, for the most part, suddenly—with chills, a sharp rise in temperature, and sore throat, but can also have the character of a mild angina at the beginning. Ulcerations and necroses are not usually limited to the tonsils alone but spread to the palate, the inner surface of the lips, the gums, the larynx, and the trachea. The temperature reaches 40° and often has a septic character. The liver and spleen, as well as erythrocytes, do not present any characteristic changes. Sometimes hemorrhages into the skin, mucous membranes, and lungs are observed. Pathological-anatomical examination reveals numerous necrotic foci in various organs, but especially along the digestive tract. Neither in the bone marrow, nor at the border of the necrotic areas, nor in other parts of the organism is it possible to detect a single granulocyte (granular leukocyte). The duration of the disease ranges from 3-4 days to 3-4 weeks, averaging 14 days. Initially, the disease was considered absolutely fatal, but now individual cases of recovery are known; it affects, mainly, women; age is of no significance. The causative agent of the disease is unknown: in different cases, cultures revealed the presence of hemolytic streptococcus, pneumococcus, staphylococcus, etc. Therapy has not been precisely established: in individual cases, improvement was observed after neosalvarsan, protein therapy, and blood transfusions in large quantities.