COMA (grech, koma a deep sleep) — the most considerable extent of pathological braking a main line' ache a nervous system, characterized by a deep loss of consciousness, lack of reflexes on external irritations and disorder of regulation of the vital functions of an organism.
To. is the terrible complication of various diseases significantly worsening their forecast. At the same time the disturbances of life activity which are reflected in development To., are defined by a look and weight of the basic patol, process: in one cases they form very quickly and are patholologically irreversible (e.g., at a severe craniocereberal injury), in others — these disturbances have nek-ry staging in the development and the possibility of partial or their full elimination at timely and adequate therapy remains. The last circumstance defined a wedge, the relation to To. as to an acute patol, the state demanding emergency treatment at perhaps earlier stages. Therefore practically the diagnosis To. is established not only in the presence of the full symptom complex characterizing To., but also at symptoms of less expressed oppression of c. N of page, napr, at a loss of consciousness with preservation of reflexes if they are regarded as a stage of development of a coma. Thus, the wedge, the maintenance of the concept «coma» not always matches its definition. This concept reflects only the deepest extent of braking of c in traditional sense. the N of page, edge is differentiated with other its degrees — an oglushennost (see. Devocalization ), a stupor (see. Struporous states ), a sopor (see. Devocalization ), and also with various disorders of consciousness, including with a delirium (see. Delirious syndrome ), apallichesky syndrome (see), akinetic mutism, lethargy (see), etc. The clinical diagnosis To. is based on understanding of the general patterns of its development, and also on knowledge of basic diseases and patol, processes which in the current can become complicated To. (e.g., diabetes mellitus, uraemia, poisoning with hypnotic drugs). Ambiguity terminological and a wedge, the maintenance of the concept «coma» is shown that the diagnosis To. usually it is not put if it makes only a part of manifestations of another terrible patol, states. So, carried to To. disturbances of consciousness at terminal states (see), at different types of shock, in particular at acute anaphylaxis (see) as a result of postvaccinal complications, are not considered as independent patol, states as, e.g., To. at a diabetes mellitus.
- 1 The AETIOLOGY
- 2 PATHOGENY AND PATHOLOGICAL ANATOMY
- 3 The GENERAL SYMPTOMATOLOGY AND the CURRENT
- 4 The DIAGNOSIS
- 5 TREATMENT AND the FORECAST
- 6 SEPARATE TYPES of the COMA
- 6.1 The alcoholic coma
- 6.2 The hypoglycemic coma
- 6.3 The hypoglycemic coma
- 6.4 The Gipokortikoidny coma
- 6.5 the Hypothyroid coma
- 6.6 A hungry coma
- 6.7 The diabetic coma
- 6.8 A coma at diseases of a nervous system
- 6.9 The hepatic coma
- 6.10 A respiratory coma
- 6.11 The Hlorgidropenichesky coma
- 6.12 The Atsetonemichesky coma at children
- 7 Table 1. The short characteristic of main types of a coma and acute management at them
- 8 Table 2. The main clinical and biochemical differential diagnostic characters of comas at patients with a diabetes mellitus
Diseases which can become complicated To., are diverse. Division according to an etiology (1950, 1962) includes more than 30 types in N. K. Bogolepov's classifications To., from which a part belongs not to individual diseases, and to groups of diseases or syndromes. It is possible to believe, however, that a proximate cause To., except To. at primary pathology of c. the N of page, is not a basic disease, a current to-rogo not necessarily becomes complicated To., and the related certain frustration biochemical, a homeostasis, a hemodynamics or others patol, the processes in an organism breaking normal activity of a brain. In this sense an etiology To. is defined by features of a current of a basic disease and matches initial links of a pathogeny most To.
Conditional systematization To. it can be by origin presented by their following division.
1. To., caused by primary defeat, a disease of c. N of page, or neurologic coma. Carry to this group apoplectic To. (at strokes), apoplektiformny To., epileptic To., traumatic To. (at a craniocereberal injury) and To. at inflammations and tumors of a brain and its covers.
2. To. at endocrine diseases, caused by disturbance of metabolism owing to insufficient synthesis of hormones (diabetic To., gipokortikoidny To., hypothyroid To., hypopituitary To.), their excess products or overdose to lay down. hormonal drugs (thyrocardiac To., hypoglycemic To.).
3. To., initially connected with loss of electrolytes, water and power substances. From them have independent value hlorgidropenichesky To., developing at patients with persistent vomiting, in particular at a pyloric stenosis, and alimentary and dystrophic, or hungry, To.
4. To., caused by disturbance of gas exchange. Main types To. this group are: a) hypoxemic To., connected with insufficient intake of oxygen from the outside (a hypobaric anoxemia, a suffocation) or with disturbance of transport of oxygen blood at anemia, heavy acute circulatory disturbances; b) respiratory To. (respiratory and cerebral, respiratory atsidoticheskaya), or To. at respiratory insufficiency, caused by a hypoxia, a hypercapnia and acidosis owing to considerable disturbances of gas exchange in lungs.
5. Toxic To., connected with endogenous intoxication at toxicoinfections, various inf. diseases, pancreatitis, a hepatic unsufficiency and kidneys (hepatic To., uraemic To.) or with influence of exogenous poisons (To. at poisoning with organophosphorous connections, alcoholic To., barbituric and other pharmakotoksichesky To., etc.).
Such division To. reflects the value only conducting, prevailing separate patol, processes in an etiology To. and partially orients in accessory of some types To. to competence of certain medical specialties. However not always the leading reason To. it is possible to carry unambiguously to any of listed etiol, factors. So, reckoning so-called thermal is doubtful To. (at excessive overheating of a body) to neurologic. Besides, secondary defeats of c. the N of page causing To. at diseases of internals, can become more considerable, than all other manifestations of a basic disease, napr, at eclamptic To.
PATHOGENY AND PATHOLOGICAL ANATOMY
Pathogeny. The comas different in an etiology, usually have distinctions and in a pathogeny. The general for a pathogeny of all types To. communication of its development with dysfunction of bark of cerebral hemispheres, subcrustal educations and a brainstem is that leads to disorders of consciousness. Special value has defeat of a reticular formation of a brainstem with loss of its activating influence on bark of big hemispheres, disorder of reflex activity of a trunk and oppression of the vital vegetative centers. In an origin of these disturbances the following pathogenetic factors can have major importance.
1. Disturbances of cellular respiration and exchange of energy in a brain. In their basis there can be an anoxemia, anemia, frustration of cerebral circulation with a secondary cellular hypoxia; blockade of respiratory enzymes cytotoxic poisons; acidosis (at respiratory, diabetic, uraemic and some other types To.); deficit of power substances or blockade of their utilization (at alimentary and dystrophic To., hypoglycemic To.). Practically at all types To. in development of a hypoxia of a brain disorders of microcirculation are of great importance. Owing to a hypoxia in cells of a brain processes of oxidizing phosphorylation are broken, maintenance and use of ATP and phosphocreatinine decreases, the quantity of ADF, milk to - you and ammonia increases.
2. Balance upsets of electrolytes with change of cellular potentials and processes of polarization of membranes of neurocytes, and also with disturbance of the osmotic relations in cellular and intercellular spaces. Disorders of exchange of potassium, sodium, magnesium and calcium usually in combination with disturbance of acid-base equilibrium which play a role in development diabetic, hepatic, uraemic, hlorgidropenichesky and some other types To have the greatest value.
3. Disturbances of education and allocation of mediators in synapses of c. N of page. In their basis there can be hormonal frustration at endocrine diseases, and also disturbances of exchange of amino acids, napr, at hepatic To., and secondary insufficiency of cellular enzymes and ATP at a hypoxia and influence of cellular poisons.
4. Changes of physical properties and structure of a brain and intracranial .obrazovaniye. Swelling and wet brain and a meninx have pathogenetic value, increase in intracranial pressure which strengthen disturbances of haemo-circulation and a likvorodinamika activities aggravate a hypoxia of nervous cells and their oppression fiziol. The bruise of cells of a brain plays a role in development To. at a craniocereberal injury, hematencephalons, tumoral processes in a head cavity.
Each of the listed pathogenetic factors at separate types To. can have the leading value, but at many To. these factors work jointly and are interdependent. At deep To. disorders of regulation of vegetative functions usually lead to additional heavy disturbances of metabolism in an organism, including in a brain, and create «vicious circle» in a pathogeny To.
Pathoanatomical data at To. are not specific, they are a little expressed in comparison with the prevailing signs of a basic disease and hl come to light. obr. in a brain.
Macroscopically swelling of a brain, sometimes sites of «enlightenment» in bark, small hemorrhages and ochazhka of a softening are defined. Microscopically find disturbances in a microcircular bed: a trichangiectasia with stazy blood in them, plasmatic treatment and necrobiotic changes of vascular walls, perivascular hypostasis, dot hemorrhages. Changes in; cells of a brain correspond to the changes revealed at acute hypoxias (see). In neurocytes — signs of acute swelling, dystrophic changes, a cytolysis. Glybchaty intracellular inclusions, pycnosis, a hyperchromatosis, a chromatolysis at reduction of number of ribosomes and the raised vacuolation of protoplasm are defined. Glial cells dystrophic are changed * in some cases proliferation of an oligodendrogliya comes to light.
These changes have various degree - expressivenesses depending on a look To. and duration of coma are also combined with the changes caused by a basic disease.
At To., connected with primary disease of c. the N of page, in a brain is found a picture of the basic patol, process — inflammatory, tumoral, traumatic or characteristic of a stroke.
At eclamptic To. signs of swelling of a brain, increase in liquid in subarachnoid space, expansion of perivascular spaces with dot hemorrhages prevail. Same morfol, the picture is observed at uraemic To., edges it is characterized by also more expressed hypostasis of a meninx, an uneven krovenapolneniye of a brain, change of cells of bark of big hemispheres and a cerebellum with a chromatolysis (generally in IV and in the V layers of brain bark), vacuolation, pycnosis, dystrophic changes.
The changes found in a brain at hepatic To., to some extent depend on features of development of a liver failure. At its acute development of change have diffusion character; microcirculator disorders, signs of swelling and wet brain and meninx prevail. At subacute and hron, a current cellular changes with preferential localization in gray matter of bark, in a striate body and a cerebellum prevail that reminds morfol, a picture of hepatolenticular dystrophy (see. Hepatocerebral dystrophy ).
An originality morfol, changes at separate types To. does not reach value of specific manifestations. Therefore the posthumous conclusion about the nature To. the wedge, data is based on set morfol, signs of a basic disease with the obligatory account.
The GENERAL SYMPTOMATOLOGY AND the CURRENT
Development To. can be very bystry, almost instant, or gradual — within several hours or days.
Bystry development is possible at To. to any etiology, but a thicket it is observed at epilepsy, a hypoglycemia, a craniocereberal injury, strokes. The patient suddenly faints and the next minutes or hours all signs of deep K. Otmechayetsya the noisy, often stertorozny (snoring) breath, breath like Cheyn — Stokes develop (see. Cheyna — Stokes breath ) and other types of disorder of breath, fluctuation of the ABP with a tendency to decrease, an anizovazotoniya (especially at nevrol. To.), various disturbances of a rhythm and rate of cordial reductions, disorders of functions of pelvic bodies.
Slow development To. includes the period of a prekomatozny state with gradual deepening of disorders of consciousness and oppression of reflex reactions. In the beginning slackness of mental processes, sometimes the periods of mental and motive excitement is observed, the drowsiness which is replaced by hibernation then a soporous state develops. The patient wakens only under the influence of strong sound or pain stimulations for a short time, does not answer questions or answers in monosyllables, indistinctly, often incorrectly. In the period of a sopor of the patient can swallow of water and liquid food, independently turns in a bed. Upon transition of a soporous state in coma with its subsequent deepening pog reflexes on all types of irritations are sedately lost, decrease or lack of reaction of pupils to light, then loss of corneal and gag reflexes is noted, disturbances of vegetative functions and change on EEG progress.
N. K. Bogolepov (1963) on weight of coma distinguishes 4 degrees To.: easy, expressed, deep and terminal, or «ultraboundary».
The first degree To. it is characterized by loss of consciousness and reactions of patients to strong irritants, but psychomotor avtomatizm, unconscious coordinate gesticulations come to light; pupillary, corneal and gag reflexes are kept, skin — are lowered or are absent, tendinous — are raised or reduced. The dispersing squint and the pendulum movements of eyeglobes are defined. On EEG — moderate diffusion disturbances in the form of irregular alpha activity, low-amplitude slow activity and emergence of a so-called bezdominantny curve.
The second degree To. corresponds to deeper braking of bark and a subcortex with counterinhibition of trunk and spinal avtomatizm. The spontaneous movements become less difficult and less coordinate. The pupillary test on light dies away, pupils are often narrowed. Corneal and gag reflexes are kept. Cutaneous reflexes are absent, pyramidal reflexes come to light (see. Reflexes pathological ), protective reflexes (see), gormetoniya (see) and muscular dystonia. Tachypnea, stertorozny breath, various disturbances of a respiratory rhythm are noted. On EEG — the alpha rhythm is absent, slow activity dominates, paroxysmal flashes of slow or acute waves with their dominance in front departments of parencephalons are bilateralno registered.
The third degree To. it is characterized by switching off of functions of a mesencephalon and the bridge of a brain. Pupils are usually narrowed, do not react to light, corneal reflexes are absent, hypotonia of circular muscles of an eye, diffusion decrease in tendon jerks and a tone of skeletal muscles is noted. Decrease body temperature and the ABP, breath is broken, cyanosis is often expressed. On EEG — diffusion slow activity of low amplitude, the periods of «bioelectric silence».
The fourth degree To. differs in deep disturbance of functions of a myelencephalon with the termination of spontaneous breath and the progressing decrease in the ABP. The bilateral mydriasis and full areflexia is defined. On EEG signs of bioelectric activity are absent. Life of the patient is supported only special to lay down. actions. At long artificial ventilation of the lungs emergence of signs of reflex activity of a spinal cord is possible.
The given degrees To. treat the periods of its development, the corresponding deep disorders of consciousness. For early diagnosis To. as patol, states a wedge, allocation of the periods of a prekoma matters. It is for this purpose reasonable to distinguish 4 stages of development To., from which the first two correspond to a prekoma:
The I stage — mental concern, drowsiness in the afternoon at excitement at night; a lack of coordination of conscious movements, initial changes on EEG.
The II stage — a somnolention with sharp braking of reactions to strong irritants, including painful; increase, then weakening of tendon jerks; changes of EEG correspond described for the first and second degrees To.
The III stage — a deep sleep; patients do not come into contact, however painful sensitivity at some patients is kept; muscular dystonia, spastic reductions of separate groups of muscles are observed; the urination and defecation are involuntary; the expressed changes of EEG.
The IV stage — deep To. with a full areflexia, heavy disorders of vegetative functions; sharp easing of bioelectric activity on EEG.
During the escaping of coma under influence to lay down. actions gradual recovery of functions of c is observed. N of page usually as it should be, the return to their oppression. In the beginning corneal, then pupillary reflexes are recovered, extent of vegetative frustration decreases. Recovery of consciousness takes place stages of the confused consciousness, oglushennost, the nonsense and hallucinations are sometimes noted. Quite often during escaping To. the sharp motive concern with the chaotic dicoordinated movements against the background of the deafened state is observed. At patients with hypoglycemic To. and at some other its types during the escaping To. convulsive attacks with the subsequent twilight condition of consciousness are possible.
At developed a wedge, a picture K. the diagnosis is not difficult. Timely recognition of a prekomatozny state is more difficult that requires special attention to little changes of mentality, behavior and frustration of a dream at patients with diseases which course can become complicated To. — at a diabetes mellitus, insufficiency of adrenal glands, acute and hron, hepatitis, uraemia, toxicosis of the second half of pregnancy, respiratory insufficiency, poisonings, etc.
The differential diagnosis between To. a different origin, their wedge, manifestations and in connection with frequent impossibility of obtaining anamnestic data is very difficult because of a community. To the correct recognition etiol, option K. promote poll of the relatives and persons surrounding the patient, the accounting of features of a current To., and also identification of objective symptoms of a basic disease.
Poll can supply with the information on earlier established diagnosis of a disease or its signs (changes of appetite, thirst, existence of vomiting or diarrhea, convulsive attacks, etc.); about the first manifestations To., speed of its development.
At survey pay attention to outward of the patient, a condition of skin and hypodermic cellulose, the nature of breath, and also to a pose, edges can have features at patients with meningitis (an opisthotonos, the bent position of legs), with wet brain, in particular at uraemia (edgewise position with the bent and given legs), with defeat of one of parencephalons at a stroke (asymmetry of the person, position of a body and activity of extremities). Sharp weight loss, cachexia allow to suspect hron, a debilitating disease of internals, damage of a hypophysis, a thyrotoxicosis. Patients with a diabetes mellitus, alcoholism can have an obesity, and also is frequent at patients with apoplectic To. Hypostases, their distribution and character allow to suspect an eclampsia, diseases of kidneys and heart. Discolorations of skin help recognition hepatic To. (intensive jaundice), anemic and hemolitic To. (sharp pallor or pale yellow coloring), poisonings with carbon monoxide (pink coloring). The expressed xeroderma and mucous membranes is characteristic for diabetic and uraemic To. For hypoglycemic To. excess perspiration is characteristic, edges happens also at a hypercapnia, a thyrotoxicosis.
Stertorozny breath is more often observed at apoplectic and eclamptic To., kussmaulevsky breath at a diabetes mellitus. The same changes of breath are possible at uraemic and hepatic To. Diagnostic value has establishment of an unusual smell in expired air: acetone or rotten apples — at diabetic To., alcohol — at alcoholic To., urine — at uraemic To., «crude meat» — at hepatic To.
High temperature of a body is noted at infectious and toxic, thyrocardiac, apoplectic To. also excludes hypothyroid To., proceeding with a hypothermia. Decrease in body temperature is peculiar to many types To., it is often observed at gipokortikoidny, diabetic, charcoal To.
Increase in the ABP happens at apoplectic, eclamptic, uraemic To. and at poisonings with nicotine, organophosphorous connections. Falloff of the ABP with a collapse is characteristic for gipokortikoidny and hypothyroid To., it is observed also at diabetic, hlorgidropenichesky, barbituric, many toxic To. Unconsciousness at a collapse of not clear genesis obliges to an electrocardiographic research for an exception apoplektiformny To. at a myocardial infarction.
The polyuria is inherent diabetic To. also demands an obligatory research of urine on sugar and acetone. The oliguria and an anury in the absence of a collapse indicate damage of kidneys in connection with poisoning or a disease (eclamptic To; uraemic To.).
Nevrol, inspection facilitates diagnosis at To., the c caused by primary defeat. N of page if characteristic symptoms of focal disturbances or symptoms of defeat of covers of a brain come to light.
To specification of the diagnosis To. the lab promotes purposeful., rentgenol. and tool inspection of the patient using an electroencephalography, an ekhoentsefalografiya, biochemical, blood analyses, urine, cerebrospinal liquid, etc.
TREATMENT AND the FORECAST
Treatment To. in each case is defined by its etiology and a pathogeny. Nek-raya a community of pathogenetic mechanisms at different types To. causes for part of them and the community to lay down. actions. At any kind To. hospitalization is necessary. At To. ekzo-and endotoxic genesis it is carried out disintoxication therapy (see), including an osmotic diuresis, if necessary substitution of blood, a haemo sorption detoxication, peritoneal dialysis (see) or hemodialysis (see) by means of the device an artificial kidney (see). For the purpose of reduction of brain swelling, hypostasis of covers and decrease in likvorny hypertensia dehydrational therapy is carried out (see. Swelled also swelling of a brain ), in some cases it is made spinal puncture (see). At the majority To. it is shown oxygen therapy (see), and at some of them, napr, at hepatic To., an oxygenobarotherapy (see. Hyperbaric oxygenation ).
At many To. events for correction of balance upsets of electrolytes and acid-base equilibrium are held, symptomatic therapy of disorders of vegetative functions is performed (purpose of respiratory analeptics, cardiac glycosides, corticosteroid hormones etc.).
The forecast is defined by degree, character and a current of a basic disease, and also terms of the correct recognition To. and beginnings of pathogenetic therapy. To. at extensive primary damages of a brain, at uraemia, the progressing liver failure, and also at poisonings with nek-ry poisons differ in the bad forecast. It is more favorable at alcoholic, diabetic, hypoglycemic and some other types To., if adequate treatment, especially at early stages of development is carried out To. At some To., napr, at epileptic and To. at some poisonings, consciousness and other functions of c. N of page can be recovered without treatment when the pathogenic factor is terminated. The forecast at deep To. it is always heavier, than at To. easy degree. After escaping To., proceeding several days, residual changes of mentality and nevrol, the status are possible.
SEPARATE TYPES of the COMA
the Main a wedge, signs I also am urgent therapy of separate types To. are briefly presented in tab. 1, e.g. To. at poisonings with hypnotic drugs, drugs, organophosphorous connections and other poisons. Row K. it is described in separate articles: hyper thermal To. — see. Thermal shock ; hypopituitary To. — see. Shikhena syndrome ; malarial To. — see. Malaria ; pernicious and anemic To. — see. Pernicious anemia ; thyrocardiac To. — see. Thyrotoxicosis ; traumatic To. — see. Craniocereberal injury ; charcoal To. — see. Carbon monoxide ; uraemic To. — see. Uraemia ; eclamptic To. — see. Eclampsia . Below separate types are stated To., often meeting in a wedge, practice and the presenting diagnostic and therapeutic difficulties.
The alcoholic coma
the Alcoholic coma (poisoning with ethyl alcohol) is observed at considerable intoxication by alcohol (usually after a single dose more than 200 ml in terms of 96% alcohol) and is caused by preferential direct effect of alcohol on the central nervous system, and also toxic damage of other systems and development of acidosis.
To emergence To. excitement and other signs precede alcoholic intoxication (see); the epileptiform attack is sometimes observed. The person and conjunctivas are hyperemic in the beginning, vessels of scleras are injected, pulse is intense, repeated vomiting is observed; the emetic masses and expired air with a pungent smell of alcohol. In the subsequent skin becomes pale with a grayish and cyanochroic shade, cyanosis of the person and extremities can prevail. The cold clammy sweat is noted. Hypothermia. Shallow breathing. Pulse becomes frequent, becomes small; By the ABP it is lowered. Involuntary otkhozhdeniye of urine and calla. Pupils are narrowed, but at increase of respiratory frustration extend, the horizontal nystagmus comes to light. Spasms are sometimes observed. Aspiration of emetic masses with symptoms of mechanical asphyxia is possible.
Diagnosis alcoholic To. in typical cases it is not difficult, but demands a careful exception of other possible reasons To., which could accompany intoxication, first of all a craniocereberal injury, acute frustration of cerebral circulation, a myocardial infarction, and also poisoning with other poisons. Therefore at alcoholic To. expanded examination, including use rentgenol, methods, an ekhoentsefalografiya, an electrocardiography, a research of a sugar content and alcohol in blood is conducted.
Treatment. The urgent gastric lavage via the probe with the subsequent introduction to a stomach of 100 — 150 ml of 30% of solution of sodium sulfate or magnesium sulfate is necessary; intravenously kapelno 1000 ml, 5% of solution of glucose, from 300 to 800 ml of 4% of solution of hydrosodium carbonate under control of pH are entered (see. Hydrogen ion exponent ). At the same time enter lasixum (40 — 80 mg) or osmotic diuretics (30% solution of urea or 10% solution of a mannitol at the rate of 1 g of osmotically active agent on 1 kg of weight of the patient). After administration of osmotic diuretics administration of isotonic solutions of electrolytes continues.
Also symptomatic therapy — introduction of respiratory analeptics and vasoactive means — Cordiaminum on 2 ml each 3 hours, 10% of solution of caffeine-sodium benzoate on 2 ml according to indications, and also cocarboxylase (100 mg), B6 vitamin (2 ml of 5% of solution), nicotinic to - you is carried out (1 ml of 1% of solution). The oral cavity is often washed out, its contents are sucked away for the prevention of aspiration.
The hypoglycemic coma
the Hypoglycemic coma arises at the heavy course of hemolitic crisis at patients with hemolitic anemia, is more often at autoimmune and its toxic forms (see. Hemolitic anemia ). In a pathogeny To. the changes of composition of blood leading to a gemichesky hypoxia of a brain, and disturbance of cerebral circulation in connection with dystonia and thrombosis in a microcirculator bed play a role.
To development To. progressively accruing jaundice, a headache, often high temperature («hemoglobinuric fever»), the expressed short wind, muscle pains, a collapse precede. Skin of patients pale yellow with an olive shade, the Crocq's disease is sometimes expressed. Breath frequent. The ABP it is more often reduced, but maybe high, napr, at patients with an idiopathic hypertensia with the hemolysis caused by reception Methyldopa. Tachycardia. The repeated plentiful cholemesis is quite often noted. The diuresis is reduced; department of dark urine is characteristic, the urobilinuria is expressed; the anury with the subsequent azotemia is possible. Kloniko-tonic spasms are often observed. In blood define hypochromia, particles of the broken-up erythrocytes (schizocytes), substantial increase in plasma of not conjugated («indirect») bilirubin and free hemoglobin are more rare normokhromny anemia with decrease in erythrocytes to 1 000 000 and less in 1 mkl; the neutrophylic hyperleukocytosis with shift of a formula is often noted to the left. The picture of blood and a developmental character of a disease help the correct recognition of the nature To. and to its differentiation with hepatic To.
Treatment. Make transfusion of erythroweight, the washed erythrocytes (transfusion is fresher than blood and hemolysis can strengthen plasmas), in need of picked up for Koombs's test. The dose of the transfusion environment (from 200 to 500 ml) is defined by degree and speed of decrease in hemoglobin in blood. Intravenously enter reopoliglyukin, heparin. Other actions are defined by the specified diagnosis of a form of hemolitic anemia therefore are appointed only together with the hematologist or are held in gematol, department. Purpose of glucocorticoids is effective only at autoimmune hemolitic anemia. At an anury with the expressed hyperpotassemia it is shown hemodialysis (see) by means of the device artificial kidney (see).
The hypoglycemic coma
the Hypoglycemic coma can be manifestation insulomas (see), a diffusion hyperplasia of beta cells of a pancreas, diseases which are characterized by relative hyper dysinsulinism (see), but it is most often observed at patients with a diabetes mellitus at excess administration of insulin by it (insulin To.) or sugar-lowering sulfanamide drugs (especially in combination with salicylates, Etioniamidum) against the background of insufficient consumption of carbohydrates. To emergence hypoglycemic To. at patients with a diabetes mellitus alcoholism, existence of renal or heart failure, and also an intensive muscular exercise promote. In a pathogeny hypoglycemic To. major importance has decrease in utilization of glucose cells of a brain for which activity glucose is the main power source.
Hypoglycemic To. can develop almost suddenly. The thicket to it is preceded by other manifestations hypoglycemia (see) — considerable weakness, feeling of hunger, pallor of skin, cold sweat, a tremor of extremities, and just before development To. — the disturbances of mentality reminding alcoholic intoxication. The beginning To. it is shown by motive excitement, emergence of clonic and tonic spasms, the oglushennost which is quickly passing into a sopor. Vegetative frustration in the form of sharp perspiration, tachycardia, trembling are characteristic.
At assessment a wedge, manifestations hypoglycemic To. at patients with a diabetes mellitus it is necessary to carry out the differential diagnosis with diabetic To.
Unlike diabetic ketonemichesky To., at a hypoglycemic coma of the ABP, the tone of eyeglobes and skeletal muscles are normal or raised; the smell of acetone is absent; sugar of blood is lowered, there is no ketosis, except for a rare form of the hypoglycemia with a ketosis which is observed at children of early age. Hypoglycemic To. can be complicated by disturbance of cerebral circulation.
Treatment consists in bystry intravenous administration of 40 — 80 ml of 40% of solution of glucose (if necessary repeated) and hypodermic introduction of 0,5 — 1 ml of 0,1% of solution of adrenaline.
The Gipokortikoidny coma
Gipokortikoidnaya of a lump (adrenal To.) arises owing to both acute, and aggravations hron, adrenal insufficiency with falloff of products glyuko-and mineralokortikoid. It is observed at bilateral adrenalectomies (see), hemorrhage in adrenal glands, Waterhouse's syndrome — Frideriksena (see. Adrenal glands ), at addisonovy disease (see) against the background of intercurrent infections, intoxications, stressful situations, and also at the sudden termination of long glucocorticoid therapy.
To development To. prostration, pernicious vomiting, quite often abdominal pains, symptoms of the accruing dehydration, sometimes clonic spasms precede. During the period To., except spasms, the Meningeal syndrome can develop, in the presence to-rogo the differential diagnosis with is carried out To. at meningitis (see). Patients are dehydrated. At To. at patients with an addisonovy disease symptoms of dehydration often are defined against the background of considerable weight loss, the xanthopathy is expressed. Language dry. The smell of acetone from a mouth is sometimes noted. Often tachycardia (but also bradycardia is possible); low threadlike pulse. Sharply expressed hypotonia of muscles and arterial hypotension are characteristic. At a lab. researches the Hyponatremia, a hyperpotassemia, a hypoglycemia, increase in residual nitrogen and urea of blood, low content in blood of cortisol and Aldosteronum at falloff of secretion of Aldosteronum decide and 17 oxycorticosteroids on urine, gipernatriyuriya and gipokaliyuriya. Are often observed a moderate leukocytosis with an eosinophilia and the accelerated ROE.
Treatment. Make one-time parenteral administration of 125 mg of a hydrocortisone (to children at the rate of 5 mg on 1 kg of body weight) or 60 mg of Prednisolonum (to children at the rate of 1 — 2 mg on 1 kg of body weight) with the subsequent drop introduction to a vein of 5% of solution of glucose and isotonic solution of sodium chloride with a total amount up to 2000 — 3000 ml a day with addition of a hydrocortisone to 300 — 600 mg or Prednisolonum to 200 mg a day, and also noradrenaline in the presence of the collapse which is not eliminated by glucocorticoids. After introduction of the first 800 — 1000 ml of isotonic solutions 10 — 20 ml of 10% of solution of sodium chloride can be intravenously in addition entered. Intramusculary enter 4 ml of 0,5% of oil solution of cortexone (children of 0,5 — 2 ml), injections to-rogo on 1 — 2 ml are repeated by each 6 — 8 hours
the Hypothyroid coma
the Hypothyroid coma is result of sharply expressed deficit in an organism of thyroid hormones owing to hypothyroidism (see). It is observed extremely seldom, usually at elderly patients with a myxedema. To emergence To. cooling, an injury, intercurrent, especially inf promote. diseases, use of drugs, the oppressing c. N of page.
In pathogeny To. major importance have decrease in exchange processes in a brain and the hypoxia of a brain caused by pulmonary hypoventilation with a secondary anoxemia, often observed hypochromia anemia, delay of a brain blood-groove.
Usually To. develops slowly, body temperature gradually decreases, the confused consciousness periodically clears up in the beginning, then is replaced by an oglushennost; spasms are quite often observed (at the expense of a hyper carotenemia). Skin is pale, rough, dry, cold; sometimes easy yellowness. The person odutlovato, puffiness the century, hypodermic hypostasis on brushes and shins often come to light; on places of hypostases of manual impressions it is not possible to receive.
Shallow breathing, usually rare. Sharply expressed bradycardia and arterial hypotension are noted. The most characteristic symptom is the considerable hypothermia — body temperature can be lower than 30 ° (at development To. against the background of inf. process the hyperthermia is possible). The diagnosis is confirmed by definition of thyroid hormones in blood which level is sharply reduced. The hypercholesterolemia is characteristic.
Treatment. Via the probe each 12 hours to fervescence and increase in pulse rate, then on 20 — 50 mkg each 12 hours before permanent improvement of a condition of the patient enter 100 mkg of triiodothyronine. Once enter 100 mg of a hydrocortisone; in the subsequent kapelno intravenously for 5% solution of glucose or isotonic solution of sodium chloride (500 — 1000 ml a day) in addition enter Prednisolonum to 100 mg a day or a hydrocortisone to 300 mg a day. Symptomatic therapy is carried out. Artificial warming of a body is not shown.
A hungry coma
the Hungry coma (alimentary and dystrophic To.) it is observed at a part of patients with nutritional dystrophy (see) the III degrees, edges in peace time meets very seldom.
In pathogeny hungry To. the leading role is played by sharp deficit in an organism of proteins, power substances and vitamins, owing to-rogo the atrophy and funkts, insufficiency practically of all bodies, including hemadens develops; enzymatic activity is oppressed, heat production decreases. In a brain oxidation-reduction processes and water and electrolytic exchange are broken, interneural mediator function is oppressed. To development To. intoxication connected with the increased disintegration of fabrics and a cellular hypoxia owing to reduction of speed of a blood-groove and quite often observed anemia promote.
Hungry To. arises at long proteinaceous starvation, is more often at young faces of an asthenic constitution in cold season. Usually its development is preceded by faints which can be against the background of rather satisfactory condition; transition from a condition of a faint in To. it is made quickly. At inspection of the patient pallor of skin, a cachexia with an atrophy of a hypodermic fatty layer and muscles are observed. Spasms of tetanic type are periodically noted. The urination and defecation are involuntary, breath superficial, is frequent bradipnoe. Body temperature is reduced to 35 ° below. Arterial hypotension is in most cases noted, the number of cordial reductions is not changed, but bradycardia is possible as tachycardia with small, sometimes threadlike pulse, and. Cardiac sounds are more often muffled. On an ECG falloff of a voltage of a tooth of P and decrease in a segment of ST is noted, often with the two-phase or negative stretched T. V tooth of blood define leykotsitopeniya), the thrombocytopenia which is sharply expressed to a hypoproteinemia) and hypochilesterinemias). Concentration of sugar in blood is reduced, is sometimes considerable — to 40 — 50 mg of %, but a wedge, manifestations of a hypoglycemia are not expressed.
Differential diagnosis with hypopituitary To. the hl is based. obr. on data on development of a disease.
Treatment includes warming of the patient with warm hot-water bottles, introduction of 125 — 250 mg of a hydrocortisone or 30 — 60 mg of Prednisolonum, intravenous jet administration of 30 — 40 ml of 40% of solution of glucose every 2 — 3 hour (at repeated injections add insulin on 3 — 4 PIECES) or its drop introduction together with proteinaceous hydrolyzates (see) — solutions of Hydrolysinum or Aminopeptidum (see) which originally enter in number of 750 — 1000 ml with a speed of 20 — 30 thaws of 1 min., and in the subsequent increase a daily dose to 1500 — 2000 ml. Parenteral administration of 100 — 200 mg of cocarboxylase, ascorbic to - you and a pyridoxine on 100 — 200 mg is shown. For treatment hungry To. in besieged Leningrad applied also intravenous administration of alcohol (33% — 10 ml). In the presence of spasms intravenously enter 10 ml of 10% of solution of calcium chloride; according to indications other symptomatic therapy is carried out.
The diabetic coma
the Diabetic coma is caused by absolute deficit in an organism of patients with a diabetes mellitus of insulin. It is observed at untimely diagnosis of diabetes and at its decompensation (see. diabetes mellitus ).
Pathogeny diabetic To. it is studied only partially, but the important role in its development is established to a hyperglycemia, disturbances of acid-base equilibrium, balance of electrolytes in an organism and osmotic properties of extracellular liquid. According to already known leading links of a pathogeny To. at patients with a diabetes mellitus it is possible to allocate three main its pathogenetic options: 1) giperketonemicheskiya, 2) giperosmolyarny and 3) giperlaktatsidemicheskiya. Some authors allocate also option so-called brain To., which is caused by wet brain at patients with diabetes owing to uneven change of osmolarity of cells of a brain and a blood plasma at decrease in a glycemia under the influence of insulin.
Actually diabetic To. call usually giperketonemichesky hyper glycemic coma since in genesis giperlaktatsidemichesky To. the hypoxia caused by associated diseases, and giperosmolyarny is of great importance To. it is observed at special patol, states and at patients without diabetes. At the same time the overwhelming frequency of development of these types To. at patients with a diabetes mellitus does reasonable their consideration together with typical for diabetes giperketonemichesky To., since the differential diagnosis between them is carried out by hl. obr. at To. at patients with a diabetes mellitus.
1. Giperketonemichesky giperglikemicheskayakoma develops in connection with disturbance of a cycle Tricarboxylic to - t at a lack of insulin, considerable decrease in digestion of glucose, the hyperglycemia and a nedookisleniye of ketone bodies, acetone, acetoacetic and beta and hydroxy-butyric to - t are cells a consequence of what at an excess ketogenesis in a liver. Accumulation acetoacetic and beta and hydroxy-butyric to - t in extracellular liquid promotes accumulation of carbonic acid and surplus of hydrogen ions. In development of a ketosis activation gipotalamo - gipofizarno - adrenal system with the increased allocation in blood of glucocorticoids can play a pathogenetic role. The last strengthen glyconeogenesis and mobilization from depot fat to - t which partial oxidation conducts to a ketosis promote.
Alkaline reserves of an organism are spent for neutralization and removal of ketone bodies that conducts to a metabolic acidosis and loss of potassium cells. The excitement of a respiratory center caused by acidosis causes the hyperventilation promoting release of acetone with expired air. The glycosuria connected with a hyperglycemia and excess release of salts are followed by considerable increase of a diuresis that along with often observed vomiting causes dehydration of an organism and disturbance of electrolytic structure of cells with a gipokaligistiya. It leads to decrease in sokratitelny function of a myocardium, a pachemia, decrease in its circulating volume and the ABP, reduction of glomerular filtering in kidneys. Tension of the enzymatic processes directed to a reabsorption in kidneys is excessive the tubules of glucose and salts allocated in a gleam, and also disturbance of a blood-groove in kidneys and their toxic damage can be led to a renal failure with an oliguria, especially in the presence of a diabetic nephropathy or the accompanying pyelonephritis. In such cases release of glucose and ketone bodies with urine sharply decreases, the hyperglycemia and a giperketonemiya accrues, development of uraemia is possible.
At the heart of disturbances of functions of c. N of the page bringing to To., deep disturbances of metabolism of cells of a brain as owing to a lack of digestion by them of glucose and the disturbances of cellular respiration aggravated with circulatory disturbances and owing to the expressed disturbances of exchange of electrolytes and water, acidosis and toxic impact on cells of products patol lie. exchange, a part of which, napr, beta and hydroxy-butyric to - that, possesses narcotic action.
A wedge, signs indicating a possibility of development To., create the so-called period of harbingers which proceeds several days, several hours are more rare. During this period the polyuria, a polydipsia, a loss of appetite up to anorexia is observed, nausea, vomiting, weight loss. Fluid loss at diabetic To. reaches 10% of body weight, loss of sodium apprx. 500 mekv, potassium — 350 mekv, chlorides — 390 mekv. In process of increase of a ketosis block, drowsiness, then the confused consciousness appears. Vomiting amplifies, abdominal pains quite often appear. In some cases in a wedge, a picture separate symptoms prevail that formed the basis for allocation atypical a wedge, forms — gastrointestinal (reminding a picture of peritonitis, appendicitis, a gastroenteritis), the cardiovascular, shown a collapse, and renal, characterized oliguria, a hyperazotemia, emergence in urine of protein and cylinders.
During the period To. the hyperemia of the face, the sunk-down eyeballs, a xeroderma, decrease in its turgor, slackness of muscles, cold extremities are observed. Pupils are usually narrowed. Are characteristic deep and noisy breath like Kussmaul and a smell of acetone in expired air. Language dry, is laid often over by a brown plaque. At superficial To. reaction to pain at a palpation of a stomach can be defined. The pulse which is speeded up, weak; By the ABP it is lowered; changes of cardiac sounds are not specific, the pendulum rhythm is sometimes noted. In certain cases at development of a renal failure with a hyperpotassemia the expressed bradycardia is possible. During the listening of lungs the pleural rub sometimes is defined.
Lab. researches reveal a hyperglycemia with concentration of sugar in blood more than 400 mg of %, hyper osmolarity of plasma, a giperketonemiya, decrease in pH of blood with reduction of content of bicarbonates, increase in residual nitrogen, urea and creatinine in blood, increase in a hematocrit, concentration of hemoglobin, a neutrophylic leukocytosis. Level of immunoreactive insulin in blood is sharply reduced, and a glucagon — is increased. In urine sugar and acetone are defined.
The diagnosis is based on identification of a hyperglycemia, glycosuria, symptoms of ketoacidosis and dehydration.
2. Giperosmolyarny coma — a special look To. at a diabetes mellitus, in a pathogeny the cut plays the main role hyper osmolarity of plasma owing to a hyperglycemia and the increased concentration of electrolytes in blood. Giperosmolyarny not ketogenic To. it is described also at patients with not diabetes mellitus, at defeats of c. N of page, introduction of a large amount of glucose, Dilantinum, at long diarrhea, peritoneal dialysis and a hemodialysis, a hypothermia, acute pancreatitis, a thyrotoxicosis and after introduction of glucocorticoids. But the most often giperosmolyarny To. develops at patients with a diabetes mellitus.
Emergence To. it is connected with insufficiency of insulin and increase in a plasma glucagon, however for the reasons not clear still ketoacidosis at it does not develop. Assume that lack of a ketosis is connected with preservation of endogenous secretion of nek-ry amount of the insulin sufficient for braking of a lipolysis, but insufficient for prevention of a hyperglycemia.
Giperosmolyarny To. develops at persons more often 40 years suffering from an easy form of a diabetes mellitus and at 2/3 patients before development are more senior To. diabetes was not distinguished. Isolated cases of this look are described To. at insulin-dependent sick children and young men. Emergence To. the excess use of carbohydrates, intercurrent diseases and injuries which are especially followed by dehydration (burns, vomiting, diarrhea), treatment by immunodepressants, glucocorticoids, diuretics and also a hemodialysis, peritoneal dialysis, infusion of large amounts of salt solutions and glucose provoke.
In a pathogeny giperosmolyarny To. disturbances of hydration of a brain which cause cellular accumulation of sorbitol with the subsequent hypostasis, and also hypoxemic damage of c can be play a role. N of page. The large role is played by dehydration. The high osmotic diuresis caused approximately equally by a glycosuria and release of salts leads to bystry development of a hypovolemia, dehydration of intercellular and cellular spaces, a vascular collapse with decrease in a blood-groove in bodies, including in a brain and kidneys. Decrease in glomerular filtering against the background of dehydration is followed by a delay in blood of osmotically active agents, including urea and sugar, concentration to-rogo in plasma is sharply increased (can reach 3000 mg of % and more). It strengthens dehydration of cells and aggravates disorders of functions of all systems, first of all with c. N of page and blood circulatory system. If the water lost by an organism is not compensated, then the collapse is aggravated and there comes death at heavy disorders of haemo circulation
Klin, a picture giperosmolyarny To. in most cases develops gradually since the period of harbingers in the form of a polyuria, a polydipsia, sometimes polyphagias. Then there are circulator frustration with decrease in the ABP. At increase of dehydration an asthma, drowsiness, confusion of consciousness is noted, at 1/3 patients fever and hypovolemic shock is observed. The beginning To. often is followed nevrol, disturbances in the form of epileptiform attacks, paresis of extremities. Further the tone of muscles decreases; eyeballs of a gipotonichna, the nystagmus comes to light, symptoms of dehydration are considerably expressed: skin and mucous membranes dry, turgor of fabrics is sharply reduced. Hypostasis of the lower extremities and a scrotum is sometimes noted. Constant sign — an asthma (breath like Kussmaul is not characteristic). The smell of acetone is absent. Tachycardia is noted; The ABP it is considerably reduced at the expressed reduction of pulse pressure, pulse small, quite often is defined hardly. The diuresis is sharply reduced, up to an anury.
At a blood analysis the considerable hyperglycemia — higher than 600 mg of % with sharp increase in osmolarity of plasma — to 400 mosm/l comes to light (norm 290 — 310 mosm/l). Except the cryoscopic method, osmolarity of plasma can be estimated on an empirical formula:
The hypernatremia is defined not in all cases. Level of bicarbonate and pH of blood is usually normal. The hyperleukocytosis and the increase in a hematocrit caused by a pachemia, increase in concentration of hemoglobin, crude protein of serum, residual nitrogen, urea are characteristic. In urine sugar at negative reaction to acetone is defined.
A lethality at giperosmolyarny To. exceeds 50%. Circulator frustration, hypovolemic shock, fibrinferments and thromboembolisms of vessels of a big and small circle of blood circulation, a myocardial infarction, and also a renal failure, wet brain and other complications happen a cause of death.
3. Giperlaktatsidemichesky coma develops at a hypoxia and stimulation of the anaerobic glycolysis which is characterized by accumulation in an organism milk to - you and increase in the relation lactate/pyruvate making normal 12/1. The arising metabolic acidosis and disturbances of energy balance at patients with a diabetes mellitus promote development To. The contributing factors are bleeding, a circulator collapse, infections, administration of adrenaline and noradrenaline, use of guanyl guanidines against the background of a renal and liver failure.
To development To. usually muscular pains, a stethalgia, increase of breath, apathy, drowsiness, stupefaction precede. In process of increase of acidosis an asthma progresses, symptoms of dehydration, decrease in the ABP, a collapse with oligo-or an anury are noted. At To. substantial increase in blood of concentration milk to - you, decrease in content of bicarbonates and reserve alkalinity is defined. The hyperglycemia is expressed unsharply; cases are observed To. at a normoglikemiya.
Giperlaktatsidemichesky acidosis needs to be differentiated with the metabolic acidosis caused by a hyperchloremia and other metabolic frustration or introduction to an organism of acids (ketoglyutarovy, salicylic, etc.).
The diagnosis is based on identification of a heavy metabolic acidosis with a hyper lactacidemia and increase in the relation lactate/pyruvate in the absence of a ketosis and the expressed hyperglycemia. Lethality high.
The differential diagnosis of comas at patients with a diabetes mellitus includes not only the described pathogenetic options, but also hypoglycemic To. It is based on assessment of set of clinical and laboratory signs (tab. 2).
Treatment diabetic To. includes administration of insulin, a regidratation, compensation of loss of electrolytes and if necessary correction of acidosis.
At giperketonemichesky hyper glycemic To. insulin is entered intravenously and subcutaneously in equal quantities with an interval of 2 hours before decrease in a hyperglycemia, calculating every time the general dose of the entered insulin in terms of action as equal one tenth numbers characterizing concentration of sugar in blood in mg of %; e.g., at concentration of sugar of 400 mg of % the dose of insulin is equal to 40 PIECES. If in 2 hours after introduction of an initial dose of insulin the level of a glycemia decreases by 25% and more, then insulin is not entered before definition of concentration of sugar into blood in 2 hours. To children an initial dose of insulin define at the rate of 1 PIECE on 1 «of body weight. In an initiation of treatment enter hypotonic (0,45%), then isotonic solution of sodium chloride and 2,5% solution of hydrosodium carbonate. The total amount of the entered liquid makes 4 — 6 l (for children of early age of 150 — 180 ml on 1 kg of body weight, school age — 70 — 100 ml/kg). In 4 — 5 hours add 2 — 3 g of potassium chloride on each liter of the entered liquid for elimination of the hypopotassemia developing in these terms to solutions. Enter 200 mg of cocarboxylase, 5 ml of 5% of solution ascorbic to - you, whether 2 5% of solution of a pyridoxine. Appoint symptomatic means; at permanent decrease in the ABP enter plasma, plasma substitutes, noradrenaline, glucocorticoids.
For treatment giperosmolyarny To. recommend introduction of 2 — 5 l of hypotonic solution of sodium chloride during the first 8 — 10 hours, then fiziol, solution (total amount of liquid of 5 — 8 l) with addition of potassium chloride from 3 to 8 g a day. To children total quantity of the entered liquid is defined by equal 10 — 20% of body weight. Insulin is entered intravenously kapelno in number of 10 — 15 PIECES an hour (to children — 2 PIECES on 1 kg of body weight) depending on an initial hyperglycemia. At threat of a hypoglycemia enter 2 — 3% solution of glucose.
Treatment giperlaktatsidemichesky To. consists in intravenous administration of 2,5 — 4% of solution of hydrosodium carbonate under control of pH (1 — 2 l a day and more), small doses of insulin and 2 — 5% of solution of glucose. For the purpose of stimulation of transformation of a lactate into pyruvate enter methylene blue at the rate of 2 — 5 mg on 1 kg of weight of the patient. Carry out an oxygenotherapy. At the low ABP enter corticosteroids, plasma and plasma substitutes. In hard cases apply a hemodialysis.
A coma at diseases of a nervous system
Apoplectic coma arises at hemorrhagic or ischemic cerebral stroke (see). At a hematencephalon development To. sudden, is more often in the afternoon. Loss of consciousness can be followed by psychomotor excitement; the person is purple-red, breath loud, stertorozny, disturbance of swallowing, vomiting is observed. Pulse intense, slowed down, the ABP is more often raised. At hemorrhage under covers of a brain Meningeal symptoms are noted. Symptoms of a hemiplegia, hypotonia a century, a symptom of «sail» of a cheek and rotirovanny foot on the party of a hemiplegia, Babinsky's symptom come to light; floating movements of eyeglobes; ischuria or involuntary urination. On the party of a hemiplegia the raised, and then released extremity falls as the lash, and on other party slowly is returned to the initial position. At hemorrhage in cerebral cavities gormetonichesky spasms are observed (see. Gormetoniya ). At a hemorrhagic stroke the leukocytosis, impurity of blood in cerebrospinal liquid, subfebrile temperature come to light (several hours later).
To. at a trombotichesky ischemic stroke develops gradually, more often at night, usually after harbingers (dizziness, a faint), repeated passing disturbances of cerebral circulation. At patients pallor of the person is noted, by the ABP it is lowered, the ciliary arrhythmia, pulse of weak filling, cardiac sounds deaf sometimes comes to light, the pulsation of a carotid artery is sometimes weakened; mono - or a hemiplegia is defined. At an embolic stroke development To. can be followed by spasms. At an ischemic stroke coagulability of blood is often increased.
To diagnosis apoplectic To. help a research of cerebrospinal liquid (availability of blood at a hemorrhagic stroke), an ekhoentsefalografiya (shift of a median M-echo in the party opposite to the struck parencephalon), a cerebral angiography, an axial (computer) tomography of a brain. At differential diagnosis it is necessary to remember what at some diseases of internals develops apoplektiformny To., reminding apoplectic. Apoplektiformny To. arises at myocardial infarction (see). Its development is caused by disturbance of the general hemodynamics against the background of an acute heart failure, disorder of vasculomotor regulation from carotid receptors and development of arterial hypotension, change of reactivity of vessels of a brain with tendency to a thrombogenesis in them, reflex paresis of vessels of a brain with stazy blood in them.
Apoplektiformny To. at a myocardial infarction the wedge, manifestations of coronary insufficiency, sometimes after repeated attacks of heartaches develops sharply, more often in the first days, slightly earlier or along with typical. In nevrol, the status all-brain and focal symptoms come to light, also decrease in the ABP, speeded up is noted, is more rare (at an atrioventricular block) the slowed-down, low, arrhythmic pulse, premature ventricular contraction, a ciliary arrhythmia, an asthma, cyanosis. Psychomotor excitement, euphoria, hallucinations, epileptiform attacks, akroarteriospastichesky reflex (disappearance of pulse on arteries of extremities), abdominal and renal symptoms are possible; temperature increases, the leukocytosis, acceleration of ROE are defined. On an ECG the changes characteristic of a myocardial infarction are noted. In blood — changes of concentration of enzymes (a lactate dehydrogenase, aminotransferases).
Treatment at apoplectic To.: intravenously enter an Euphyllinum (10 ml of 2,4% of solution); the means reducing wet brain (solution of a mannitol, lasixum) are shown. At an ischemic stroke anticoagulating and fibrinolitic therapy, hemodilution, anti-aggregation drugs (Persantinum or curantyl) is recommended. At a hemorrhagic stroke appoint coagulating and anti-fibrinolitic means (Trasylolum, Contrykal), and also the drugs reducing permeability of a vascular wall (ascorbic to - that, a gluconate of calcium, Rutinum); at the raised ABP carry out hypotensive therapy (Pentaminum, etc.). At apoplektiformny To. treatment includes absolute rest, intravenous slow administration of the polarizing mix, a reopoliglyukin and others fiziol, liquids, urgent actions for stopping of a pain syndrome (1 ml of 2% of solution of Promedolum or 1 ml of 2% of solution of an omnolon in combination with 0,5 ml of 0,1% of solution of atropine, a combination of Droperidolum with fentanyl), to elimination of an acute heart failure (strophanthin or Korglykonum) and arterial hypotension (pressor amines). In the absence of contraindications enter anticoagulating (heparin) and fibrinolitic drugs, antiarrhythmic and improving conductivity, dehydrating, spasmolytic and sedatives.
Coma at meningitis. To. it can be observed at meningitis of various etiology, preferential purulent. Development To. it is caused by inflammatory changes in covers of a brain, likvoro-and hemodynamic disturbances in substance of a brain, venous stagnation. Acute development is characteristic To. against the background of initial symptoms of meningitis (a febricula, a hyperthermia, the general hyperesthesia, a headache, vomiting). At a research the Meningeal syndrome comes to light, a hemorrhagic enanthesis, delay or increase, and also arrhythmia of pulse and breath, asymmetry of tendon jerks and a muscle tone, loss of function of cranial nerves are possible. At children convulsive attacks or development of the convulsive status are quite often observed.
Diagnosis To. at meningitis is based on a research of cerebrospinal liquid. At the same time increase in its pressure, a high pleocytosis (neutrophylic comes to light at purulent meningitis, lymphocytic at serous), moderate increase in protein content, at purulent and tubercular meningitis — falling of a sugar content and chlorides. On an eyeground the hyperemia of disks of optic nerves is noted.
Treatment To. at meningitis it is carried out in the conditions of a specialized hospital. Appoint antibiotics according to indications; at Waterhouse's syndrome — Frideriksena (infectious and toxic shock with the disseminated intravascular coagulopathy) — drugs of glucocorticoid hormones, dehydrating, antihistaminic, symptomatic and fortifying agents.
Coma at encephalitis. Development To. at encephalitis of various etiology (see. Encephalitis ) it is caused by inflammatory changes in substance of a brain. It usually begins suddenly in the first - second day of a disease. It is preceded by a febricula, a hyperthermia, a hyperemia of a pharynx, drowsiness, slackness or psychomotor excitement, a headache, dizziness, vomiting. To. is followed by tachycardia, a tachypnea, sometimes repeated convulsive attacks, at children development of the convulsive status. At nevrol. a research the general and brain symptoms connected with wet brain, and also the focal, caused by preferential localization defeats come to light: squint, a ptosis, paralysis of a look, hyperkinesias, a plastic hypertension, is more rare hypotonia of muscles, paralyzes, paresis.
For diagnosis the research of cerebrospinal liquid matters. At encephalitic To. build-up of pressure of cerebrospinal liquid, xanthochromatic or hemorrhagic (is noted at hemorrhagic encephalitis) its coloring, increase in protein content and sugar. At an ekhoentsefalografiya signs of increase in intracranial pressure, expansion of the third ventricle are found.
Treatment encephalitic To. it is directed to fight against wet brain (intravenous administration of 150 — 300 ml of 10% of solution of a mannitol, 40 — 60 mg of lasixum), a metabolic acidosis (150 — 300 ml of 4% of solution of hydrosodium carbonate intravenously). Intravenously enter corticosteroids. Carry out the desensibilizing and anticonvulsant therapy, use the drugs strengthening a vascular wall (Rutinum, ascorbic acid, drugs of calcium), according to indications — resuscitation actions.
Epileptic coma arises at the epileptic status (see. Epilepsy ). In its development play a role haemo - and liquorodynamic, and also metabolic disturbances in a brain. The beginning To., as a rule, sudden; consciousness of the patient in the convulsiveless mezhpristupny period is not normalized. The hyperthermia, decrease in the ABP, arrhythmia of pulse and breath, oppression of corneal and tendon jerks, vomiting are observed by «a coffee thick». During resuming of spasms — sharp cyanosis of the person, foam from a mouth, tension of veins of a neck, hoarse, stertorozny breath, the low speeded-up pulse, the urination and defecation are involuntary. Consciousness is broken also in the period of postepileptic prostration; the patient is not mobile, with pale cyanochroic complexion, the hyperthermia is noted, a mydriasis, eyeballs are taken aside, the floating movements of eyeglobes can be observed less often, the general hypomyotonia, an areflexia, a tachypnea, tachycardia is characteristic. Not stopped epileptic status leads to deepening To., to decrease and then to lack of tendon jerks and a muscle tone, reduction of duration of the convulsive attacks having preferential tonic character. Disorders of breath and cardiovascular activity accrue; breath becomes superficial, gradually passing into periodic breathing of Cheyn — Stokes, arterial hypotension, tachycardia is aggravated. In a terminal phase there are no spasms, pupils are expanded, there is no photoharmose, duration of an apnoea increases, symptoms of a hypoxia and wet brain come to light, acidosis accrues.
At establishment of the diagnosis it is important to specify whether the epileptic status is primary or display of other disease (neuroinfections, tumors of a brain, etc.). Along with studying of the anamnesis, a wedge, data the great value is attached a lab. to methods of a research, electroencephalography, ekhoentsefalografiya, lumbar puncture, axial (computer) tomography of a brain.
Treatment shall be complex. It begins with the moment of detection of the patient in the epileptic status, proceeds in the ambulance car and the intensive care unit or chamber of an intensive care. Upper respiratory tracts exempt from slime, emetic masses. Intravenously slowly enter 2 ml of 0,5% of solution of Seduxenum into 20 ml of 40% of solution of glucose. At continuation of spasms administration of drug is repeated. Intramusculary enter the lytic mixes including 1,0 ml of 2,5% of solution of aminazine, 1,0 ml of Pipolphenum, 1,0 ml of 50% of solution of analginum in 2 ml of 2% of solution of novocaine. In the absence of effect apply a geksenalovy or tiopentalovy anesthesia — 8 — 10 mg/kg of 1% of solution of hexenal or thiopental intravenously. Use dehydrating drugs: Mannitolum, glitserol, lasixum, Uregitum. The lumbar puncture can give therapeutic effect. For elimination of acidosis intravenously enter 100 — 300 ml of 4% of solution of hydrosodium carbonate. According to indications appoint cardiac glycosides, pressor amines, metabolic active means (ATP, cocarboxylase), hold events for decrease in temperature.
Control of treatment is exercised by means of an electroencephalography — with effect paroxysmal categories disappear and desynchronization of rhythms appears.
The hepatic coma
the Hepatic coma develops at the heaviest degree of a liver failure (see. Hepatargy ) at patients with various diseases of a liver, it is especially frequent at hepatitises (see. Hepatitis , viral hepatitis ).
On the main kliniko-pathogenetic syndromes allocate endogenous hepatic To., caused by sharp reduction of number of hepatocytes, exogenous To., connected with intoxication due to «shunting» of portal blood in the general blood stream, electrolytic and hepatic To., K.
Endogennaya sometimes mixed hepatic To. (hepatocellular, true To., «To. disintegration or substitution of a liver») develops usually at disintegration of body (see. Toxic dystrophy of a liver ), and also at substitution of its parenchyma a tumor or cicatricial fabric (see. Cirrhoses of a liver ). Etiol, factors are a viral hepatitis In, alcoholic, and also medicinal intoxications (a halothane, levomycetinum, an isoniazid, etc.), acute circulatory disturbances («a shock liver»), heavy bacterial injuries of a liver, etc.
Exogenous hepatic To. (portal and hepatic, ammoniac, or «To. the disconnected liver») meets more often endogenous, usually at patients with a syndrome of portal hypertensia. Intestinal bleedings, emergence so provoke its development. naz. ascites peritonitis, gross violations of a diet, including alcohol intake.
Electrolytic and hepatic, or «false», To. it is connected with disturbance of water and electrolytic exchange (especially with a hypopotassemia). At patients with a liver failure these disturbances proceed especially hard and often are complicated by encephalopathy. Disorders of electrolytic exchange are provoked by the use of saluretics, a laparocentesis, intercurrent diseases which are followed by a hypoxia and disturbance of acid-base equilibrium.
Division hepatic To. on separate options to a certain extent conditionally also reflects only the leading value of separate disturbances in an origin To.; usually these disturbances are combined. With the expressed participation in development To. each of the described disturbances speak about mixed K.
Patogenez of any of options hepatic To. it is connected with funkts, a hepatic unsufficiency, first of all with decrease in its anti-toxic function.
It is known that products of bacterial decarboxylation of amino acids and other transformations of proteins and fats in intestines usually come on portal system to a liver where will be transformed to non-toxic substances. At damage of a liver or considerable development of collaterals between portal system and extrahepatic vessels in blood toxic products collect. The main role in a pathogeny To. allocate for accumulation in an organism of ammonia, phenols and other toxic products of exchange. This mechanism hepatic To. it was experimentally reproduced by I. P. Pavlov at the end of the last century (meat, or carbamic, poisoning).
Y. F. Fischer et al. (1976) attach independent pathogenetic significance to one of products of bacterial decarboxylation of amino acids in intestines — to tyramine, surplus to-rogo causes strengthening in blood of an oktopamin. Oktopamin forces out from synapses of c. N of page the main mediators of excitement — noradrenaline and a dopamine that leads to
K. V development a pathogeny sharply developing hepatic To. the role of disturbances of allocation is established to cookies of toxic polypeptides about a pier. it is powerful (weighing) more than 1500 and molecules of the average sizes connected with protein.
One of the main pathogenetic mechanisms of development hepatic To. disturbance of products is the affected liver of a number of the enzymes providing a lemon and acid cycle (first of all coenzyme A). The perversion of one of side reactions of a lemon and acid cycle leads to accumulation of such tserebrotoksichesky products as methyl-acetyl carbinol, butylene glycol, etc.
In a pathogeny of endogenous option hepatic To. all listed pathogenetic factors play a role. In development exogenous To. the leading role is assigned to excess hit in blood from intestines of decarboxylates of amino acids and to accumulation in synapses of c. N of page of an oktopamin. Disturbances of electrolytic exchange are caused by restriction of participation of a liver in regulation of content of the hormones controlling a water salt metabolism. In particular, emergence of a hypopotassemia is promoted by the secondary hyper aldosteronism which is observed at patients with severe damages of a liver.
A clinical picture hepatic To. in most cases develops gradually, but in some cases To. happens as if sudden, sometimes it develops against the background of the seeming recovery.
Endogenous To. proceeds most hard with rather bystry (in several hours) development of deep stages and a high lethality. To development To. increase of weakness, drowsiness, quite often the periods of psychomotor excitement precede. Usually jaundice, dispeptic and hemorrhagic frustration accrues. The beginning To. it is characterized by increase of frequency and depth of breath, its rhythm is broken. There are muscular twitchings, a clonus of feet, the hypertension of muscles accrues, reflexes, a nystagmus, expansion of pupils are noted patol. In the subsequent the tone of muscles decreases. At inspection of the patient yellowness of scleras and skin, often raschesa on skin, a petechia, hematomas in places of injections come to light. Fervescence with the subsequent its decrease is possible. Breath like Kussmaul is defined, breath like Cheyn — Stokes or difficult disturbances of his rhythm is more rare. Often «the hepatic smell» (a smell of crude meat) from a mouth is defined. Usually (but not always) bradycardia comes to light. By the ABP it is lowered. As a rule, the increased and painful liver, the sizes a cut is palpated can progressively decrease in the prekomatozny and coma periods up to almost total disappearance of hepatic dullness at percussion. At a blood analysis define a leukocytosis, acceleration of ROE, strengthening of free and glyukuronirovanny bilirubin. Bromsulfaleinovy and vofaverdinovy tests, a research of activity of pseudo-cholinesterase indicate falloff of functions of a liver. Color of urine dark due to presence of bilious pigments; the urobilinuria, emergence in urine of a leucine, tyrosine is noted. Sometimes signs of toxic damage of a liver with development of a picture come to light gepatorenalny syndrome (see). By Kcal it is quite often decoloured.
Exogenous To. develops gradually and seldom reaches deep stages. The periods of the expressed excitement are not characteristic, is frequent in a prekomatozny state sick malokontaktna, are embittered, closed. Disturbances of breath and «a hepatic smell» usually are absent. Increase of jaundice and hemorrhagic manifestations are expressed less, than at endogenous To. At survey of patients symptoms of portal hypertensia, ascites are defined. (Perkutorno) are defined by Palpatorno increased both a liver, and a spleen. In blood, except the changes inherent endogenous To., but less expressed, often find anemia and substantial increase of concentration of ammonia and phenols; funkts, tests of a liver are changed unsharply.
Electrolytic and hepatic To. on a wedge, to manifestations differs from exogenous hepatic a little To. Muscular weakness is more expressed, paresis of intestines is quite often noted, the ABP more decreases, there can be expressed tachycardia and the changes of an ECG characteristic for hypopotassemias (see). The diagnosis is based on data of researches of electrolytes in blood.
A clinical picture mixed hepatic To. forms from symptoms of each of the described types. In practice mixed To. designate, apparently, and To. with a difficult pathogeny. Features of a current have, e.g., To. at the patients suffering from slowly progressing forms of cirrhosis and a diabetes mellitus. Their repeated comas lasting 7 — 10 days were observed, and in some cases — up to 40 days. At the same time jaundice and a hyperglycemia significantly amplified, ketoacidosis was absent, there were no disturbances of breath, «a hepatic smell». Gross violations funkts, tests of a liver were noted also out of coma. At the moment To. the giperammoniyemiya, a hypopotassemia, a hypomagnesiemia, decrease in concentration of phosphorus in blood serum were defined.
Treatment hepatic To. it is reasonable to carry out in chamber of intensive round-the-clock overseeing by the patient. At once intravenously kapelno 500 ml of 5% of solution of glucose with addition of 1,5 g of potassium chloride and 10 — 12 PIECES of insulin are entered; per day intravenously enter to 1 l 5% of solution of glucose with ascorbic to - that (10 ml of 5% of solution), and also Neocompensanum, Haemodesum. Intramusculary enter a pyridoxine (3 ml of 5% of solution), cocarboxylase (200 mg), Vikasolum (2 ml of 1% of solution), B12 vitamin (500 mkg). Depending on degree of acidosis under control of pH pour in from 200 to 600 ml of 2,5 — 4% of solution of sodium bicarbonate; at a hyponatremia apply sodium chloride (10 — 20 ml of 10% of solution), infusions of solution of Ringer. For the purpose of desintoxication and for partial recovery of amino-acid and enzymatic structure enter 25 — 100 ml of 1% of solution glutaminic to - you, appoint ornithine and arginine on 5 — 15 g a day, amino-acid cocktails; intravenously kapelno on isotonic solution of glucose enter 240 mg of coenzyme A, 208 mg of NADF, 65 mg a-lipoic to - you. Taking into account a pathogenetic role of deficit of mediators in c. N of page apply a levodopa from 1 to 3 g a day. Inside enter active coal (on 20 — 30 g 2 times a day), to a laktulez (50 — 100 g a day); for «sterilization» of intestinal contents appoint antibiotics.
For reduction of necrotic processes in a liver recommend high doses of glucocorticoids (to 200 — 1000 mg of Prednisolonum a day), however the effect of hormones is estimated variously and use them demands control of dynamics of electrolytes and bilirubin in blood.
At treatment hepatic To. at children the dose of glucocorticoids is defined at the rate of 4 — 5 mg of Prednisolonum on 1 kg of body weight; Neocompensanum and Haemodesum to children of early age enter in number of 10 — 15 ml on 1 kg of body weight.
The good effect gives hyperbaric oxygenation (see), edges in the absence of contraindications it has to be applied as soon as possible.
Sometimes use (so far without strict proofs of efficiency) exchange hemotransfusion (see), plasma exchange (see), cross circulation, gomo-and heterologous extracorporal perfusion of a liver, or hemosorption (see), administration of specially processed active coal, suspension of hepatocytes. In a stage of development there is a technique of liver transplantation.
A respiratory coma
the Respiratory coma (respiratory atsidoticheskaya To., respiratornotserebralny To.) develops at funkts. insufficiency of system of external respiration. The name «atsidotichesky coma» applied sometimes is unsuccessful since, first, the pathogenetic role of acidosis is known in development of many types To., secondly, a pathogeny To. at respiratory insufficiency it is not limited to disturbances of acid-base equilibrium.
Respiratory To. the hl is observed. obr. at the diseases and states which are followed by falloff of alveolar ventilation in lungs both at acute and at hron, respiratory insufficiency (see). Defeats of a respiratory center, peripheral motor nerves, skeletal respiratory muscles and a diaphragm can be the reason of pulmonary hypoventilation, except bronchopulmonary diseases; changes of a shape of a thorax and condition of pleural cavities; pain at breath; wrong carrying out artificial ventilation of the lungs (AVL) or assisted ventilation. Respiratory To. it is observed sometimes at patients in time or after the surgery performed under the general anesthesia using muscle relaxants.
At patients hron. bronchopulmonary diseases (bronchial asthma, hron, pneumonia, pneumoscleroses, pneumofibroses, etc.) to development To. often the exacerbation of pneumonia and intercurrent infections, a circulatory unefficiency in connection with a decompensation promote pulmonary heart (see), use for its treatment of the diuretics blocking a karboangidraza, the long asthmatic status, overdose of adrenomimetichesky bronchial spasmolytics, increasing the need of an organism for oxygen, use of the muscle relaxants and drugs oppressing a respiratory center, and also the wrong performing oxygen therapy at decrease in sensitivity of a respiratory center to carbonic acid.
In pathogeny respiratory To. the hypoxia, a hypercapnia, a metabolic acidosis and the related disturbances of electrolytic balance and microcirculation have major importance. Respiratory insufficiency at hron, bronchopulmonary diseases is shown first of all by an anoxemia and hypoxia (see). The lack of oxygen leads to decrease in cells of a brain of content of creatine phosphate and to deficit of ATP in an organism. At the same time glycolysis is activated; stocks of a glycogen, including in a brain are as a result exhausted, and contents in an organism of a lactate and pyruvate increases that along with accumulation of other nedookislenny products promotes development of a metabolic acidosis. At the long and sharply expressed hypoxia also glycolysis is oppressed, there is a necrobiosis of cells, especially in tensely functioning bodies. The hypoxia and acidosis lead to changes of electrolytic structure of various environments that first of all is shown by a gipokaligistiya and strengthening of extracellular potassium, and also swelling of cells of a brain. The described disturbances cause funkts, insufficiency of all bodies and systems, including cardiovascular, with widespread frustration of the central hemodynamics and microcirculation which aggravate degree of a hypoxia. At considerable decrease in lung ventilation of disturbance of gas exchange are supplemented hypercapnia (see), the head leading to decrease in a tone of vessels and playing a role in developing of paresis of vessels of a microcirculator cerebral bed. In the conditions of a hypercapnia affinity of hemoglobin to oxygen decreases that worsens transport function of blood; oxygen consumption by fabrics decreases, the thermolysis at reduction of heat production increases, excitability of a respiratory center decreases and there are additional disturbances of depth, speed and a respiratory rhythm. To. develops in connection with hypoxemic braking, and then and damage of cells of a brain, the direct oppressing impact on c. N of page of a hypercapnia and owing to disturbances of polarization of membranes of neurocytes at redistribution of electrolytes in the conditions of a metabolic acidosis.
Clinical picture To. is defined by the leading reason of respiratory disturbances and speed of development of a hypoxia. At acute respiratory insufficiency, including the caused obstruction of respiratory tracts, rapid development a wedge, manifestations — psychomotor excitement with the subsequent bystry loss of consciousness, the progressing asthma, disturbances of a respiratory rhythm, arrhythmia of heart, often fibrillation of ventricles of heart can be observed. Death comes from the termination of breath or from a cardiac standstill. At an aggravation hron, respiratory insufficiency respiratory To. develops slowly, within several days; influence of provocative factors, napr, use of drugs, can accelerate considerably emergence To., however and in these cases its development takes, as a rule, not less than several hours that the nek-swarm is explained by adaptation of patients to a hypoxia, apparently, at it hron, a current.
To slow development To. progressing of signs of respiratory insufficiency — strengthening of an asthma, diffusion cyanosis, tachycardia, increase of venous hypertensia and peripheral hypostases precedes at a dekompensirovanny pulmonary heart. There is an irritability, a headache, then slackness, drowsiness (sometimes after the period of euphoria), a black-out with its periodic clearings. Passing delirious states and other psychotic syndromes are in some cases observed at night. Often there are convulsive twitchings of separate muscles, sometimes more widespread clonic and tonic spasms. Development of a soporous state has wavy character in the beginning, then disturbances of consciousness go deep; reactions to strong irritations are weakened. During this period pupils are more often narrowed; if adrenomimetik are not applied, the anisocoria is quite often observed. Tendon jerks are raised, the tone of muscles is lowered, pyramidal and Meningeal symptoms are sometimes noted. In process of increase of a hypercapnia the minute volume of breath increases in the beginning, then decreases; cyanosis gets a crimson shade, large drops of sweat on face skin and an upper half of a trunk appear; The ABP raises, sometimes considerably, in the subsequent it decreases; frustration of a cordial rhythm are aggravated; body temperature decreases.
Diagnosis respiratory To. at knowledge of the anamnesis, preliminary observation of the asthmatic status or signs of a prekomatozny state does not represent difficulties. At the first inspection of the patient with To. without data of the anamnesis the diagnosis is based on objective data. Survey diffusion cyanosis of skin and mucous membranes comes to light; patients with hron, a hypoxia can have it sharply expressed («pig-iron» cyanosis); at a considerable hypercapnia coloring of the person is more often crimson or cyanochroic-pink. Extremities are cold, body temperature is reduced. The person is bloated, the cervical veins which often bulked up; peripheral hypostases, ascites can be defined. Breath is arrhythmic, superficial. At percussion of lungs reveal a bandbox sound and omission of borders, extensive areas of dullness at massive pneumonia or a pleural exudate or a «mosaic» percussion sound — alternation of sites of a bandbox sound with areas of dullness at patients hron, pneumonia. Auskultativno is defined by wet and dry rattles, sometimes breath is not listened on all fields or in certain sites. At the expressed emphysema the loudness of cordial tones in standard points of listening is sharply reduced, but they can well be listened under a xiphoidal shoot and in an anticardium where the pulsation of the increased right ventricle of heart quite often is defined. Often arrhythmia against the background of tachycardia comes to light. Size ABP depends on a stage To. and from degree of a hypercapnia. Choreoid hyperkinesias, fibrillations of muscles are characteristic; generalized spasms are possible. At deep To. the respiratory rhythm is sharply broken, is lowered by the ABP, pulse small, arrhythmic, muscles of a gipotonichna, reflexes are oppressed, pressure of cerebrospinal liquid is increased.
In blood the leukocytosis and a polycythemia often is defined; at To. in the outcome of the asthmatic status the eosinophilia is possible; pO2 is sharply lowered, pCO2 is raised, pH and an alkaline reserve are lowered. The hypercapnia can be established by express definition of concentration of CO2 in expired air by means of a kapnometriya. On an ECG in most cases reveal a hypertrophy and an overstrain of the right departments of heart, signs of diffusion disturbances of repolarization of a myocardium, nodal and ventricular escapes, in some cases — nodal tachycardia, atrial fibrillation, disturbances of conductivity, including sometimes passing, imitating premature ventricular contraction) a syndrome of WRW (see. Wolff-Parkinson-Whyte syndrome ).
Treatment consists in correction of disturbances of gas composition of blood and a metabolic acidosis, and also in elimination of the reasons of ventilating insufficiency and in recovery of functions of external respiration. The general for treatment respiratory To. any etiology are: urgent oxygen therapy (see) by means of artificial ventilation of the lungs (see. Artificial respiration ), since inhalations of oxygen at natural breath in the conditions of a hypercapnia create threat of an apnoea; intravenous administration of 125 mg of a hydrocortisone or 60 mg of Prednisolonum for the purpose of reduction of necrotic processes in cells; drop intravenous administration of 400 ml of 4% of solution of hydrosodium carbonate with its further additional introduction according to indications under control pH loudspeakers and an alkaline reserve of blood before their normalization; drop intravenous administration of 400 ml of 5% of solution of glucose after correction of a metabolic acidosis together with 6 — 8 PIECES of insulin for reduction of a gipokaligistiya; at a hypopotassemia add potassium chloride to 1 — 1,5% of its concentration to solution and increase total quantity of the solution entered per day depending on degree of deficit of potassium; intravenous, intramuscular or rectal (at ventricular premature ventricular contraction) introduction of 0,24 g of an Euphyllinum for the purpose of improvement of zone ventilation and a blood-groove in lungs and increases in a renal blood-groove; intravenous or intramuscular administration of 200 — 300 mg of cocarboxylase, 40 — 60 mg of a pyridoxine, 200 — 400 mg ascorbic to - you in days. Recovery of functions of external respiration, etiol, and symptomatic therapy are individual — according to the nature of respiratory insufficiency in each case and character accompanying funkts, frustration.
Purpose of respiratory analeptics in an initiation of treatment at use of artificial ventilation of the lungs is not shown: even in high doses they do not increase significantly ventilation, and moderate doses of Cordiaminum, Corazolum at the expressed hypoxia can cause emergence of spasms. If necessary drugs of this group are appointed before the termination IVL after reduction of a hypoxia and acidosis. If To. developed against the background of use of drugs, enter Nalorfinum on 2 ml of 0,5% of bucketed solution of 10 — 20 min. to effect, but no more than 4 injections.
At To. in the outcome of the asthmatic status in one step intravenously struyno enter 125 mg of a hydrocortisone or 60 mg of Prednisolonum and continue drop injection (or combine ways of introduction) glucocorticoids to 200 — 300 mg of Prednisolonum a day. Parenteral use of adrenomimetik is not shown because of falloff of their bronkhodilatiruyushchy effect at acidosis while the increase in oxygen requirement caused by them and a direct impact on adrenoceptors of a myocardium and c. N of page can worsen a current To. Intra tracheal introduction of Isoproterenolum happens reasonable. For the prevention of a condensation of a phlegm increase the volume of the entered alkaline solutions at the corresponding reduction of concentration of bicarbonate. Make long drop injections of isotonic solutions of sodium chloride and glucose, and also the reopoliglyukin improving microcirculation). Carry out a bronchial lavage of 1,3% solution of hydro-sodium carbonate with addition 50 — 70 mg of chemical opsin or acetyl of cysteine to 1 g on 1 l of solution. The most effectively posegmentarny bronchial lavage with use of a bronkhoskopiya. Transdermal catheterization of a trachea (microtracheostomy) with infusion of the solutions containing bronchial spasmolytics, Mucolyticums, antibacterial agents is applied.
At inflammatory process in lungs enter parenterally antibiotics of a broad spectrum of activity. Semi-synthetic are preferable to initial antibacterial therapy Penicillin (see) or cephalosporins, napr, Oxacillinum, Methicillinum or tseporin.
Despite often available signs of a decompensation of blood circulation, use of cardiac glycosides in an initiation of treatment To. contraindicated. Their trial careful use is possible only after considerable reduction of degree of a hypoxia and an anoxemia — at pO 2 ≥ 60 mm of mercury. in an arterial blood. Before bloodletting of 400 — 500 ml is made. It is reasonable to apply diuretics at reduction of a hypoxia against the background of IVL. At a cardiac standstill it is made defibrillation (see), electrostimulation of heart and other methods resuscitation (see).
The Hlorgidropenichesky coma
the Hlorgidropenichesky coma (hloroprivny To., gipokhloremichesky To.) it is caused by disturbance of water and electrolytic exchange and acid-base balance owing to considerable losses by an organism of water and salts, first of all chlorides. The main reason for these disturbances — pernicious vomiting at toxicosis of the first half of pregnancy, at diseases of kidneys, poisonings, food toxicoinfection, at acute and hron, diseases of the digestive system (a pyloric stenosis, pancreatitis, a gastroenteritis, intestinal impassability, etc.)*. To development To. the electrolyte-deficient diet, reception or injection of alkalis, diarrhea, a plentiful diuresis after use of saluretics, evacuation of large amounts of ascitic liquid, the strengthened sweating, and also a hypoparathyrosis, insufficiency of kidneys, adrenal glands can promote, to a liver.
In pathogeny the loss by an organism of acid ions conducting to a metabolic alkalosis and also his dehydration against the background of losses of the main osmotic cations — sodium and potassium plays a role. Initial redistribution of water is characterized by a pachemia and a cellular overhydratation. Decrease in sokratitelny function of heart and an intravascular hypovolemia cause insufficiency of a hemodynamics and disorder of microcirculation in bodies, including in a brain. Content of the ionized calcium in plasma owing to an alkalosis decreases that leads to increase in neuromuscular excitability and emergence of spasms. Education milk to - you at spasms and accumulation of nedookislenny products as a result of disorders of microcirculation reduce degree of a metabolic alkalosis, but disturbance of hydration of cells, their electrolytic structure, oppression of cellular enzymes at the same time progresses.
Clinical picture develops gradually. To emergence To. repeated vomiting, the progressing weakness, fatigue, thirst, sometimes a headache, preferential frontal localization precedes. Weight loss at the expense of dehydration accrues. The ABP goes down. In an orthostatics pulse pressure considerably decreases, tachycardia, dizziness is observed; faints are possible. The diuresis is reduced. Spasms are quite often noted. The rhythm of a dream is broken, drowsiness prevails afterwards, patients become indifferent to surrounding. The condition of prostration is replaced by a deep oglushennost, a sopor, then a coma.
At inspection of the patient with hlorgidropenichesky To. considerable weight loss, falloff of turgor of fabrics comes to light. Skin and mucous membranes dry, features are pointed, the eyeballs which sank down. Body temperature is lowered. Breath is frequent, superficial. Pulse is small, quite often threadlike, frequent, can be arrhythmic. Sometimes the embryocardia is defined. The ABP it is considerably reduced with a small pulse pressure. Often anury. Quite often tetanic spasms. Tendon jerks are oppressed; Meningeal symptoms are possible.
At a blood analysis signs of its condensation with increase in a hematocrit and an azotemia come to light, concentration of cholesterol is reduced; quite often high leukocytosis.
Differential diagnosis it is carried out with uraemic To., at a cut there are usually multiple displays of uraemia, most often widespread hypostases and high the ABP.
Treatment begin with intravenous administration 30 — 40 ml of 10% of solution of sodium chloride (to children at the rate of 1 ml for 1 year of life) with the subsequent drop administration of salt isotonic solutions, a reopoliglyukina, Haemodesum, 5% of solution of glucose with a total amount up to 3 l a day. Subcutaneously enter 1 — 2 ml of 10% of solution of caffeine-sodium benzoate, 2 ml of Cordiaminum. At a collapse apply a phenylephine hydrochloride (1 ml of 1% of solution). For stopping of spasms enter 5 — 10 ml of 10% of solution of calcium chloride intravenously, in need of 5 — 10 mg of Seduxenum. Treatment of a basic disease is carried out.
The Atsetonemichesky coma at children
the Atsetonemichesky coma at children develops at disturbances of a lipometabolism more often aged from 1 year up to 10 years. Among the reasons of such disturbances note irrational food (underfeeding, violent feeding, an overfeeding fats), hron, frustration of food, various infectious diseases, hepatitises. Predisposition to development of this look To. is available for children with neuroarthritic diathesis. Development To. it is connected with accumulation in blood of ketone bodies and acetone, intoxication, acidosis, disorder of functions of c. N of page, kidneys, liver.
Before emergence To. patients note weakness, a headache, abdominal pains, then there is vomiting, edges arises often without the visible reasons, from 2 — 3 to 20 times a day. Emetic masses contains slime, impurity of bile. There can be a hyperthermia with development on its background of spasms. In process of progressing of vomiting there is a thirst, perspiration is replaced by dryness of integuments. The child has a motive concern, irritability, emotional lability. Abdominal pains often amplify, become skhvatkoobrazny, at the same time the delay of a chair is noted. At increase of intoxication and ketoacidosis emergence of nonsense is possible, meningeal symptoms, excitement is replaced by slackness, drowsiness, «load», a loss of consciousness. At survey in time To. note the pointed features, blue under eyes. Integuments are pale gray, often wet, but at is longer to vomiting with dehydration — dry; turgor of fabrics is reduced. The hypomyotonia and a hyporeflexia is noted. Breath deep (like Kussmaul); smell of acetone from a mouth. Pulse is frequent, weak filling, cardiac sounds are muffled, the ABP low. In blood the giperketonemiya at nek-rum is defined decrease in concentration of sugar in blood (sometimes its increase to 120 — 140 mg of %), acidosis. Find traces of protein, leukocytes, cylinders in urine. Kal contains a large number of droplets of fat at minor changes from other indicators.
Treatment. In a prekomatozny state at identification of the first signs of a ketonemiya appoint plentiful drink: 5% solution of glucose, sweet tea, alkaline mineral waters, Ringer's solution, isotonic solution of sodium chloride. At the repeated vomiting expressed to intoxication treatment begin with a gastric lavage 1 — 2% with the solution of hydrosodium carbonate cooled to 16 — 18 ° for fight against a hyperthermia; then enter 100 — 200 ml of isotonic solution of sodium chloride for completion of chlorides at frequent vomiting into a stomach.
At coma intravenously kapelno enter in the equal volume of 20% solution of glucose, Ringer's solution, isotonic solution of sodium chloride in the total quantity approximately equal to 10% of body weight of the child. At a hypopotassemia add 1% solution of potassium chloride (at the rate of 3 ml on 1 kg of body weight of the child). If concentration of sugar in blood is increased, then enter 4 — 6 PIECES of insulin and the level of a glycemia is constantly controlled. Acidosis korrigirut introduction of 2 — 4% of solution of hydrosodium carbonate iod control of pH. For the purpose of desintoxication apply Neocompensanum, plasma, Haemodesum. Symptomatic therapy includes spasmolysants, febrifugal, cardiovascular means (but not adrenaline). After removal from To. the patient appoint a rational diet and drugs of digestive enzymes (pepsin, abomin, Pancreatinum).
Table 1. The short characteristic of main types of a coma and acute management at them
Table 2. The main clinical and biochemical differential diagnostic characters of comas at patients with a diabetes mellitus
Bibliography: Bogolepov N. K. Comas, M., 1962; Cooper 3. A. Clinical hepathology, page 24, M., 1970, bibliogr.; Hemosorption, under the editorship of Yu. M. Lopukhin, M., 1977; L at N and - to about in E. A., D and and e in V. H. and Fir-s about in H. H. Fundamentals of resuscitation at acute poisonings, M., 1977, bibliogr.; M and x e of l with about V. A. N and M and N of e in and the p A. 3. Bases of an intensive care and resuscitation in pediatrics, M., 1976, bibliogr.; The multivolume guide to neurology, under the editorship of N. I. Grashchenkov, t. 4, p.1, page 9, M., 1963; The Multivolume guide to pediatrics, under the editorship of Yu. F. Dombrovskaya, t. 8, page 493, etc., M., 1965; Acute management in pediatrics, under the editorship of V. M. Sidelnikov, Kiev, 1976; The Guide to clinical endocrinology, under the editorship of B. G. Baranova, L., 1977, bibliogr.; The guide to endocrinology, under the editorship of B. V. Alyoshin, etc., M., 1973, bibliogr.; Smetnev A. S. and Petrova L. I. Medical emergencies in clinic of internal diseases, page 134, M., 1977, bibliogr.; Bennett D. R. and. lake of Atlas of electroencephalography in coma and cerebral death, EE G at the bedside or in the intensive care unit, N. Y., 1976; Handbook of clinical neurology, ed. by P. J. Vin-ken a. G. W. Bruyn, v. 11-12, pt 1 — 2, Amsterdam a. o., 1975.
H. K. Bogolepov, E. I. Gusev, V. P. Zhmurkin; G. S. Zefitzova (and.), V. P. Lebedev (ped.), A. I. Hazanov (gastr.); authors of tab. E. I. Gusev, S. M. Kamenker.