Presentation on theme: "Diagnostic and emergency assistance in Coma"— Presentation transcript:
1Diagnostic and emergency assistance in Coma Prepared by: C.m.s., assistant professor of outpatient therapy and emergency medical emergency KSMU A.R. Alpyssova
2The purpose of the lecture After completing the lecture, students should focus on issues of diagnosis and emergency care at koma in the amount of the first medical care (doctor's line crews), and depending on the patient - in the amount of specialized care (intensive care team, intensive care team).
3The plan of the lectureComa: determination, etiology, pathogenesisClinic pictureDifferential diagnosisTips caller, mandatory questions in the diagnosis, indications for hospitalizationUndifferentiated therapyThe specific treatment of individual comatose states
4ETIOLOGY AND PATHOGENESIS ComaComa - a state of CNS disease, characterized by a violation of its coordination activities, autonomous operation of individual systems, graduating at the level of the whole organism the ability to self-regulate and maintain homeostasis, clinically manifested loss of consciousness, a violation of motor, sensory and somatic functions, including vital.ETIOLOGY AND PATHOGENESISTo evaluate the prognosis and treatment selection is very important to determine the cause of coma:Focal lesion hemispheres and / or brain stem with a volume effect and the development of dislocation syndrome.Diffuse lesion of the cortex and brain stem.The first option is typical for the primary and the latter is observed almost exclusively in secondary koma.
5All causes of whom can be reduced to four categories: Intracranial processes that lead to increased intracranial pressure (vascular, inflammatory, tumor, brain injury, etc.).Hypoxic conditions (respiratory, circulatory, hemic, tissue, etc.).Metabolic disorders (primarily in the pathology of the endocrine system).Intoxication (both exogenous and endogenous).
6Despite the diversity of the etiology of comatose states in the pathogenesis of many things in common, and the factors that serve as the primary causes of some types of components, are the pathogenic basis for others.A direct mechanism for cerebral insufficiency are violations of education, distribution and transmission of nerve impulses in the brain cells due to inhibition of tissue respiration, metabolism and energy. This is due to the reduction of oxygen supply and nutrients to the brain (ischemia, venous congestion, microcirculation, vascular stasis, perivascular edema), changes in acid-base and electrolyte balance, increased intracranial pressure, edema and swelling of the brain and the meninges, the latter can lead to dislocation of the brain from mechanical damage to the vital centers in the brain stem.
7If any coma at some point it develops tissue hypoxia of varying severity. Disturbances of acid-base status often have the nature of metabolic acidosis, although the primary lesion of the respiratory system develops respiratory acidosis. More rarely, such as persistent vomiting, there is metabolic alkalosis, hyperventilation and respiratory alkalosis leads to. Characterized by a combination of various metabolic and respiratory disorders.Among the most significant electrolyte disturbances consider changes in the concentration of potassium (hypokalemia as well as hyperkalemia) and hyponatremia. Last played an important role in the pathogenesis of brain edema. Slow metabolism have histotoxic action. With the deepening coma develop respiratory failure, and subsequently circulation.
8CLINIC PICTUREThe clinical picture is dominated by the coma of any disturbance of consciousness with loss of perception of the environment and oneself, depression of reflexes to external stimuli and disturbances of regulation of vital functions. Patients in a coma can not "wake up“ any, even the most energetic events. Allocate the following shape changes in the level of consciousness: Stun (shallow and deep), sopor, who (I-III degree). The degree of severity of disorders of consciousness can be assessed by a simple but informative clinical scale of Glasgow.Stun (13-14 balls on the scale of Glasgow) is characterized by drowsiness, disturbances of attention, loss of cohesion of though and action. With stunning patient is awake, but can not perform a task requiring sustained attention. for example, consistently take 7 from 100.
9Stun (13-14 balls on the scale of Glasgow) is characterized by drowsiness, disturbances of attention, loss of cohesion of thought and action. With stunning patient is awake, but can not perform a task requiring sustained attention. for example, consistently take 7 from 100.Coma surface (I degree, 7-8 on a scale of Glasgow): wake up the patient is impossible to pain stimuli it responds to the simplest, erratic movements, not localizing pain.Deep coma (II degree, 5-6 on a scale of Glasgow): The patient is responsible motor responses to pain stimuli.Coma atonic (III degree, 3-4 on a scale of Glasgow): complete lack of response of the patient, even on very strong pain stimulation. Atony, are flexia, impaired or absent breathing, possibly inhibition of cardiac activity.
10Depression of consciousness and the weakening of reflexes (corneal, pupillary) tendon, skin), progressing to full extinction of the deepening coma. For focal lesions characterized by unilateral neurological symptoms. Meningeal signs - stiff neck, Kernig and Brudzinski signs, observed in lesions of the meninges (meningitis, meningoencephalitis), can also be caused by brain swelling and irritation of the meninges.Progression of cerebral insufficiency with the fading of central nervous system leads to various respiratory disorders with hypo-or hyperventilation and respiratory related shifts the acid-base status. Gross violations of hemodynamics is usually attached to a terminal state other clinical manifestations, the rate of development of coma, clinical history is usually quite specific for different versions of components.
11DIFFERENTIAL DIAGNOSIS Coma differentiated from a pseudocomasyndrome (isolated psychogenic are activity, abulic status, inconvulsive status epilepticus)Here are the features most frequently observed coma.Alcoholic coma may develop against the background of prolonged alcohol abuse, and the first use of alcohol, usually develops gradually, beginning with alcohol intoxication, ataxia, coma, much less sudden onset of a convulsive seizure. Objectively say congestion and cyanosis of the face, alternating with pallor, pendulum-like movement of the eyeballs, bronhoreia, hyperhidrosis, hypothermia, decreased skin turgor, muscle atony, hypotension, tachycardia, smell of alcohol, according to which, however, can not reject any other, in particular traumatic or hypoglycemic coma etiology.
12When hyperthermia coma (heat stroke), history of present indications of overheating (the most adverse effects of heat with high humidity). Coma develops gradually: the characters sweating, increasing weakness, headache, dizziness, tinnitus, nausea, vomiting, palpitations, shortness of breath, fainting. Objectively say hyperthermia, flushing of the skin, tachypnea, less breathing Cheyne-Stokes or Kussmaul, tachycardia, hypotension, anuria or oligouriyu, dilated pupils.
13Hyperglycemic ketoatsidotic coma. Information about diabetes can not be. Coma may be preceded by fasting, infection or other acute diseases (myocardial infarction, stroke), physical or mental injury, pregnancy, termination of hypoglycemic therapy. Coma occurs gradually, against the background of weight loss increases the overall weakness, thirst, polydipsia and polyuria, pruritus. Immediately prior to the development of coma appear anorexia, nausea, can be confusing for intense abdominal pain until the symptoms of "acute abdomen", headache, sore throat, and esophagus. Against the background of acute inter current illness coma may develop rapidly with no obvious predecessor. Physical examination reveals signs of dehydration (dry skin and mucous membranes of the mouth, decreased skin turgor and the eyeballs, the gradual development of anuria), general pallor and local congestion in the area of the zygomatic arch, chin, forehead, cold skin (but low-grade fever is possible) muscular hypotonia, hypotension, tachypnea or Kussmaul breathing, acetone odor from the mouth.
14Unketoatsidotic hyperglycemic hyperosmolar coma may develop mild diabetes or impaired glucose tolerance and triggered by factors causing dehydration and increased osmotic pressure of blood vomiting, diarrhea, polyuria, hyperthermia, burns, diuretics, and large doses of glucocorticoids, administration of hypertonic solutions. This coma develops slowly More than hyperglycemic ketoatsidotic coma, possible harbingers of the same (but usually there is no pain in the abdomen) may be orthostatic syncope. Typical signs of dehydration, hypotension up to hypovolemic shock, shortness of breath, possible hyperthermia, muscular hypertonicity, focal or generalized seizures, bulbar disturbances, meningeal signs, and aphasia in a shallow depression of consciousness, the smell of acetone from the mouth is missing.
15Hypoglycemic coma. There may be instructions for lowering drugs, although the lack of information about diabetes and hypoglycemic therapy does not exclude hypoglycaemia. Note the acute onset (as an exception - a gradual), a short period of precursors (with atypical course, caused dysmetabolic neuropathy, precursors may be absent), weakness, sweating, palpitations, trembling all over, a keen sense of hunger, fear, excitement (hypoglycemia may be unusual mental disorders, such as euphoria, delirium, amentia). On examination reveals hyperhidrosis, hypothermia, marked pallor of the skin with an unmodified color of mucous membranes, generalized tonic-clonic seizures, muscular hypertonicity, muscle hypotonia revocable, tachycardia, hypotension (may be uncharacteristic of hypoglycemia autonomic dysfunction (hypertension, bradycardia, vomiting)), breathing modifications and focal neurological symptoms.
16Gipokortikoidic coma (adrenal) develops or against the background of chronic adrenal insufficiency Coy (with inadequate replaces therapy in a variety of stressful situations) or as a result of various acute pathological conditions (haemorrhage in the adrenal glands with meningococcal and severe viral infections or trauma, acute thrombosis H, DIC, abrupt withdrawal of glucocorticoid therapy), as well as in times of stress (infection, trauma and other pathology) on the background or after discontinuation of glucocorticoid therapy. Coma may develop gradually with the increase obshey weakness, fatigue, anorexia, nausea, diarrhea, hypotension, orthostatic collapse, fainting, under the influence of adverse factors coma develops rapidly, and in case of hemorrhage in H, such as severe infections - with lightning speed ( syndrome Waterhouse-Friderihsen). Found note hypotension until redistributed shock, shortness of breath (perhaps Kussmaul breathing), hyperthermia, dilated pupils, convulsive seizures, muscle rigidrit, are flexia. In a number of possible CA-bronze color of the skin and giperpigm-Ia (гиперпигм-ия ) skin folds, weight loss, hemorrhagic rash.
17Alimentary dystrophic coma Alimentary dystrophic coma. When hungry (alimentary dystrophic) coma present indications inadequate and insufficient food for a long time. Characterized by sudden onset of: after a period of excitement growing faint, rapidly turning into a coma. On examination reveals hypothermia, pale peeling skin, it is possible acrocyanosis. Face pale icteric, and sometimes swollen. Characterized by muscle atrophy, may tonicity convulsions, hypotension, shallow breathing rare.Opiate coma. For opiate coma use of drugs is often hidden from medical professionals. Relatively fast growing drug intoxication is transformed into a coma. Depressed respiration (shallow, irregular, Cheyne-Stokes equations, sleep apnea), cyanosis noted, hypothermia, bradycardia. Possible hypotension until the collapse, is rare - pulmonary edema. Almost always reveal the point pupils (except poisoning promedolom or in combination with atropine). Multiple traces from injections and other signs of drug use do not exclude the other (eg, trauma) etiology of the coma.
18Traumatic coma. There are indications of injury and disease often develops quickly, however, possible, and the presence of a "bright period" during which the patient can be confusing for a sharp headache, nausea, vomiting, psychomotor agitation. Cerebral symptoms may be associated with meningeal signs and symptoms of focal brain lesions. Bradycardia and a rare breath replaced at later stages of tachycardia and tachypnea.Cerebrovascular coma develops against the background of hypertension and cardiovascular disease, although data on hypertension, atherosclerosis, vasculitis, aneurysms of the cerebral arteries can not be. The rate of development and the presence or absence of precursor role in the diagnosis did not play because the pre-hospital differential diagnosis of hemorrhagic and ischemic stroke is not carried out. Characterized by cerebral and focal neurological, meningeal symptoms against a background of various disorders of hemodynamics.
19Eсlampsic coma occurs between the 20th week of pregnancy and the end of the 1st week after birth. Coma develops after a period of pre-eclampsia, which lasts from minutes to hours, rarely weeks, accompanied by a painful headache, dizziness, visual disturbances, epigastric pain, nausea, vomiting, diarrhea, mood changes, restlessness or adynamia appearing on the background of nephropathy. Pre-eclampsia is diagnosed when a pregnant facial swelling or hands, blood pressure reaches 140/90 mm Hg or systolic blood pressure by 30mmHg, and diastolic - by 15 mmHg, or proteinuria detected. Eсlampsic coma develops after a convulsive seizure, which begins fibrillar contractions of muscles in the face and hands, which are replaced by generalized tonic, and then clonic seizures. Possible recurrence of attacks against the unconscious. Characterized by hypertension, bradycardia, hyperthermia can be. In some cases, coma develops without seizures (inconvulsive form).
20Epileptic coma. There may be indications of seizures, head injury, stroke history. Coma develops suddenly, often after a brief aura shutdown of consciousness and seizures begin simultaneously. In the first period (the period of status epilepticus), tonic seizures, frequent, revocable clonic seizures, cyanosis face, foam on his lips, his tongue, stridoroz breathing, tachycardia, swollen neck veins, involuntary urination and defecation, and expansion are activity pupils. In the second period (the period of postepilepticus sleep) reveals hypotension mouse, are flexia, abnormal signs iambic, flushing, pallor or cyanosis of the face, open mouth, eyes in the direction of abstraction, mydriasis, tachypnea, tachycardia.
21ADVICES FOR CALLERYou can not transfer the patient to lift his head and put patient; should leave it where he is and not change the position of the body.You should not undertake activities that affect the body temperature (dew patient with water, put hot water bottles to the feet, the ice on his head, etc.).You can not try to drink and to check whether the patient swallows. Should not be given to the patient to smell ammonia.Recommended gently turn a head slightly to one side, remove dentures, leftover food from the mouth.
22OBLIGATORY QUESTIONSIn the diagnosis of coma necessarily should try to gather history from relatives and witnesses (the inability to collect a history of the patient significantly reduces the value of information obtained). Necessary to clarify the following points.The presence of chronic disease (diabetes, hypertension, liver and kidney disease, thyroid disease, epilepsy, stroke and traumatic brain injury history, etc.),intoxications and abuse of alcohol or drugs, as well as receiving a present or past drug syndrome "cancellation ", which can occur coma (glucocorticoids, thyroid hormones).The presence of infection or injury.The circumstances, leading up to the loss of consciousness (changes in health, thirst, polyuria and polydipsia, excessive heat, in coordination, alcohol, seizures).The rate of development of a coma.
23INDICATION FOR HOSPITALIZATION Mandatory immediate hospitalization in an intensive care unit, in stroke - in the intensive care unit for patients with acute disorders of cerebral circulation, in brain injury or subarachnoid hemorrhage - a specialized neurosurgical department.Recommendations for abandoned homes of patients. All patients admitted to the hospital.
24Undifferentiated therapy Restore and maintain adequate breathing1. Remediation of the airways to restore their patency, installing ductwork or documentation of the language, mechanical ventilation with a mask or a tracheal tube, in rare cases - or tracheo-konikotomiya (opening between the larynx and thyroid cartilage annular).2. Oxygen (4-6 L / min via nasal catheter, or 60% by face mask, tracheal tube).3. Before tracheal intubation requires premedication of 0.1% solution of atropine (0.5-1 ml), except in cases of poisoning anticholinergic drugs.Relief of hypoglycemia. Regardless of the level of glucose (a long ill with diabetes, poor compensation hypoglycemic coma may develop against a normal glucose concentration) required bolus of 20-40 ml 40% glucose solution, in obtaining the effect, but the shortcomings of its severity, the dose increases. For the prevention of acute encephalopathy Wernicke-Gaye before the appointment of glucose must enter the thiamine (in the absence of his intolerance) at a dose of 100 mg (2 ml of 5% solution).
25Restoration and maintenance of adequate blood flow By reducing blood pressure should start a drip ml (less than 1 l/m2/day) 0.9% sodium chloride, 5% glucose solution and ml of dextran of average molecular weight 50-70 million (poliglyukina ) with the accession of the ineffectiveness of pressor amines infusion therapy - dopamine, norepinephrine.In the case of coma, occurred against a background of hypertension, correction of a high blood pressure to values, exceeding the "working" at 10 mm Hg (in the absence of anamnestic data - not below /80-90 mm Hg) by reducing the intracranial pressure (see below) intravenous injection mg of magnesium sulfate (5-10 ml 25% solution ) bolus over 7-10minutes, or drip. In the presence of contraindications to magnesium sulfate, allowed the introduction of 30-40 mg bendazola (3-4 ml of \% or 6-8 ml of 0.5% solution intravenous). With a slight increase in blood pressure enough intravenous an aminophylline (10 ml 2.4% solution).Restoring adequate heart rate in arrhythmiases (mainly by defibrillation).
26Immobilization of the cervical spine in any suspicion of injury. Catheterization of peripheral veins. If a comatose state, almost all drugs administered parenterally (preferably - intravenous) through a peripheral catheter infusion is carried out, with stable hemodynamics and there is no need of detoxification slowly drip administered indifferent solution that provides a constant opportunity for the rapid introduction of drugs.Bladder catheterization. Prehospital should be performed only on strict indications (risk of infection).Setting the gastric or nasogastric tube (after intubation, which must precede premedication with atropine.
27Therapeutic and diagnostic use of antidotes Antagonist of opiate receptors naloxone is indicated for suspected intoxication drugs, respiratory rate less than 10 per minute, point pupils. Initial dose - from to 2 mg (intravenous or endotracheal) may re-introduction after minutes with repeated deterioration; acceptable combination of intravenous and subcutaneous administration to prolong the effect.If you suspect a poisoning benzodiazepine drugs (diazepam [with Relanium,seduksenium], oxazepam [tazepamom, nozepamom] medazepama [rudotelem,mezapama]) or suspicion of such, is administered flumazenil (0.2 mg intravenous for 15 seconds, followed by the introduction of if necessary to 0.1 mg every minute up to a total dose of 1 mg).
28Relief of intracranial hypertension, edema and swelling of the brain In the absence of high osmolarity of blood (which occurs, for example, hyperglycemia or hyperthermia), and the threat of development or strengthening of bleeding (eg, trauma, inability to exclude hemorrhagic stroke) for dehydration, mannitol is administered at a dose of 1-2 g / kg (in 20 % solution) for minutes, to prevent a subsequent increase in intracranial pressure and progressionof cerebral edema after mannitol infusion lead furosemide 40 mg.1. Traditionally used glucocorticoids with minimal mineralocorticoid activity -methylprednisolone or dexamethasone (dose for both - 8 mg).2. Limiting the introduction of hypotonic solutions (5% Dextrose and 0.9% solution of NaCl - not more than 1 liter / day), but this does not apply to komah proceeding against haemoconcentration (hyperglycemic, Hyperthermic, gipokortikoidic, alcohol).3. In the presence of appropriate equipment may conduct mechanical ventilation mode hyperventilation (effective against intracranial hypertension persists for 1 h).
29Neuroprotection and increasing the level of consciousness 1. When violations of consciousness to the level of surface glycine sublingually shows the coma (or cheek) at a dose of 1 g, Semax 3 drops of 1% solution in each nostril), an antioxidant etilmetilgidroksipiridina succinate (meksidol) at a dose of 30 mg (6 ml of 5% solution) intravenous, bolus, for 5-7 minutes.2. With a deep coma spend antioxidant therapy and injected SemaxActivities to cease receipt of the toxin in the body in cases of suspected poisoning.1. Gastric lavage through a tube with the introduction of the sorbent (after intubation- see above) - when you receive the poison from the mouth or during injection of the poison of the gastric mucosa.Wash skin and mucous membranes with water - when you receive the poison through the covering fabric.
30Symptomatic therapyNormalization of body temperature. When supercooling - warming the patient (without heaters) and warmed intravenous fluids. In severe hyperthermia - a natural cooling (cold compresses on his head, and large vessels, wiping with cold water or solutions of ethyl alcohol and vinegar in water) and pharmacological methods (metamizol sodium, but without the use of lytic mixtures).1. Relief of seizures: Diazepam intravenous at a dose of 10 mg.2. Relief of vomiting: metoclopramide 10 mg intravenous or intramuscularly
31The specific treatment of individual comatose states Hypoglycemic coma. Bolus 40% glucose solution at a dose of ml (not more than 120 ml because of the danger of cerebral edema), with preliminary administration of 100 mg of thiamine. If necessary, further administration of glucose - its infusion solutions in decreasing concentrations of 5/10/20% with dexamethasone or methylprednisolone at a dose of 4-8 mg for the prevention of brain edema and as kontrinsulyar factors. If you need high doses of glucose and the absence of contraindications acceptable subcutaneous injection of 0.5-1ml of 0.1% solution of epinephrine, with a duration of a coma more than a few hours is shown intravenous and 2500 mg of magnesium sulfate.Hyperglycemic ketoatsidotic and hyperosmolar not ketoatsidotic coma. Infusion of 0.9% sodium chloride in the volume, respectively, 1,000and 1,500 ml in the first hour. When hyperosmolar and prolonged coma ketoatsidotic shown heparin - up to 10 000 units intravenous.
32Alimentary dystrophic coma. Rewarming the patient, infusion of 0 Alimentary dystrophic coma. Rewarming the patient, infusion of 0.9% sodium chloride solution (with addition of 40% glucose solution at the rate of 60 ml per 500 ml) with an initial rate of 200 ml / 10 min under the control of respiratory rate, heart rate, blood pressure and lung auscultatory pattern, fractional administration of vitamin - thiamine (100 mg), pyridoxine (100 mg), cyanocobalamin (200 mg), ascorbic acid (500 mg);Hydrocortisone 125 mg, with adequate hemodynamic failureinfusion therapy and signs of stagnation - pressor amines (dopamine, norepinephrine).
33Alcoholic coma. Bolus of 0. 5-1 ml of 0 Alcoholic coma. Bolus of 0.5-1 ml of 0.1% solution of atropine, and after tracheal intubation through a gastric lavage tube - expedient for 4 h after the last intake of alcohol) to clean the wash water (10-12 liters of water at room temperature) and the introduction of enterosorbent, warm infusion of 0.9% sodium chloride solution with an initial rate of 200 ml/10 min under the control of respiratory rate, heart rate, blood pressure and lung auscultatory pattern with a possible subsequent transition to the Ringer's solution, bolus or drip 120 ml 40% glucose solution, the introduction of fractional vitamins - thiamine (100 mg), pyridoxine (100 mg), cyanocobalamin(200 mg), ascorbic acid (500 mg), with hemodynamic failure of adequate fluid therapy - pressor amines (dopamine, norepinephrine).Опиатная кома. Введение налоксона (см. выше); при необходимости интубации трахеи обязательна премедикация 0,5—1 мл 0,1% р-ра атропина.
34Cerebrovascular coma. Since prehospital currently assisting impossible differential diagnosis of ischemic and hemorrhagic strokes, spend only a general treatment.When hypertension - blood pressure reduction to a level higher than the usual valueof 10 mm Hg, and in the absence of anamnestic data - not below /80-90mm HgRelief of arterial hypotension is carried out in three stages: - intravenous slow introduction of methylprednisolone (dexamethasone) in doses of 8-20 mg or prednisolone at a dose of 60-150 mg; - After failure - a dose of 50-100 polyglukin ml intravenous bolus, then infusion of up to ml; - With inefficiency - the dopamine drip (5-15In severe to reduce the capillary. permeability, improving of μ-the circulation and Haemostasis - bolus of 250 mg etamzilata to suppress proteolytic activity - a dripin the vine aprotinin KIE (КИЕ).Neyroprotective therapy: in prevalent symptoms centre of defeat crust of big hemisphere (vocal defeats and etc. changes of upper phsyhic functions ) under common brain symptomatic (clear conscious or easy deaf) admitted the injection of piracetam (6-12 g. intravenous).
35Eclampsic coma. 3750 mg bolus of magnesium sulfate for 15 min Eclampsic coma. 3750 mg bolus of magnesium sulfate for 15 min. while maintaining the seizures, diazepam bolus of 5 mg to relieve cramps, a drip of Ringer's solution (INN (МНН) - sodium chloride complex pp) at ml / h, dextran [cf. Mol. weight 30 000-50 000] (reopoliglyukin) (100 ml / h).Hyperthermic coma (heat stroke). Cooling, the normalization of respiratory, infusion0.9% sodium chloride solution with an initial speed of ml / h to 125 mg hydrocortisone.Gipokortikoidic (adrenal) coma. Bolus 40% glucose and thiamine (see above), hydrocortisone 125 mg, infusion 0.9% sodium chloride solution (with addition of40% glucose solution at the rate of 60 ml per 500 ml, taking into account the number already entered) with an initial velocity ml / h under the control of respiratory rate, heart rate, blood pressure and auscultatory pattern in the lungs.