Intensive therapy for septic shock is carried out by an obstetrician-gynecologist together with a resuscitator.
Measures to combat shock should be focused on restoring tissue blood flow and correcting metabolic disorders and on maintaining adequate gas exchange.
The first two problems are solved by performing infusion therapy, which must be started as early as possible and carried out for a long time. As nifusion media in the first stages of treatment, it is preferable to use derivatives of dextran (400-800 ml of rheopolyglucin and/or polyglucin) and polyvinylpyrrolidone (400 ml of hemodez). The speed and amount of fluid infused depends on the patient’s response to the therapy.
The total amount of fluid on the first day is usually 3000-4500 ml, but can reach 6000 ml. Against the background of replenishment of the bcc and improvement of the rheological properties of blood, the mandatory use of cardiac and vasoactive agents is necessary to correct hemodynamics and restore tissue blood flow. Along with the normalization of hemodynamics, the goal of infusion therapy for septic shock should be the correction of acid-base and electrolyte homeostasis.
With septic shock, metabolic acidosis develops quite quickly, which at first can be compensated by respiratory alkalosis.
To correct acidosis, it is necessary to include 500 ml of lactasol, 500 ml of ringer lactate or 150-200 ml of 4-5% sodium bicarbonate solution in the infusion therapy. Along with the restoration of hemodynamic disorders and correction of metabolic disorders, ensuring adequate oxygenation is of great importance. The introduction of oxygen must begin from the first minutes of treatment, using all available means for this, up to artificial ventilation lungs. Along with anti-shock measures, infection control is an integral part of intensive care for septic shock.
Antibacterial therapy for septic shock is emergency. At the same time, semi-synthetic penicillins are widely used.
Methicillin sodium salt administer 1-2 g every 4 hours and ampicillin sodium salt (pentrexil) - 1.5-2 g every 4 hours or 2 g every 6 hours intramuscularly or intravenously (maximum dose 8 g). Cefamezin is prescribed 1 g every 6-8 hours, intravenously or intramuscularly, the maximum daily dose is 4 g. In addition, the fight against shock includes eliminating the source of infection. The experience of obstetric and gynecological practice shows that the approach to eliminating the source of infection in septic shock should be purely individual.
The most radical way to fight is to remove the uterus. To obtain the desired effect, surgery must be performed in a timely manner.
According to the majority of domestic and foreign authors, surgery should be resorted to if intensive conservative therapy carried out within 6 hours is unsuccessful.
The operation of choice is hysterectomy with removal of the fallopian tubes, drainage of the parametrium and abdominal cavity. In some cases, in patients in extremely serious condition, in the absence of macroscopic changes in uterine tissue, supravaginal amputation of the uterus is permissible. In these cases. removal of the fallopian tubes and drainage of the abdominal cavity is mandatory. Treatment of late stage septic shock with the appearance of hemorrhagic syndrome, including uterine bleeding, requires a differential approach.
Depending on the coagulogram parameters, replacement therapy(“warm” donor blood, lyophilized plasma, dry, native and fresh frozen plasma, fibrinogen) and/or antifibrinolytic drugs (trasylol, contrical gordox) are administered.
In this article we will talk about severe pathology. We will review the pathophysiology of septic shock, clinical guidelines for it, and its treatment.
Features of the disease
Septic shock is the terminal phase of a generalized (extended to all organs) septic process (blood poisoning), which is characterized by active development pathological processes in the body that practically do not respond to intensive resuscitation therapy.
Basic:
- critical decrease in blood pressure (hypotension);
- severe disruption of blood supply the most important organs and tissues (hypoperfusion);
- partial and complete failure of several organs to function simultaneously (multiple organ dysfunction).
Considering the commonality of internal and external manifestations, septic shock is considered in medicine as successive stages of a single organism-wide pathological process. Another name for the disease is bacterial toxic shock, septic infectious toxic shock. Septic shock develops in almost 60% of cases severe sepsis. As a result of such serious disorders in the functioning of body systems, deaths from septic shock are common.
According to ICD-10, septic shock has code A41.9.
The development of shock is most often observed during an attack on the body by gram-negative flora (Klebsiella, coli, Proteus), and anaerobes. Gram-positive microorganisms (staphylococci, diphtheria bacteria, clostridia) cause the critical phase of sepsis in 5% of cases. But the difference between these pathogens is the release of toxins (exotoxins), which cause severe poisoning and tissue damage (for example, necrosis of muscle and kidney tissue).
But not only bacteria, but also protozoa, fungi, rickettsia and viruses can cause a state of septic shock.
This video talks about septic shock:
Stages
Conventionally, in a state of shock during sepsis, three phases are distinguished:
- warm (hyperdynamic);
- cold (hypodynamic);
- irreversible.
Manifestations during different phases septic shock Table No. 1
| Stages (phases) of septic shock | Manifestations, characteristics of the condition |
|---|---|
| Warm | It has been proven that in case of shock caused by gram-positive flora, the course and prognosis are more favorable for the patient. Characterized by the following conditions:
|
| Cold shock phase | The course of “cold shock,” most often provoked by gram-negative organisms, is more severe and more difficult to respond to therapy, lasting from 2 hours to a day. This form is observed at the stage of centralization of blood circulation due to vascular spasm (outflow of blood from the liver, kidneys, peripheral vessels to the brain and heart). The “cold phase” is characterized by:
|
| Irreversible phase | Severe organ failure of several organs and systems is observed (respiratory and, with depression of consciousness up to coma), a critical drop in blood pressure. Functions cannot be restored even with resuscitation measures. The comatose state leads to the death of the patient. |
Immediate and competent therapy state of shock in case of sepsis, carried out from the beginning of the “warm phase”, often stops the development of pathological processes, otherwise septic shock goes into the “cold phase”.
Unfortunately, due to its short duration, the hyperdynamic phase is often overlooked by physicians.
Causes
The causes of septic shock are similar to the causes of severe sepsis and the inability to stop the progression of the septic process during treatment.
Symptoms
The complex of symptoms during the development of septic shock is “inherited” from the previous stage - severe sepsis, differing in even greater severity and further increase.
The development of a shock state during sepsis is preceded by severe chills against the background of significant fluctuations in body temperature: from sharp hyperthermia, when it rises to 39 - 41 ° C, lasting up to 3 days, and a critical decrease in the range of 1 - 4 degrees to (up to 38.5) , normal 36 – 37 or falling below 36 – 35 C.
The main sign of shock is an abnormal drop in blood pressure without previous bleeding or not corresponding in severity, which cannot be raised to the minimum norm, despite intensive medical measures.
General symptoms:
In all patients, at the early stage of shock (often before the pressure drops), signs of damage to the central nervous system are observed:
- euphoria, overexcitation, loss of orientation;
- delusions, auditory hallucinations;
- further - apathy and numbness (stupor) with a reaction only to strong painful stimuli.
Increasing severity of manifestations of severe sepsis are expressed in the following:
- tachycardia up to 120 – 150 beats/min;
- the shock index rises to 1.5 or more when the norm is 0.5.
It is a value equal to the heart rate divided by the systolic blood pressure. Such an increase in the index indicates the rapid development of hypovolemia - a decrease in circulating blood volume (CBV) - the amount of blood in the vessels and organs.
- breathing is uneven, shallow and rapid (tachypne), 30–60 respiratory cycles per minute, indicating the development of acute acidosis (increased acidity of tissues and body fluids) and a state of “shock” lung (tissue damage preceding edema);
- cold sticky sweat;
- redness of the skin in a short “warm phase”, then a sharp pallor of the skin in the “cold stage” with a transition to marbling (whiteness) with a subcutaneous vascular pattern, the limbs become cold;
- bluish coloration of lips, mucous membranes, nail plates;
- sharpness of facial features;
- frequent yawning if the patient is conscious, as a sign of oxygen deficiency;
- increased thirst (decreased amount of urine) and subsequent anuria (stopping urination), which indicates severe kidney damage;
- in half of the patients - vomiting, which, as the condition progresses, becomes like coffee, due to tissue necrosis and bleeding in the esophagus and stomach;
- pain in the muscles, abdomen, chest, lower back, associated with a disorder of blood supply and hemorrhages in tissues and mucous membranes, as well as an increase in acute renal failure;
- strong;
- yellowness of the skin and mucous membranes becomes more pronounced as liver failure worsens;
- hemorrhages under the skin in the form of pinpoint, cobweb-like petechiae on the face, chest, abdomen, folds of the arms and legs.
Diagnosis and treatment of septic shock are described below.
Diagnostics
Septic shock, as a phase of generalized sepsis, is diagnosed by the severity of all the symptoms of the pathology in the “warm” and “cold” stages and clear signs of the last stage - secondary or irreversible shock.
The diagnosis must be made immediately - based on the following clinical manifestations:
- the existence of a purulent focus in the body;
- fever with chills, followed by a sharp drop in temperature below normal;
- acute and threatening drop in blood pressure;
- high heart rate even at low temperatures;
- depression of consciousness;
- pain in different areas of the body;
- acute decrease in urine output;
- hemorrhages under the skin in the form of a rash, in the whites of the eyes, nosebleeds, necrosis of areas of the skin;
- convulsions.
In addition to external manifestations, when carrying out laboratory tests observe:
- deterioration of all indicators of laboratory blood tests in comparison with the first phases of sepsis (severe leukocytosis or leukopenia, ESR, acidosis, thrombocytopenia);
- acidosis, in turn, leads to critical conditions: dehydration, blood thickening and blood clots, organ infarctions, impaired brain function and coma;
- the change in the concentration of procalcitonin in the blood serum exceeds 5.5 - 6.5 ng/ml (an important diagnostic indicator for the development of septic shock).
Diagram of septic shock
Treatment
Treatment combines medications, therapeutic and surgical methods, used simultaneously.
As in the phase of severe sepsis, emergency surgical treatment is carried out for all primary and secondary purulent metastases (in internal organs, subcutaneous and intermuscular tissue, in joints and bones) in the most short time, otherwise any therapy will be useless.
In parallel with the sanitation of purulent foci, the following are performed: urgent measures:
- Perform artificial ventilation to eliminate manifestations of acute respiratory and heart failure
- To stimulate heart function, increase blood pressure, and activate renal blood flow, Dopamine and Dobutamine are infused.
- In patients with severe hypotension (less than 60 mmHg), Metaraminol is administered to ensure blood supply to vital organs.
- Massive intravenous infusions of medicinal solutions are carried out, including dextrans, crystalloids, colloid solutions, glucose under constant monitoring of central venous pressure and diuresis (urine excretion) in order to:
- elimination of blood supply disturbances and normalization of blood flow indicators;
- removal of bacterial poisons and allergens;
- stabilization of electrolyte and acid-base balance;
- prevention of pulmonary distress syndrome ( acute failure breathing against the background of the development of edema) - infusion of Albumin and Protein;
- relief of hemorrhagic syndrome (DIC) in order to stop tissue bleeding and internal bleeding;
- replenish fluid loss.
- When cardiac output is low and vasoconstrictors are ineffective, the following are often used:
- Glucose-insulin-potassium mixture (GIK) for intravenous infusion;
- Naloxone for bolus - rapid jet injection into a vein (if a therapeutic effect is obtained, after 3 - 5 minutes they switch to infusion).
- Without waiting for tests to identify the pathogen, antimicrobial therapy is started. Depending on development internal pathologies systems and organs, penicillins, cephalosporins (up to 12 grams per day), aminoglycosides, and carbapenems in large doses are prescribed in large doses. The combination of Impinem and Ceftazidime is considered the most rational, which gives a positive result even in the case of Pseudomonas aeruginosa, increasing the survival rate of patients with severe concomitant pathology.
Important! The use of bactericidal antibiotics can worsen the situation, as a result of which a switch to bacteriostatic drugs (Clarithromycin, Dirithromycin, Clindamycin) is possible.
To prevent superinfection (re-infection or complications during antibacterial therapy), Nystatin 500,000 units up to 4 times a day, Amphotericin B, bifidum are prescribed.
- Suppress allergic manifestations by using glucocorticosteroids (Hydrocortisone). The use of Hydrocortisone in a daily dose of up to 300 mg (up to 7 days) for shock can accelerate the stabilization of vascular blood flow and reduce deaths.
- Administration of the activated APS protein drotrecogin-alpha (Zigris) for 4 days at a dose of 24 mcg/kg/hour reduces the likelihood of patient death during the critical phase of acute renal failure (contraindication - no risk of bleeding).
In addition, if it is established that the causative agent of sepsis is staphylococcal flora, add intramuscular injections antistaphylococcal immunoglobulin, infusion of antistaphylococcal plasma, human immunoglobulin, are engaged in restoring intestinal motility.
Prevention of septic shock
To prevent the development of septic shock, you must:
- Timely surgical opening and sanitation of all purulent metastases.
- Prevention of the deepening development of multiple organ dysfunction with the involvement of more than one organ in the septic process.
- Stabilization of improvements achieved during the severe shock stage.
- Maintaining blood pressure at minimally normal levels.
- Prevention of the progression of encephalopathy, acute renal and hepatic failure, disseminated intravascular coagulation syndrome, development of the state of “shock” lung, elimination of the state of acute anuria (urinary retention) and dehydration.
Complications of septic shock are described below.
Complications
- At worst– death (if this result can be considered as a complication).
- At its best– serious damage to internal organs, brain tissue, central nervous system with long-term treatment. The shorter the period of recovery from shock, the less severe tissue damage is predicted.
Forecast
Septic shock represents mortal danger for the patient, therefore it is extremely important both early diagnosis, and emergency intensive treatment.
- The time factor is crucial in predicting this condition, since irreversible pathological changes in tissues occur within 4–8 hours; in many cases, the time for providing assistance is reduced to 1–2 hours.
- The probability of death with septic shock reaches more than 85%.
This video talks about septic shock due to TBI:
Emergency care for infectious-toxic shock begins to be provided at the prehospital stage. The ambulance team stabilizes the hemodynamic state (blood pressure, pulse), stabilizes breathing and returns adequate diuresis. To do this, vasopressors are administered intravenously: 2 ml of a 0.2% solution of norepinephrine (norepinephrine) with 20 ml saline solution or 0.5-1 ml of 0.1% solution of epinephrine (adrenaline), and glucocorticosteroids: 90-120 mg prednisolone intravenously or 8-16 mg dexamethasone intravenously. Oxygen therapy and artificial ventilation are performed in cases of severe respiratory failure and respiratory arrest.
Hospitalization is carried out in the intensive care unit or intensive care unit where further emergency care is provided. Catheterization in progress Bladder to control diuresis, catheterization of the subclavian vein and monitoring the state of the respiratory and cardiovascular systems.
To maintain hemodynamics and vital important functions body is used:
Inotropic agents:
200 mg of dopamine (5 ml of a 4% dopamine solution must be dissolved in 400 ml of a 5% glucose solution) is administered intravenously at a rate of 3-5 mcg/kg/min, followed by an increase to 15 mcg/kg/min;
40 mg of norepinephrine (norepinephrine) (2 ml of 0.2% norepinephrine solution dissolved in 400 ml of 5% glucose solution) is administered intravenously at a rate of 2 mcg/kg/min and then increased to 16 mcg/kg/min.
Glucocorticosteroids:
Prednisolone is used intravenously up to 10-15 mg/kg/day. Up to 120 mg is administered one-time and if a positive effect is observed, then after 4-6 hours the procedure is repeated.
Oxygen therapy:
Inhalation of humidified oxygen is performed at a rate of 5 l/min.
To correct hemorheological disorders the following is used:
Colloidal and crystalloid solutions:
400 ml of rheopolyglucin;
100 ml of 10% albumin solution;
400 ml 5% glucose solution
400-800 ml saline solution
The total volume of fluid should not exceed 80-100 ml/kg/day.
Antithrombins:
Unfractionated heparins are administered: the first dose is 5000 units intravenously, then 3-4 times a day is administered subcutaneously at a rate of 80 units/kg/day.
Antienzyme therapy:
1000 IU/kg/day Contrical or 5000 IU/kg/Sutgordox is administered intravenously 3-4 times a day, dissolved in 500 ml of saline.
Also, after emergency care for infectious-toxic shock, you should switch to bacteriostatic antibiotics (erythromycin, lincomycin) or reduce the dose of the antibiotic that was previously used to treat the disease that caused the shock.
118. Basic and the most urgent measure to treat and prevent progression hemorrhagic shock should be considered the search for the source of bleeding and its elimination.
The second fundamental action that decides the issue of preserving the patient’s life is the speed of restoration of blood volume. The infusion rate is determined by the most accessible indicators - blood pressure, heart rate, central venous pressure and minute diuresis. Moreover, in the case of ongoing bleeding, it should advance the rate of blood flow by approximately 20%.
Such a speed of solution administration can be achieved only if there is reliable access to the central venous vessels using a large-diameter catheter. Therefore, catheterization of the subclavian or jugular vein is included in the range of emergency measures.
We should not forget about the simultaneous catheterization of preferably two peripheral vessels, necessary for long-term, strictly dosed administration of drugs, as well as the installation of a catheter in the bladder.
(Option 2): To eliminate fluid loss during compensated shock (the initial stage of hypovolemic shock), an isotonic sodium chloride solution and a 5% glucose solution are prescribed, a 5% albumin solution - 10 ml/kg, rheopolyglucin - 10-15 ml/kg. kg.
In case of subcompensated and compensated shock, the total volume of colloids should be at least a third of the infusion volume, and crystalloids - 2/3.
In the case of decompensated (that is, the most severe) hypovolemic shock, emergency surgical correction of hemodynamic disorders includes injections of a 5% albumin solution, a 6% rheomacrodex solution and plasma-substituting solutions: a 6% hemacel solution, a 6% plasmasteril solution, a 6% solution hydroxyethyl starch or hydroxyethylamylopectin, 5% solution of jellyfundol.
The crystalloid volume should include sodium bicarbonate and glucose-salt solutions. It is not recommended to administer potassium chloride outside the hospital due to the risk of hyperkalemia.
If shock progresses, moving into the subcompensated and then into the decompensated stage, and therapy does not give the proper effect, sympathomimetics are prescribed (dopamine - 1-5 mcg/kg per minute).
119. Emergency care for an attack of bronchial asthma.
1. It is immediately necessary to remove causally significant allergens or minimize the patient’s interaction with him.
2. Provide access to fresh air, unbutton the patient’s clothes.
3. Give one of the drugs that has a bronchospasmolytic effect: Berotec N, salbutamol, Berodual. 1-2 doses are administered using a dosing aerosol inhaler or through a nebulizer (the interval between inhalations is 2 minutes).
4. You can give the patient 1 tablet of aminophylline.
5. If there is no effect, repeat inhalation after 20 minutes.
120. Status asthmaticus does not respond for treatment with inhalers. To treat status asthmaticus, it is necessary to regularly use aerosols and parenteral administration antibiotics such as epinephrine and prednisone. Also used to treat status asthmaticus is parenteral administration of terbutaline, the use of magnesium sulfate, which helps to relax the muscle tissue around respiratory tract, and a leukotriene inhibitor, which has an anti-inflammatory effect. During an attack of status asthmaticus that is not responding to regular asthma medications, you may also need a ventilator to help your lungs and airway muscles work. In this case, use a breathing mask or snorkel, which is inserted into the nose or mouth. These aids are temporary, the need for them disappears as soon as the acute attack passes and lung function is restored. It is possible that after such an attack you will need to spend some time in the intensive care unit.
To avoid the need for urgent hospitalization, it is necessary to begin treatment for asthma at the first, even minor, signs and symptoms of status asthmaticus.
121pneumothorax. First aid: stop bleeding and the flow of air into the pleural cavity by applying a tight, airtight bandage. Naturally, it will not be sterile, since improvised means will be used, but the cleanest available must come into direct contact with the wound. It would be nice to add a plastic film or oilcloth on top of the bandage for a more convincing seal.
To make breathing easier, the injured person should be placed in an elevated position, again using available means. This must be done carefully so as not to cause additional suffering.
If you faint, bring a strong-smelling product to your nose. Ammonia is not always at hand. It can be replaced by perfume, nail polish remover, gasoline, finally. For pain, give analgin, aspirin, if available. And wait for the ambulance doctor to arrive.
Health care
An X-ray examination will give an objective picture of the lesion. Normally, the ribs and lungs with a characteristic pulmonary pattern are clearly visible on the x-ray. You can also judge the degree of displacement of the heart and second lung. With pneumothorax, a thickening of the pulmonary pattern in the compressed lung is visible, and the presence of gas is indicated by the absolute transparency of the lateral section chest(no pulmonary pattern).
What surgeons do: An open pneumothorax is converted to a closed one by suturing the wound.
The gas is then sucked off, restoring negative pressure.
Measures are taken to combat shock by administering painkillers.
They combat a sharp decrease in blood pressure due to blood loss with blood transfusions, and the resulting shock with medications that stimulate the vascular and respiratory centers.
Valvular pneumothorax is converted to closed pneumothorax by excision of the valve.
Then the gas is evacuated using a special apparatus.
35. PROTOCOL: HURTICS. ANGIONEUROTIC EDEMA (ANGIONEUROTIC EDEMA)
Hives. Angioedema (Quincke's edema)– acute allergic diseases caused by hypersensitivity immune system to various exogenous antigens (allergens). They are characterized by sudden onset, unpredictable course, high risk life-threatening states.
Localized urticaria manifests itself with a sudden appearance in a limited area skin urticarial elements with clear boundaries, usually red, with a diameter of several elements to several centimeters, against a background of hyperemia, accompanied by itching.
Generalized urticaria characterized by total damage to the skin; a merging of the elements described above is often observed.
Quincke's edema (angioedema) manifested by local swelling of the skin, subcutaneous tissue and/or mucous membranes. It most often develops in the area of the lips, cheeks, eyelids, forehead, scalp, scrotum, hands, and dorsal surface of the feet. Allergic swelling of the gastrointestinal tract is accompanied by intestinal colic, nausea, and vomiting. With Quincke's edema, localized in the larynx, cough, hoarseness, difficulty swallowing, suffocation, and wheezing are observed. In 50% of cases, angioedema is combined with urticaria.
Generalized urticaria and angioedema (Quincke's edema) are severe (prognostically unfavorable) acute allergic diseases.
HURTICS Termination by Quincke's edema
allergen steps
Diphenhydramine 1% -2 ml intravenously
Prednisolone
intravenously 90-150 mg
When swelling spreads to the larynx and pharynx:
adrenalin
intravenously 0.3 ml of 0.1% solution in 20 ml of 0.9% sodium chloride solution
Oxygen therapy.
Readiness for emergency restoration of patency of the upper respiratory tract (tracheal intubation, conicotomy)
Hospitalization (for generalized urticaria and Quincke's edema)
36. PROTOCOL: LYELL'S SYNDROME
Lyell's syndrome (epidermal toxic necrolysis)–
This is a severe toxic-allergic dermatosis of an infectious or drug-induced nature, characterized by sudden violent necrosis of superficial areas of the skin and mucous membranes with the formation of large blisters that quickly open. Accompanied by severe general intoxication.
Diagnostics:
There is severe hyperesthesia of the affected areas. The lesion spreads to the mucous membrane of the eyes, mouth, nasal cavity, pharynx, and genitals. With the rejection of the epidermis, extensive erosion is formed. Associated infection leads to sepsis, multiple organ failure, disseminated intravascular coagulation syndrome (DIC syndrome)
Stopping the intake of allergen
Oxygen therapy
Ensuring the patency of the upper respiratory tract
Intravenous fluid administration (polyglucin, reopo-
liglucin, 0.9% sodium chloride solution or 5% glucose solution)
Adrenaline intravenously 0.3 ml of 0.1% solution in 20 ml of 0.9% sodium chloride solution
Prednisolone intravenously 90-150 mg
Diphenhydramine 1% -2 ml intravenously
For bronchospasm: | ||||
if the patient can do effectively | ||||
inhalative - salbutamol 2.5 mg | ||||
(1 nebula) or berodual 1 ml (20 | ||||
drops) through a nebulizer. | ||||
If you don't have a nebulizer or | ||||
serious condition of the patient - eu- | ||||
fillin 5-6 mg/kg (10 – 15 ml 2.4% | Protocol |
|||
solution) intravenously | ||||
Hospitalization under monitoring of vital functions Use of sterile linen
37. PROTOCOL: DIABETIC COMA (HYPERGLYCEMIC)
Diabetic coma– acute disorder carbohydrate metabolism, caused by a decrease in insulin levels, a significant increase in blood glucose concentrations and associated water and electrolyte imbalances. As a rule, it is known that the patient suffers from diabetes mellitus; less often, diabetic coma becomes the first symptom of diabetes mellitus.
An increase in glucose levels can be caused by:
insufficient dose of insulin;
diet disorders;
intercurrent infectious and other diseases;
stress ( surgery, accident, psi-
There are two main forms of diabetic coma:
Diabetic ketonemic coma:
This coma is based on absolute insulin deficiency, which leads to increased levels of lipolysis, production of ketone bodies and severe metabolic acidosis. In most cases, diabetic ketonemic coma complicates type 1 diabetes mellitus, but diabetes may not be known. The main signs of diabetic ketonemic coma are unconsciousness, dehydration, acute hypovolemic circulatory failure, hyperglycemia (16 - 33.3 mmol/l), ketoacidosis, glucosuria and ketonuria. Deep, rare, noisy breathing (Kussmaul breathing), smell of acetone.
Diabetic non-ketonemic hyperosmolar coma:
As a rule, it complicates the course of unrecognized type II diabetes mellitus in patients over 40 years of age. The development of coma is gradual, characterized by neurological disorders, severe shortness of breath in all patients, sinus tachycardia, arterial hypotension, low diuresis up to anuria, glucosuria without ketonemia. Hyperglycemia more than 33.3 mmol/l. Kussmaul's breath and the smell of acetone are not typical. It is much less common than ketonemic coma.
Examination of the patient. Glucometry
Ensuring the patency of the upper respiratory tract. Oxygen therapy. Venous access.
Rehydration:
sodium chloride solution 0.9% 1 liter per hour (intravenous drip) An excessively rapid rate of rehydration can cause cerebral edema (it is necessary to reduce the rate of fluid administration and intravenous
For severe collapse, dopamine 200 mg in 200 ml of 5% glucose IV at a rate of 4-5 mcg/kg/min
For prolonged coma, heparin 10,000 units intravenously as a bolus
Hospitalization under monitoring of vital functions
38. PROTOCOL: HYPOGLYCEMIC STATE
Occurs, as a rule, in patients with diabetes mellitus during insulin therapy or therapy with sulfonamide antihyperglycemic drugs of the second and third generation: glibenclamide (Maninil), guikvidone (Glyurenorm), gliclazide (Diabeton, Predian).
The direct cause of hypoglycemic conditions in diabetes mellitus Usually there are violations of the eating pattern, an overdose of sugar-lowering drugs.
TO rare reasons Hypoglycemic conditions include insulinoma, glycogen storage diseases, and functional hyperinsulinism.
Chronic renal failure, intake of ethanol, salicylates, and adrenergic blockers potentiate the development of hypoglycemic conditions. The latter also obscure the clinical picture of hypoglycemic conditions, eliminating the adrenergic components of its manifestations.
At the precursor stage, subjective sensations are observed (not in all patients) of sudden weakness, feelings of hunger, anxiety, headache, sweating, and less often - a feeling of numbness in the tip of the tongue and lips. If at this stage the hypoglycemic state is not stopped by taking carbohydrate-containing products, then agitation, disorientation, then stupor, convulsions, and stupor develop.
At the stage of a full-blown hypoglycemic state, the patient experiences impaired consciousness or loss of consciousness, severe sweating, tachycardia, and sometimes increased blood pressure, increased muscle tone, clonic and tonic convulsions. Tissue turgor is normal.
Symptoms of a hypoglycemic state appear when the blood glucose level is below 2.78-3.33 mmol/l. Rarely, a hypoglycemic state can be combined with ketoacidosis.
Differential diagnosis
Differentiation from diabetic non-ketonemic coma is based on the absence of hyperglycemia, ketoacidosis, and dehydration in a hypoglycemic state.
Differentiation of a hypoglycemic state and acute cerebrovascular accident, as well as an epileptic seizure, is based on rapid positive effect intravenous administration of glucose in a hypoglycemic state.
Severe long-term unresolved hypoglycemia progresses to coma; convulsions and sweating stop, areflexia, progressive arterial hypotension, and cerebral edema develop; achieving normoglycemia and even hyperglycemia at this stage of the hypoglycemic state does not lead to success.
In patients with coronary disease heart and brain, a hypoglycemic state can provoke an acute violation of coronary or cerebral circulation; patients in this category require ECG registration and emergency hospitalization.
Examination of the patient. Glucometry
Ensuring the patency of the upper respiratory tract. Venous access.
Glucose 40% solution 20-50 ml intravenously.
consciousness |
|||||||||||
no effect | |||||||||||
recovery |
|||||||||||
Glucose 40% solution 20-50 ml intravenously. | |||||||||||
(until the glycemic level reaches 8-9 mmol/l) | |||||||||||
no effect | |||||||||||
Prednisolone 30-60 mg intravenously | |||||||||||
no effect | |||||||||||
Feed carbohydrate-containing |
|||||||||||
pressing products |
|||||||||||
Hospitalization | |||||||||||
(sugar, bread, potatoes) |
|||||||||||
39. PROTOCOL: SEPTIC SHOCK
Septic shock on prehospital stage diagnosed if the following are present clinical symptoms:
presence of a focus of infection (not always)
systolic blood pressure below 90 mm Hg. Art.;
disturbance of consciousness;
oliguria;
the number of respiratory movements (RR) is more than 20 per minute;
the number of heart contractions (HR) is more than 90 per minute;
body temperature is above 38o C or below 36o C;
Therapy Notes:
The rate of drug administration should be adjusted to stabilize systolic blood pressure above 90 mmHg. Art.
Administration of polyionic solutions of no more than 1000 ml during the period of assistance (administration of large volumes of crystalloid solutions with increased permeability of the vascular wall can lead to an increase in edema of the lungs, brain and other organs, and worsening multiple organ failure)
Emergency hospitalization in the intensive care unit is carried out after stabilization of blood pressure against the background of ongoing mechanical ventilation and infusion therapy.
EMERGENCY CARE FOR SEPTIC SHOCK
If the respiratory rate is more than 40 per minute - Septic shock, tracheal intubation and mechanical ventilation.
Oxygen therapy.
Monitoring of vital functions. Venous access. Oxygen therapy.
Infusion colloidal solutions(polyglucin, rheopolyglucin, hydroxyethyl starch)
Prednisolone
intravenously 90-150 mg
Infusion of crystalloid polyionic solutions
Hospitalization after stabilization of blood pressure
40. PROTOCOL4: PNEUMONIA
Diagnostic algorithm
SYMPTOMS: | |||||||||||||||||||||||
appeared or intensified | |||||||||||||||||||||||
chest pain associated with breathing | |||||||||||||||||||||||
the presence of purulent mucous membrane | |||||||||||||||||||||||
fever 38.0 C or more. | |||||||||||||||||||||||
Pneumonia | |||||||||||||||||||||||
unlikely | |||||||||||||||||||||||
physical symptoms | |||||||||||||||||||||||
wet rales; | |||||||||||||||||||||||
There is not a single symptom | bronchial breathing; | ||||||||||||||||||||||
shortening of percussion | |||||||||||||||||||||||
Availability at least | weakening of breathing | ||||||||||||||||||||||
one symptom | limited area. | ||||||||||||||||||||||
PNEUMONIA | |||||||||||||||||||||||
disturbance of consciousness; | |||||||||||||||||||||||
Not severe | |||||||||||||||||||||||
NPV 30 per minute or more; | |||||||||||||||||||||||
Blood pressure less than 90/60 mm Hg. | pneumonia | ||||||||||||||||||||||
poor prognosis: | |||||||||||||||||||||||
Age over 60 years; | pneumonia | ||||||||||||||||||||||
Treatment algorithm
Mild pneumonia Outpatient
Severe pneumonia
Protocols: “Acute respiratory failure”, “Septic shock”, “Pulmonary edema”
For arterial hypotension:
Lay the patient down at an angle of 15-20° lower limbs; IV jet-plasma-substituting solutions (polyglucin, reopolyglu-
kin, gelatinol, 5% glucose solution); the total volume of infusion therapy is at least 1000-1500 ml; glucocorticoid hormones IV infusion in terms of prednisolone
vasopressors (norepinephrine) 2 - 4 ml 0.2% IV drip or dopamine 200 mg per 200 ml plasma replacement solution, increasing the infusion rate until a systolic pressure of 90-100 mm Hg is achieved. Art.; oxygen therapy with an oxygen-air mixture with an oxygen content of no more than 30-40%; heparin 5000-10000 units intravenously by drip or stream.
For delirious syndrome:
reliable fixation of the patient;
intravenous diazepam 0.2-0.3 mg/kg; repeated administration no earlier than 15 minutes until sedative effect; if the effect of diazepam administration is insufficient - 40-50 ml 20%
sodium hydroxybutyrate solution (80-100 mg/kg) intravenously slowly.
Hospitalization
41. PROTOCOL: BRONCHIAL ASTHMA
Clinical picture:
often at the onset – cough;
extended exhalation;
noisy wheezing;
in some cases stridor;
tachycardia and arterial hypertension;
anxiety, fear, sweating;
swollen neck veins;
“Alarm symptoms” of a life-threatening attack of bronchial asthma:
rapidly increasing shortness of breath (in adults, more than 25 per minute);
inability to speak due to shortness of breath;
participation in breathing of auxiliary muscles;
tachycardia more than 110 per minute;
Signs of life threatening:
cyanosis of the skin with a grayish tint;
confusion or coma;
weak inspiration, respiratory rate more than 30 per minute or less than 12 per minute;
Heart rate more than 120 per minute or bradycardia;
arterial hypotension;
respiratory sounds are not heard during auscultation (“silent lung”);
Therapy Notes:
Contraindicated: psychotropic drugs, narcotic analgesics, sedatives, antihistamines first generation, mucolytic agents for thinning sputum, antibiotics, sulfonamides, novocaine, calcium preparations, diuretics, acetylsalicylic acid, atropine.
Avoid massive hydration.
It is preferable to use inhalation therapy via nebulizer and infusion forms medicines.
Selective B2-adrenergic agonists short acting used if heart rate is less than 130 per minute.
EMERGENCY CARE FOR BRONCHIAL ASTHMA
Mild attack: | ||
RR up to 22/min., | through a nebulizer for 5 – 15 minutes; |
|
Heart rate 100 per minute; | ||
wheezing breathing | berodual 1 ml (20 drops) |
|
at the end of exhalation | ||
In the absence of a nebulizer or ineffective |
||
After cupping | effectiveness of nebulizer therapy: |
|
aminophylline 5 - 6 mg/kg (10-15 ml 2.4% i.v. |
||
patient's attack | ||
for 5-7 minutes) |
||
you can leave it at home | ||
Moderate attack:
RR 25-30 per minute, heart rate 100-120 per minute on auscultation: wheezing on inhalation and exhalation
After stopping the attack, the patient can be left at home
Severe attack:
RR > 30/min., HR > 120/min; on auscultation:
loud wheezing breathing when inhaling and exhaling
Salbutamol 1.25 - 2.5 mg (0.5 - 1 nebula)
through a nebulizer for 5 – 15 minutes; or
berodual 1 ml (20 drops)
through a nebulizer for 10 - 15 minutes.
If a nebulizer is not available or nebulizer therapy is ineffective:
aminophylline 5 - 6 mg/kg (10-15 ml 2.4% i.v.
within 5-7 minutes)
Prednisolone 60 – 150 mg IV.
Oxygen therapy(mixture containing 30-
40% oxygen).
No effect - hospitalization
If necessary, call a resuscitation team
42. PROTOCOL: ALCOHOL WITHDRAWAL
Alcohol withdrawal syndrome (AAS) develops with long
body (from 3 days or more) alcoholization, as a response of the body to the withdrawal of alcohol.
The severity of AAS is determined by the severity of adrenergic syndrome.
Mild degree: Symptoms appear on the first day after reducing the amount of alcohol you usually drink or completely stopping its use.
Adrenergic syndrome (+):
Heart rate up to 100/min;
diastolic blood pressure not less than 100 mm Hg. Art.,
normal temperature bodies.
criticism saved;
absence of delirium and hallucinosis.
In the absence of complications, patients can stay at home.
Average degree: Symptoms appear a day or more after stopping ethanol, reaching a maximum by 2-3 days, and include: insomnia, tremor, anxiety, nausea, hyperhidrosis, hyperreflexia.
Adrenergic syndrome (++):
Heart rate 100-120 per minute;
diastolic blood pressure 100-110 mm Hg. Art.,
low-grade fever (up to 38°C) or normal body temperature;
Criticism is preserved (perceptual deceptions are assessed by the patient
volume critically). Absence of delirium and hallucinosis. Patients require detoxification and observation.
Severe: Symptoms appear 2 days or more after stopping ethanol, reaching a maximum by 2-4 days. Adrenergic syndrome:
Heart rate more than 120/min;
diastolic blood pressure more than 110 mm Hg. Art.;
increase in body temperature (38°C and above);
Criticism, as a rule, is preserved. Possible disorientation
visual hallucinations, delirium, convulsions.
Patients require hospitalization in the ICU or ICU. Transportation in the supine position.
EMERGENCY CARE FOR AAS
Alcohol withdrawal syndrome
Ensuring the patency of the upper respiratory tract. Monitoring of vital functions.
Infusion therapy: glucose solution 5% 400 ml
Thiamine 100 mg intravenously slowly
At arterial hypertension (systolic blood pressure > 160 mm Hg,
diastole Blood pressure > 110 mm Hg. Art.):
nifedipine (orally) 10 mg, propranolol 20-40 mg (orally), diazepam 20-40 mg (intramuscular);
if ineffective: diazepam 20 mg idroperidol 2.5-5 mg (intramuscular). If ineffective, repeat the administration of the drugs after 20-30 minutes.
For arterial hypotension (systolic blood pressure< 90 мм рт. ст.):
Reopoliglucin 400 ml;
- if ineffective - prednisolone 30-60 mg intravenously;
- in case of ineffectiveness dopamine drip (at a rate not
required to maintain SBP within 100-110 mm Hg. Art.)
For coma: thiamine 100 mg intravenously slowly in fractions; naloxone 0.4 mg in 40 ml of 40% glucose solution (the substances are compatible with each other)
For seizures: protocol “Convulsive syndrome”
Hospitalization of a patient with severe and (or) complicated AAS.
43. PROTOCOL: MEDIATOR SYNDROMES
Sympathetic syndromes Adrenergic syndrome: mydriasis, pupils are not changed, hypertensive
Zia, reflex bradycardia (with stimulation of β-adrenergic systems), tachycardia (with stimulation of β-adrenergic systems), loud heart sounds, gallop rhythm, 3rd tone; dry mucous membranes, pale, moist skin (with excitement - adrenergic systems), reduced intestinal motility, muscle hypertonicity, rhabdomyolysis.
Toxic agents: cocaine, ephedron, amitriptyline (in the early phase of action), cold remedies with adrenomimetics, synthetic amphetamines, aminophylline, caffeine, phencyclidine, LSD, MAO, thyroid hormones.
Sympatholytic syndrome: miosis, hypotension, bradycardia, muffled, bifurcated heart sounds, respiratory depression, decreased intestinal motility, muscle hypotension.
Toxic agents: sympatholytics, clonidine, (β-blockers, calcium channel blockers, reserpine, opiates and their homologues (in the late phase of action).
Parasympathetic syndromes Cholinergic syndrome: miosis, spasm of accommodation, bradycardia, tachycardia, muffled heart sounds, bronchorrhea, wheezing in the lungs, diarrhea, moist skin and mucous membranes, lacrimalia, salivation, defecation, urination, myofibrillation, convulsions.
Toxic agents: FOS, insecticides (carbamates).
Anticholinergic syndrome: excitement/agitation, delirium,
mydriasis, accommodation paralysis, tachycardia, increased heart sounds, 3rd tone, normotension, dry mucous membranes and skin, warm, pink skin (increased body temperature in children), decreased intestinal motility, impaired urine outflow.
Toxic agents: antihistamines, antidepressants, antipsychotics with sedative effects, anticholinergics, belladonna alkaloids.
Toxic agents, in case of poisoning which may cause symptoms of an “acute abdomen”:
Cholinomimetics and choline-sensitizing agents - cardiac glycosides, reserpine, mushroom poisoning; botulinum toxin; heavy metals (lead, arsenic, mercury); spider venom (black widow); thiazide diuretics; steroid hormones; azathioprine; corrosive poisons; oral contraceptives; anticoagulants.
Odors of some toxic compounds
Substance, state | ||
Bitter almonds |
||
Hydrogen sulfide, mercaptans, teturam | Rotten eggs |
|
Phenol, creosote | Disinfectants |
|
Phosphorus, tellurium, selenium, thallium, arsenic | ||
Marijuana, opium | Burnt grass |
|
"Alcohol" smell |
||
Chloroform, trichlorethylene, | ||
methyl chloride, isopropanol | (sweet, fruity) |
|
Ammoniacal |
||
Diabetes, ketoacidosis | Fruit |
44. PROTOCOL: ACUTE POISONING
Poisoning is a pathological condition caused by the penetration of toxic substances of various origins into the human body from outside.
The severity of the condition in case of poisoning is determined by the dose of the poison, the route of its entry, the exposure time, the premorbid background of the patient, complications (hypoxia, bleeding, convulsive syndrome, acute cardiovascular failure, etc.).
A pre-hospital medical worker must:
observe “toxicological alertness” (the environmental conditions in which the poisoning occurred may pose a danger to the ambulance crew);
find out the circumstances surrounding the poisoning (co-
where, what, how, how much, for what purpose ), in the patient, if he is conscious, or in those around him;
collect material evidence (medicine packages,
powders, syringes), biological media (vomit, urine, blood, washing water) for chemical-toxicological or forensic chemical research;
register the main symptoms (syndromes) that were observed in the patient before treatment medical care, including mediator syndromes resulting from increased or suppressed sympathetic and parasympathetic
If there is no antidote, it is necessary to correct the indicators of hemodynamic and respiratory depression.
Assessment of the patient's condition.
Identification of poison and the route of entry of poison into the body
Ensure normalization of breathing and cardiac activity
Antidote therapy
If there is no antidote, it is necessary to correct hemodynamic and respiratory parameters.
Stopping the entry of poison into the body
Oral | Inhalation | Percutaneous |
|||||||||
poisoning | poisoning | poisoning |
|||||||||
Probe rinsing | Delete by | ||||||||||
onion with water (up to 180 C) | suffering | ||||||||||
Reactions to neutralize poison in | from an infected | ||||||||||
do not carry out the stomach! | |||||||||||
atmosphere | skin drain |
||||||||||
The presence of blood is not | |||||||||||
solution |
|||||||||||
contraindication for breast cancer | |||||||||||
antidote |
|||||||||||
Enterosorption | |||||||||||
(up to 180 C) |
|||||||||||
Cleansing enema | |||||||||||
Measures aimed at removing absorbed poison |
|||||||||||
Infusion therapy | Hyperventilation | Artificial fur- |
|||||||||
followed by forced | detoxification methods |
||||||||||
bath diuresis | (hemo- and plasmasorb- |
||||||||||
tion, peritoneal |
|||||||||||
dialysis, etc.) |
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Symptomatic therapy | |||||||||||
Septic shock– this is the most common complication in the development of a purulent-infectious process caused predominantly by gram-negative bacteria. As a result of the destruction of all these types of bacteria, the active release of endotoxin occurs, which is a kind of provocative mechanism for the development of such pathology as infectious-septic shock. When exposed to gram-positive bacteria, the pathogenesis of septic shock almost never develops. In addition to the above types of bacterial flora, anaerobic flora in the form of Clostridiaperfringens, rickettsia, herpes viruses and cytomegalovirus, and somewhat less often, fungi and protozoa, can also provoke the development of septic shock.
This pathology, in its pathogenesis, largely depends on the state of the general individual resistance of the human body, as well as the concentration of the pathogen and the degree of its pathogenicity. Considering these features of pathogenesis, the most common clinical form of this pathology is septic shock in obstetrics.
Such a fairly common pathology as septic shock in gynecology, in turn, is divided into etiopathogenetic forms such as septic out-of-hospital abortion, infectious and post-infectious abortion performed in a gynecological hospital. The early development of septic shock in gynecology and obstetrics is due to the fact that the pregnant uterus is a kind of entrance gate for the penetration of infectious agents, blood clots act as nutrient medium for the proliferation of microorganisms, during this period there is a change in hormonal status female body, as well as development, aggravating the course of shock.
It should be borne in mind that the clinical picture of septic shock can also be complicated by the development of limited or diffuse peritonitis, which is an extremely unfavorable factor and can cause death.
Causes of septic shock
This complication of blood poisoning has been sufficiently studied; the pathogenesis of septic shock represents a wide range of pathological reactions of the human body, each of which directly depends on the individual characteristics of the patient’s body. As factors that have a stimulating effect on the development of septic shock, it should be noted: features of the pathogenicity of the pathogen, localization of the primary inflammatory focus, duration of sepsis, features clinical course background infection, pathogen concentration, age and function of the patient’s immune system, the presence of additional traumatic exposure.
The initial link in the pathogenesis of septic shock is the direct entry of toxins secreted by microorganisms into the general bloodstream, accompanied by the destruction of cell membranes of endothelial cells, as well as platelet and leukocyte blood cells. As a result of these changes, there is an active release of lysosomes containing proteolytic enzymes that activate vasoactive substances such as kinin, histamine, serotonin, catecholamine, renin.
Thus, the peripheral circulation undergoes primary pathological changes, manifested by vasoplegia in the capillary network, leading to the development of a sharp decrease in peripheral resistance. In the initial stage they are triggered compensatory mechanisms in the form of an increase in cardiac output, as well as the development of regional arteriovenous shunting. And at the same time, already at this stage of septic shock there is a decrease in capillary perfusion, a disruption in the absorption of oxygen by the brain and other vital structures of the human body.
Septic shock is characterized by early development and a lightning-fast increase in the intensity of DIC as a result of hyperactivation of the platelet and procoagulant components of hemostasis. These changes have an extremely Negative influence on the course of metabolic processes occurring in all tissues of the human body, which is accompanied by excessive accumulation of under-oxidized products.
With the continued damaging effect of toxic substances released in high concentrations by microorganisms, circulatory disorders deepen. As a result of increased permeability of the vascular walls of the capillary network, blood plasma and individual blood elements leak into the interstitium, which causes the development. At this stage of the pathogenesis of septic shock, compensatory mechanisms cease to be effective and an increase in peripheral hemodynamic disturbances occurs.
The development of septic shock occurs as a result of deterioration of coronary circulation, the negative effects of bacterial toxins, and a decrease in the response of the heart muscle to adrenergic stimulation. The first pathogenetic sign of the onset of cardiac dysfunction in septic shock is sharp and persistent, which corresponds to the hypodynamic phase of septic shock.
The severe clinical picture of septic shock is largely due to the development of changes in the structure and function of the respiratory system, accompanied by the development of the so-called pathogenetic stage of “shock lung”. The above changes provoke the development of mechanisms of acute respiratory failure, accompanied by a profound disruption of oxygen transport throughout the patient’s body.
Symptoms and signs of septic shock
Septic shock is characterized by the development of pathognomonic clinical symptoms, often allowing even at an early stage of development this complication verify the diagnosis. The intensity of a particular clinical manifestation of septic shock has a correlation dependence on the pathogenetic stage of shock, the duration of pathomorphological changes, the degree of influence of the pathogenicity of the pathogen and the presence of any severe background somatic pathology that worsens the course of septic shock. Extremely severe clinical symptoms Septic shock is different in obstetrics. In general, septic shock in gynecology and surgery is the most common cause of death.
Debut clinical picture septic shock is always acute, since its development is most often associated with the presence of an extensive infected wound surface. Before the appearance of clinical symptoms pathognomonic for septic shock, there is always a short-term pyretic reaction of the hectic type organism lasting no more than three days. Also, at the onset of the clinical picture of septic shock, the development of undulating fever, characterized by rapid attack and relief of hyperthermia, accompanied by severe chills and profuse sweating.
At the same time, the most characteristic clinical marker of septic shock, which also appears in other etiopathogenetic variants of shock, is sudden bleeding without obvious signs. In the early stages of the development of septic shock, compensatory mechanisms are “triggered”, and therefore, within an hour the patient experiences a hyperdynamic phase of shock, characterized by a moderate decrease in systolic blood pressure. This is the so-called stage of “imaginary well-being”, in which verification of the diagnosis is somewhat difficult. With the onset of the hypodynamic phase of septic shock, sharp persistent arterial hypotension is noted. A feature of the clinical course of septic shock is the development of arterial hypotension in the patient, combined with severe tachycardia and a shock index of more than 1.5, which is an indirect sign of a rapid decrease in blood volume.
In addition to the above clinical manifestations, septic shock is characterized by the early development of respiratory disorders, manifested by severe shortness of breath, indicating the development of increasing tissue dyspnea. Insufficient oxygen supply to the structures of the central nervous system has an extremely negative impact on the patient’s condition, which is manifested by the appearance of unmotivated agitation and disorientation in person, time and place, quickly giving way to lethargy. In some patients, these neurological disorders may precede severe arterial hypotension.
Long-term clinical markers of septic shock include icterus and dry skin, increasing and petechial, which is a manifestation of multiple organ failure. Some patients experience the development of nonspecific abdominal pain syndrome, as well as severe headache, which is caused by impaired blood supply to the tissues. When septic shock occurs, which develops in 98% of cases, vomiting is noted. coffee grounds"and widespread hemorrhages in the mucous membranes and skin.
Emergency care for septic shock
The beginning of resuscitation measures for septic shock consists of performing mechanical ventilation in cases where respiratory distress syndrome develops. When determining the tidal volume for mechanical ventilation, a calculation method of 6 ml per kg of patient weight is used, so that the pressure in the respiratory tract during exhalation does not exceed 30 cm of water column. When performing mechanical ventilation for septic shock, hypercapnia is allowed, however, the inspiratory pressure should be reduced, and SaO2 should be maintained at 88–95%. Besides, positive influence During oxygenation, the patient is positioned on his stomach, as well as the head end of the bed is elevated by 45°.
When the patient has moderately severe hypoxemia, responding to low levels of PEEP, as well as stable hemodynamics, independent clearance of secretions from the airways through a mask is allowed, however, it should be borne in mind that at any time the patient may need emergency tracheal intubation.
In the case when the patient, during mechanical ventilation, has stabilization of hemodynamic parameters, a safe FiO2 indicator, cessation of sedation and the appearance of spontaneous cough, as well as paO2/FiO2 exceeds 200 mm Hg. Weaning from the respirator is permissible. In a situation where weaning from a respirator is accompanied by an increase in the frequency of respiratory movements and heart contractions, as well as critical arterial hypotension, it is necessary to immediately resume mechanical ventilation.
In the severe condition of a patient in need of emergency mechanical ventilation, it is imperative to carry out emergency sedation, for which bolus or continuous parenteral administration of drugs from the group of muscle relaxants is used, which allows not only to reduce the duration of mechanical ventilation, but also to reduce the likelihood of tracheostomy.
The standard set of emergency measures for septic shock must include an insulin infusion, if available, until the blood glucose level reaches no more than 8.3 mmol/l. At the same time, when administering insulin, it is necessary to carry out a glucose infusion with mandatory monitoring of blood glucose levels at intervals of 1 hour.
When considering the use of sodium bicarbonate as an emergency treatment for septic shock, blood pH should be assessed. Thus, when the pH is 7.15, sodium bicarbonate should not be administered, since in this situation there is no correction of hemodynamic disturbances and the need for the use of vasopressors is not reduced.
As an emergency preventive measure for septic shock, preventing its characteristic development, the patient should be prescribed low doses of unfractionated Heparin in the early period. TO absolute contraindications for the use of drugs of this pharmacological group should include the patient's thrombocytopenia, severe coagulopathy, ongoing bleeding, intracerebral hemorrhage. In this situation, one should resort to mechanical methods of emergency prevention in the form of mechanical compression.
When carrying out emergency medical measures in relation to a patient suffering from septic shock, the task of the attending physician is to explain to his family members about the types of resuscitation treatment used, as well as possible outcomes of this disease.
Diagnosis of septic shock
In some situations, with known anamnestic data and existing pathognomonic clinical manifestations in the patient, it becomes possible to establish a primary clinical diagnosis already at the pre-laboratory stage. And at the same time, an assessment of the severity of septic shock can be determined diagnostically only after a comprehensive examination of a person, including not only laboratory, but also high-precision instrumental techniques.
Thus, at the debut of pathogenetic changes in sepsis, the development of septic shock is indicated by the appearance of severe thrombocytopenia less than 100 109/l, an increased level of C-reactive protein, an increased level of procalcitonin more than 6.0 ng/ml, a positive test for endotoxin, as well as a positive result blood culture identification of the pathogenic causative agent of sepsis.
Indisputable clinical diagnostic markers of developed septic shock are the appearance in the patient of sudden and persistent arterial hypotension against the background of tachycardia of more than 100 beats/min and tachypnea of more than 25 respiratory movements per minute. Additional indirect clinical criteria for septic shock also include the development of oliguria, as evidence of renal failure, short-term or deep violation consciousness caused by severe hypoxemia and hypercapnia, widespread hemorrhagic rash and higher level blood lactate more than 1.6 mmol/l.
In order to dynamically assess the severity of the condition of a patient suffering from septic shock, in the intensive care unit, round-the-clock monitoring of hemodynamic parameters, respiratory rate, blood gas composition, hourly and daily diuresis, pyrometry, blood acid-base balance, platelet count and indicators is performed. coagulation.
To additional diagnostic measures for septic shock includes continuous electrocardiographic examination, ultrasound scanning and standard radiography of organs chest cavity to exclude infiltrative changes in the pulmonary parenchyma. Most laboratory parameters are determined to exclude or confirm the development of multiple organ failure, which often occurs with septic shock. Indirect laboratory markers of septic shock, in addition to the above, also include the detection of neutrophilic leukocytosis with a shift to the left or severe leukopenia, morphological changes in neutrophilic leukocytes in the form of toxic granulation, the appearance of Dole bodies and vacuolization.
Since the development of septic shock is most often observed in various infectious pathologies, high diagnostic value has a method for determining the leukocyte index of intoxication, determined by calculation. The normal threshold value is 1, and if a value of 4-9 is detected, it should be assumed that the patient has severe endogenous intoxication, which significantly aggravates the course of septic shock. And at the same time, an extremely unfavorable prognostic diagnostic sign is the detection of leukopenia against the background of a high leukocyte index of intoxication, since in this situation there is a significant risk of developing a fatal outcome of septic shock.
Treatment of septic shock
Since such a pathology as septic shock is a severe pathological condition with high level mortality and inaccessibility therapeutic measures, all the efforts of international specialists are aimed at developing algorithms and effective drug therapy regimens for such patients. The last randomized studies on this issue were carried out in 2008, after which modern ones were developed therapeutic methods correction of septic shock.
Primary or so-called emergency medical measures should be provided to the patient if the development of septic shock is suspected already at the prehospital stage. Among the indicators of the effectiveness of emergency measures taken for septic shock, the achievement of a central venous pressure threshold of 110–160 mm H2O, a systolic component of blood pressure - 65 mm Hg, diuresis - 0.5 ml/kg/hour and a degree of oxygen saturation of 65% are considered. in mixed venous blood. In a situation where emergency measures taken during the first 6 hours of septic shock do not lead to the achievement of the target CVP threshold ScvO2, then preference should be given to the administration of red blood cells and Dobutamine at a dose of 20 mcg/kg/min.
In the case of bacterial origin of septic shock, the fundamental etiopathogenetically substantiated part of the patient’s treatment is the use of antibacterial drugs. Preferably before the first dose of empirical antibacterial drug carry out a two-time bacterial culture of the blood of a patient suffering from septic shock, and additional culture of other biological secretions of the patient is also allowed. In case of isolation of the same pathogen from different biological environments of the patient, identification of the microorganism and determination of sensitivity are carried out various antibiotics To this type pathogen. Delay in the use of antibiotic therapy worsens the prognosis for recovery of a patient suffering from septic shock.
The preferred route of administration of antibacterial drugs for septic shock is parenteral through a venous access, separate from the access used for administering infusion solutions. The initial stage of antibacterial therapy is the use of empirical broad-spectrum antibiotics until the pathogen is reliably identified. The process of selecting an empirical antibacterial drug is influenced by factors such as individual intolerance to individual components of the drug, the specificity of clinical manifestations, the level of dehydration, the rate of infusion, the functional state of the liver and kidneys, and the level of toxicity of the drug. Antibacterial therapy for a patient with septic shock is necessary only under constant laboratory monitoring of the concentration of the active substance in the blood.
In the case where Pseudomonas acts as the causative agent of septic shock, the initiation of antibacterial therapy involves the use of a combination of antibacterial drugs for up to seven days. An increase in the duration of antibiotic therapy for septic shock usually occurs in undrained lesions against the background of severe immunosuppression.
The fundamental clinical criteria for the positive pharmacological effect of an antibacterial drug in septic shock are the improvement of the patient’s general well-being, the disappearance of neurological and intoxication symptoms, and the elimination of hemodynamic disturbances.
Drugs for septic shock
Carrying out any intensive medicinal methods for correcting septic shock should be carried out only under the joint supervision of doctors of various profiles. Everything introduced into the patient's body medications in septic shock they can have both a positive pharmacological effect and provoke the development of negative pathological reactions, therefore the implementation of drug therapy for this pathological condition is carried out under the dynamic control of various clinical and laboratory indicators in the form of thermometry, assessment of the condition of the skin, respiratory rate and pulse, central venous pressure and hematocrit, hourly and daily diuresis, proteinogram and coagulogram.
All medications used for septic shock must be pathogenetically justified, namely, have a preventive effect in preventing the development of complications in the form of acute renal or respiratory failure, as well as massive bleeding. The positive pharmacological effect of drugs in septic shock also lies in improving tissue perfusion and relieving metabolic disorders.
Due to the fact that with septic shock there is a need for constant introduction of various groups into the human body pharmaceuticals, it is preferable to perform central venous access with the installation of a permanent catheter in the subclavian vein.
The initial drugs in the treatment of septic shock are various kinds of infusion solutions in the form of Reopoliglucin in a volume of 800 ml or Hemodez in a volume of 400 ml. The action of this group of drugs is aimed at restoring and improving the rheological properties of blood, eliminating aggregation of platelet blood cells and improving microcirculation.
In order to carry out the reverse transportation of the liquid part of the blood from the interstitial space into the lumen of the vessel during septic shock, it is necessary to use protein preparations in the form of a 5-10% Albumin solution in a volume of 400 ml, which prevents a critical decrease in the level of protein in the blood, which often occurs during septic shock. In addition, in practical activities, resuscitators in general scheme drug treatment a transfusion of dry plasma is administered, which promotes rapid restoration of circulating blood volume.
In addition to the above medications, the so-called infusion therapy for septic shock often includes the administration of up to 500 ml of a 10% Glucose solution along with the administration of Insulin. Concentrated glucose solutions can quickly replenish the body's energy resources.
Considering the fact that with septic shock there is an early development of hemodynamic disturbances, in early For the development of this pathological condition, specialists recommend prescribing vasoactive drugs in the form of a 0.05% solution of Strophanthin in a dose of 1 ml, 0.06% solution of Korglykon in a volume of 0.5 ml. When there is a pronounced decrease in the systolic component of blood pressure, specialists use the administration of small doses of Dopamine at the rate of 1-5 mcg/kg/min.
Septic shock - which doctor will help?? If you have or suspect the development of septic shock, you should immediately seek advice from doctors such as a resuscitator, infectious disease specialist, or hematologist.
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