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BURN SHOCK

In burn shock a total or partial destruction of skin and underlying tissues arises. All injured tissues produce or release different mediators of inflammation (BAS, histamine, thromboxan, cytokinins) that lead to the increase of capillary permeability in the region of burn wound and in remote target-organs. Of particular aggression are leukotrienes C4, D4, E4 and interleukin — 6 causing a development of hypovolemia.

A severity of shock is defined by means of severity index of injury (SII):

1% I—II degree burn — 1 unit SII

1% Ilia burn — 2 units SII

l%IIIbburn — 3 units SII

1% IV degree burn — 4 units SII.

For thermal injury of respiratory tracts they add from 15 to 45 units SII. By its severity the burn shock makes up:

I degree (mild) — 30 U SII

II degree (medium) — 31-60 U SII

III degree (grave) — 61-90 U SII

IV degree (extremely grave) — > 90 U SII.

General tasks of the burn shock treatment:

— compensation of the lost volume of liquid;

— maintenance of VCB;

— decrease of edema formation;

— normalization of AAB;

— restoration of electrolytes and proteins in plasma;

— increase of perfusion of organs and tissues.

To fulfil these tasks the main emphasis is given to the infusion-transfusion therapy (Table 24) directed to restoration of VCB.

Table 24 Scheme of infusion-transfusion therapy of the burn shock

1.The first 24 hours

a) daily amount of crystalloids (Ringer-Lactate) 4 ml/kg body mass x % of burned surface;

b) rate of diffusion:

— 50% of calculated dose in the 1-st 8 hrs;

— 25% of calculated dose from 8 to 16 hrs;

— 25% of calculated dose from 16 to 23 hrs.

b) DO NOT INTRODUCE colloids in the 1-st 24 hours!

2.The second 24 hours

a) minimal needs in water 1500 ml/m² daily;

b) losses of water at the expense of evaporation through a wound surface: for adults ml/hour = (25 + % of burn) x S m² of body surface;

for children ml/hour = (35 + % of burn) x S m² of body surface;

c) total volume of infusion is equal to physiologic and pathologic losses;

d) to replenish VCB deficit 0.9% NaCl solution and 5% glucose solution are used. To each liter of infused solutions 20 meq K⁺ are added.

One starts to introduce plasma and albumin in the fourth 8 hours after a burn.

A gross error is the application of poliglucin in the first hours of burn injury.

Low-molecular colloids and proteins are used in 8-12 hrs.

In the acute period after a burn a parenteral feeding (PEF) is inexpedient.

AAB correction is made by the analyses achieving an alkaline reaction of the urine. After VCB replenishment a stimulation of diuresis (euphyllin, lasix, osmodiuretics) is carried out with maintenance of diuresis no less than 50 ml/ hour.

Anticoagulative therapy — heparin 20-40 thnd U daily and deaggregation therapy (curantyl, trental, xantinol nicotinat) and prevention of thromboembolic complications by means of low-molecular heparins (clexane and others).

A complex of group B vitamins, antioxidants, spasmolytics, glucocorticoids (strictly by indications, if a prolonged infusion therapy does not lead to substantial improvement of condition, prednisolon in a daily dose of 30 mg/kg), inhibitors of proteases, anesthesia with nonnarcotic anesthetics, perftoran (the first 24 hours 3-6 mg/kg, the third 24 hrs., 2-4 mg/kg), antibiotics, ensuring a patency of respiratory tracts and maintenance of respiration up to APV

ACUTE BLOOD LOSS IN OBSTETRICS

The process of blood coagulation may be triggered as a result of coarse manipulations on the uterus in obstetric aid. Owing to a lesion of vessels a great number of tissue thromboplastin is released into the blood and factors of blood coagulation are activated. All this contributes to the formation of thrombi according to the following scheme: prothrombin converts into thrombin the latter activates fibrinogen and a thrombus is formed (hypercoagulatory phase ofDIC).

A massive thrombogenesis contributes to a depletion of blood coagulation system. At the same time, enzymatic degradation of fibrinogen with formation of products of its degradation is observed in the thrombi themselves. As a result, a hypocoagulation phase of DIC develops.

At present, DIC is considered as a complex nonspecific pathologic process, assuming a cause and effect coexistance of the two opposite (but actually closely pathogenetically connected between themselves) processes: disseminated micro-thrombformation and progressing bleeding.

In high total maternal mortality from DIC in obstetrics (by the data of 1994

it was 8 times higher in Russia than in Europe — 51.8 and 6-9 per 100.000 deliveries, respectively) the first place among the causes was taken by hemorrhage, then — sepsis and gestoses.

Practical recommendations of A.I. Vorob'ov (1999), namely: a use of fresh frozen plasma (95 ml/kg), salt solutions, after surgical homeostasis — a correction of globular volume (plasma/packed red cells ratio 3/1) allowed to decrease significantly a death rate in obstetric hemorrhages (from 22-47% down to 4.4-13.2%).

Physiological self-protection of the organism in blood loss:

1. Activation of thrombocytes in blood loss (pseudopodia release) contributes to hypercoagulation by means of formation of the primary thrombocytic thrombus.

2. Centralization of blood circulation as a result of spasm of peripheral vessels, as well as vessels of spleen, mesentery and other inner organs. It is necessary for maintenance of blood flow in coronary, pulmonary and cerebral vessels. Clinically similar changes are manifested by dryness in the oral cavity, decrease of diuresis, enteroparesis.

Correction of globular volume before a surgical arrest of bleeding interferes with compensation and adaptation process of the primary thrombi formation, and elevated AP tears off some thrombi having had the time to form that leads to intensification of hemorrhage. Besides, in taking a decision of hemo­transfusion one should take into account that the organism, being at rest, does not need in that amount of blood that circulates in its vessels with the expectation of motor activity, as long as the inflow of blood to the relaxed muscle is 20 times lesser than that to the working one.

Proceeding on all this, tactics of treatment of acute blood loss must be the following:

1) rest;

2) arrest of hemorrhage;

3) oxygen therapy;

4) maintenance of AP at the minimal level — 80/40 mm Hg;

5) infusions of salt solutions, albumin, fresh frozen plasma;

6) surgical arrest of hemorrhage;

7) correction of globular volume at the expense of packed red cells;

8) prevention of thromboembolic complications (clexane and others). Septic shock (toxoinfectious, endotoxic, bacteriemic) — develops in

peritonitis, infections of urinary tracts and biliferous ways, pneumonia, pancreanecrosis, septic deliveries and abortions and so on. Most often it arises under the action of Gram-negative bacteria (E. coli, Klebsiella, Proteus), but it may occur under the effect of agents (Gram-positive bacteria, anaerobes, viruses, fungi, protozoa).

Features of pathogenesis depend, in significant degree, on the causative agents of sepsis. So, a Gram-negative flora, in its degradation, release endotoxins causing proteolysis with subsequent formation of plasmokinins, under the effect of which a paralysis of vessels advances. A contractile function of myocardium is disturbed under the influence of toxins and hypoxia, pachyemia contributes to aggravation of hemodynamics, particularly pronounced in peritonitis and pancreatitis. ARF develops because of the "shock lungs", disorder of respiratory muscles, tachypnea as a compensation of metabolic acidosis, effect of hyperthermia and direct effect of bacterial toxins on respiratory center. As a result of tissue ischemia and toxemia a hepatic insufficiency often arises causing a disturbance of blood coagulability by:he type of DIC-syndrome, ARF on the basis of necronephrosis, lesion of pancreas with subsequent hyperglycemia, excessive activation of kinins that cause an increased permeability of vascular walls and decrease AP and hemorrhagic gastroenterocolitis.

In clinical picture symptoms of infection (hyperthermia, chills, bacteriemia, changes of red and white blood cells), neuropsychic, hemodynamic tnd respiratory disorders, injury of parenchymatous organs (liver, kidneys, pancreas), disorders of homeostasis (coagulopathy by the type of DIC, disorders of AAB, WEE, dysproteinemia) are combined.

Treatment of septic shock includes elimination, primarily surgical, of the focus of infection, correction of hemodynamic disorders (glycosides, for example, digoxin 0.025% solution — 1.0 ml in dilution per 10 ml of 5% glucose intravenously, slowly; dopamin causing, in the dose of 0.5-2,«g/kg/min, a dilatation of renal vessels and contributing to the increase of renal function, in the dose of 2-lO^g/kg/min intensifies cardiac function and decreases vascular resistance, and in the dose of 10^g/kg/min and more produces vasoconstriction, tachycardia and dysrhythmias); coronarolytics and antiaggregants (curar.tyl 0.5% — 2 ml and isoptin 0.25% — 2 ml in dilution per 100 ml 5% glucose intravenously, drop-by-drop), rheologic agents (reopoliglucin to 1500 ml, neohemodex up to 500 ml drop-by-drop, i/v), LMH instead of traditionally applied NFH (clexane 20 mg once a day subcutaneously in the course of 7-10 days up to patient's activation), application of which is safe even in case of threat of hemorrhage. These preparations ensure not only prevention of TEO, decrease of hemorrhages, improvement of tissue blood flow, decrease the frequency of pneumonias, but influence the development of cytokin cascade reactions in sepsis development.

They ensure an adequate pulmonary ventilation, replenish losses of liquid, high-caloric (no less than 4000 kcal) parenteral feeding at the expense of amino acids and carbohydrates (lipid emulsions are not applied because of the threat of RES block).

Metabolic disorders are carefully corrected by introduction of glucose at the rate of 1 g/kg/h with addition of insulin 1U per 2.5-3 g glucose; anabolic hormones (testosterone-propionate 2 ml in a day, retabolil 1 ml every 7-10 days); glucose-alcohol mixture to inhibit ADH a release of which increases in septic shock; protease inhibitors (contrycal up to 60000 U/day); significant doses of vitamins — C, B,, B,₂, cocarboxylase (0.05-1.0 per day i/m or i/v), phosphaden 2 ml of 2% solution 3-4 times per day.

A fight is going on with ARF, treatment of enteroparesis (normalization of WEE, stimulation of motility with hypertonic enemas, diadynamic currents, administration of proserin 0.05% solution 1 ml 2 times per day, subcutaneously).

Immunity is also corrected (antistaphylococcic immunoglobulin to 4 doses every other day for 5 days i/m, antistaphylococcic plasma, i/v, bio-preparations since the 1-st day: pantoglobin, sandoglobin, monoclonal antibodies).

One should introduce antibiotics, primarily, of bactericidal action (penicillins including semisynthetic, aminoglycosides (gentamicin up to 240-400 mg/day), cephalosporins to 12 g/day), derivatives of fluoroquinolone (levofloxacin (tavanik), exceeding twice the effect of ofloxacin by 250-500 mg once per day), carbapenems in high doses (tienam 0.5-1 g every 6-8 hours).

Bacteriostatic agents (tetracycline, laevomycetinum, macrolides) are not expedient. For superinfection protection — antimycotic preparations (nystatin, levorinum, intestopan, amphotericin B, and the most effective diflucan 50-400 mg/day) are applied. To prevent dysbacteriosis bio-preparations are prescribed.

Anaphylactic shock arises as an acutely pronounced manifestation of anaphylaxia (allergic reactions of immediate type in parenteral introduction of allergen) or atopy (allergic disease with hereditary predisposition to sensibilization).

A particular feature of pathogenesis lies in the presence of reaginic antibodies in the organism (immunoglobulins E) contributing to a release of histamine from mast cells under the effect of which grave disorders of respiration and vascular tone develop.

A true anaphylactic shock is preceded by sensibilization — an immune reaction as a result of which reaginic antibodies appear, that is the patient, prior to a shock origin, must have, at least once, a contact with an allergen. But, sometimes, shock develops at the first contact, as long as some substances are able to cause a release of histamines without participation of antibodies (for example, radiopaque preparations containing iodine), though methods of treatment of such shock do not differ from a true anaphylactic one.

In clinical picture of anaphylactic shock the following forms are distinguished:

— lightning-like — it is characterized by a sudden development of paleness or cyanosis, dilatation of pupils, agonal respiration and in the next 10 minutes a clinical death comes;

— grave form with precursors of the impending catastrope in the form of complaints of diffiult breathing and circulation, whereupon the same symptoms develop as in the lightning-like form;

— medium severity forms are encountered in several variants:

a) cardial, the most prevalent one. Spasm or dilatation of peripheral vessels
interferes with peripheral and later with central hemodynamics with a drop of
AP. Respiration does not suffer;

b) asphyctic — asphyxia as a result of edema of larynx, trachea or
bronchospasm;

c) cerebral — with a symptomatology resembling status epilepticus or acute disorder of cerebral blood circulation;

d) abdominal — with a symptomatology of hollow organ perforation or ileus.

A diagnosis of anaphylactic shock of medium severity is facilitated by skin eruption that arises in this form of shock.

Treatment of anaphylactic shock depends on its form. In the lightning-like and grave forms of anaphylactic shock one should proceed, immediately, to resuscitation — APV and a closed-chest cardiac massage with intravenous or intracardiac administration of 0.5 ml — 0.1% solution of adrenalin (1 ml 0.1% adrenalin solution is diluted in 10 ml of NaCl physiologic solution and 5 ml of this mixture are introduced).

After a renewal of cardiac activity in the lightning-like and grave forms, as well as in other variants of anaphylactic shock of medium severity, they recommend an intermittent (bolus) administration by 0.1-0.2 ml 0.1% adrenalin solution diluted in NaCl physiologic solution, as indicated above (i.e. by 1-2 ml of mixture) in every 5-10 min to stabilization of hemodynamics, as long as adrenalin plays a role of the antagonist of humoral factors causing a development of anaphylactic shock. A mixture with adrenalin may also be introduced drop-by-drop as infusion.

After adrenalin antihistaminic preparations (dimedrol, suprastin, diprazin, tavegyl in the dose of 0.5-1 mg/kg intravenously) are administered. Then corticosteroids (hydrocortison 125-500 mg and other preparations in adequate doses) are introduced remembering that they do not exert their action immediately.

In cardial variant, in addition, VCB is replenished with infusion of crystalloids. Colloid solutions are avoided because of their potential allergic effect.

In asphyctic variant because of the edema of larynx and trachea administration of antihistaminic preparations is particularly indicated, as well as adrenalin and corticosteroids having their effect against edema, and in case of bronchospasm 2.5% euphyilin is introduced in the dose of 6 mg/kg/hour

(for adults 20 ml) in the course of 15 min., and then by 0.5 mg/kg/hour (for adult 15 ml/hour). In absence of effect from indicated medicamentous therapy an intubation of trachea or tracheostomy is carried out.

In cerebral variant, besides adrenalin, antihistaminic agents and corticosteroids, they administer diazepam 0.5% 2-3 ml, in 8 hours repeatedly, lasix (furosemid) 2% 2-3 ml i/v.

In abdominal variant a careful differential diagnosis is carried out in order to avoid groundless surgeries.

After removal of symptoms of shock antihistaminic agents and corticosteroids continue to be introduced for 2-3 days, and, finally, allergen is revealed to prevent a patient's contact with it in the future.

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