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Eng / Emergency situation

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PATHOGENESIS OF INFECTIOUS-TOXIC SHOCK AT

THE LEVEL OF ORGAN SYSTEMS

relative and absolute hypovolemia

development of acute renal failure

"shock lung"

EARLY PHASE OF INFECTIOUS-TOXIC SHOCK ( 1st DEGREE)

arterial hypotension may be absent

tachycardia, decreased pulse pressure

shock index up to 0.7-1.0 (ratio of heart rate to maximum blood pressure, normally it is 0.6, with shock 1.2-1.5 or more)

signs of intoxication: muscle pain, abdominal pain of uncertain localization, severe headache

CNS disorders: depression, anxiety, agitation, hyperreflexia

from the urinary system: a decrease in the rate of urination less than 25 ml / h

Second degree (phase of severe shock, subcompensated ITSH)

BP drops to 90 mm Hg. and below

Tachycardia over 100 beats per minute

Muffled heart sounds, ECG - signs of diffuse myocardial hypoxia

Shock index up to 1.0-1.4

Decreased T to subnormal numbers

Lethargy and apathy

Anuria (urine output less than 1.0 ml/hour)

Increasing shortness of breath, moist rales in the lungs

The skin is cold, moist, acrocyanosis.

The gradient of skin and rectal T -8-15° is growing - an indicator of the centralization of blood circulation

Development of DIC

Third degree (decompensated TSS)

Critical drop in blood pressure below 50 mm Hg. Art.

Tachycardia, thready pulse

Shock index 1.5 or more

Increasing acrocyanosis

cold skin, cyanotic spots on the trunk and extremities

MON: shortness of breath, oliguria, anuria, sometimes jaundice

Impairment of consciousness up to coma

body temperature below 36˚С

Involuntary defecation

Laboratory diagnostics of TSS

Definition of KOS

Blood gas status

electrolyte balance

Hematocrit

Hemoglobin

Leukogram

Blood glucose, urea, creatinine, ALT, AST

Hemostasis status (platelets, clotting and bleeding time, coagulogram)

In the early phase of TSS develop:

Respiratory alkalosis

metabolic acidosis

Accumulation of lactic acid and increased lactate/pyruvate ratio

Reduced clotting time

In the phase of severe shock:

Consumption coagulopathy is on the rise

Thrombocytopenia

The level of fibrinogen decreases to 1g/l and the activity of 2,5,8 and 12 factors

Fibrin monomers and fibrinogen breakdown products appear

Thrombohemorrhagic syndrome

disseminated intravascular coagulation (DIC)

consumption coagulopathy

Violation of the hemostasis system

at first, the process of hypercoagulability predominates (an increase in the content of fibrinogen and other coagulation factors),

then there is a loss of fibrin in small vessels with the formation of blood clots.

As a result of thrombosis of large vessels, gangrene of the fingers of the extremities may develop.

The subsequent decrease in the content of fibrinogen in the blood (consumption coagulopathy) often causes massive bleeding and hemorrhages in various tissues and organs.

Classification DIC syndrome

There are 3 main types: Acute DIC syndrome. Subacute DIC syndrome. Chronic DIC syndrome.

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