Pathology of Septic Shock

2021-01-26 12:00 AM

The development of Gr Yin septic Shock often has some easy conditions such as Bad Geography, the elderly, children, people with chronic illness

Define

Septic shock is a clinical condition that results from the circulatory failure of tissues caused by sepsis that is usually Gram-negative. The decrease in circulation in the organs are many pathological factors:

Peripheral resistance increased. Stasis of blood in the blood vessels. Reduced cardiac output. Lack of air in the tissue.

Whole disease

Sometimes due to bacteria Gr (+) but less severe Hot shock, despite hypotension, but has peripheral vasodilation, squeezing cardiac output and normal blood flow. In fact, Shock infection is usually caused by Gr (-) especially intestinal bacillus, led by Escherichia Coli, Streptococcus Faecili, other bacteria such as Pseudomonas aeruginosa, Proteus, Klebsiella. The bacteria Gr (-) endocrine toxin that induces pathological reactions and is directly responsible for Shock.

The development of Gr (-) septic Shock often has some easy conditions such as Bad sites, the elderly, children, people with chronic illnesses.

Indiscriminate use of antibiotic against Gr (+) destroys all Gr (+), dominant Gr (-) bacteria.

Mechanism of pathogenesis

Recall the concept of necessary physiology and pathophysiology

The concept of α and β receptors of the sympathetic system:

α causes total vasoconstriction, including vasculature, but less constriction of vasculature because a smooth muscle in the vein wall is thin.

β vasodilatation and cardiovascular stimulation both in frequency and intensity.

The distribution of these two organs is very different, α is abundant in blood vessels, skin, muscles and internal organs, but less in the brain and heart. On the contrary, the β system is much in the heart of the brain but less in other organs.

The concept of capillary sphincter:

Normally the sphincter at the ends of the capillaries closes in some of the capillaries. These capillaries are affected by many different substances. In particular, the posterior capillary sphincter is contracted by catecholamine (Adrenaline and Noradrenaline). Capillary sphincter opened by metabolic acidosis.

Clogged arteries and veins:

Normally the clogged junction closes, if for some reason the sphincter opens, such as septic shock, the blood will enter the junction resulting in the clogging phenomenon, causing the tissue to be anaemic.

Mechanism of pathogenesis

In humans, Shock infection has two stages.

Increased movement stage (see table).

Water and plasma are out of range.

Cardiac output (CO) decreases due to decreased circulation and decreased contractility of the myocardium. Produces factor MDF (Myocardial Depressant Factor). MDF is produced by cell target enzymes in the abdominal region with anaemia. The nature of heart failure is left heart failure (left end-diastolic pressure increase).

Patients often have metabolic acidosis.

If not treated immediately, many organs will suffer heart, lung, kidney, liver, digestive tract, pancreas.

Table: Two Stages of Septic Shock.

Stage

CI

RPT

HE HAS

CVP

MVO2

DAVO2

PH

Increase mobility

(Hyperkinetic)

Increase

Reduction

Mitigation

Mitigation

Increase

Reduction

Increase

Reduce exercise

(Hypokinetique)

Reduction

Increase

Reduction

Change

Reduction

Reduction

Reduction

CI (Cardiac index): Heart index.

CO (Cardiac output) Number of hearts measured by thermal dilution. CVP: (Central venous pressure): Central venous pressure.

DAVO2: Dynamic-venous blood oxygen difference. RPT: Total peripheral resistance.

MVO2: Oxygen consumption.

On experiments, it was found that in endotoxin Shock cells were damaged through 4 contractions:

Cell damage due to endotoxins.

White blood cells release the enzyme Lysosome (Enzyme that targets cells). Activate the complement system.

Metabolic disorder due to lack of oxygen cells. Damage to endothelial cells, white blood cells cause:

Increases vascular permeability. Makes water drain out of the space, effectively reducing blood volume.

Thrombocytopenia: Destroyed platelets will release intermediates such as Serotonin, Adrenaline, and Thromboxane 2 causing vasoconstriction.

Decreased granulocytes: Destroyed white blood cells release cytostatic enzymes and Arachidonic derivatives via complement and Properdin sugars

The macrophage produces TNF and Interleukin that cause rapid vasodilation, metabolic acidosis, activation of the coagulation system, haemorrhage of the pancreas, adrenal.

Lack of oxygen cells cause:

Glycogen formation dysfunction, Krebs cycle disorder, bile production disorder, hyperlactatemia. Endotoxins cause spasm of smooth muscle before and after capillaries (effects on α receptors to stagnate blood in the lungs, abdomen, kidneys).

Through Hageman Factor (XII) activates Bradykinin, which is a vasodilator that causes blood stasis in peripheral organs. Bradykinin also increases capillary permeability.

Arachidonic acid and endogenous opium (Endorphin) have been reported to be harmful. Using Imidazole to prevent the formation of Thromboxane A2 or using Prostacyclin to antagonize Thromboxane A2 will not cause Endotoxin Shock. On the kidneys and kidneys are two organs affected by endotoxin Shock first: kidney Shock, lung Shock.

The first stage: the secretion of endotoxins has the same effect as moderate amounts of Catecholamine, so it causes moderate vasoconstriction due to the effect of α Causing vasoconstriction in the skin, muscles, kidneys, organs) blood accumulation for heart, kidney, brain At the same time, stimulating and must increase cardiac output, this stage is beneficial for the patient, but in the kidneys because of vasoconstriction, the amount of urine has been reduced.

Later stage: Excessive production of endotoxins causes excessive contraction of blood vessels due to the effect of α, especially post-capillary sphincter, blood stasis in capillaries not returning to heart, reducing total blood flow body. The whole-body stasis will also create a lack of oxygen in the tissues, in the organization. The cells will react by anaerobic metabolism, leading to the production of metabolic acidosis products that expand the capillary sphincter, causing additional blood stasis in normal blood capillaries and also the capillaries. Usually there is no blood. As a result, more blood becomes stagnant in the capillaries, leading to a further decrease in circulation. At the same time, the stagnation will increase the hydrostatic pressure, the electric water will be released. This will decrease blood flow even more. In short, there are two main consequences

Reduced circulation. Anaemia, lack of oxygen in the tissue.

And these two consequences are the definition of Shock.

The stitches in the pathogenesis further catalyse each other to go in an irreversible vicious cycle, thus worsening Shock, eventually leading to scattered intravascular coagulation (CIVD: Coagulation intravascular disseminate). diffuse of capillaries and blood vessels due to lack of oxygen causes local blood clots in the vessel walls, thereby depleting clotting factors leading to diffuse bleeding in all organs.

Symptoms and diagnosis

Circumstances appear

Concept:

Any local or systemic infection usually occurs in:

Urinary tract: Stones, postoperative.

Gastrointestinal: cholecystitis, appendicitis, after surgery.

Respiratory: Including tracheostomy, pneumonia.

Genital: After birth, abortion.

Mach province: Hemodynamic exploration, infusion.

Skin: Skin ulcers, butt ulcers, dermatitis.

Most of them are gram negative.

Common in emergency procedures.

40% are septicaemia.

60% Occurs on poor atopic sites.

Some clinical features

Due to brain tissue: Shock appears rapidly, bleeding under the skin, meningeal syndrome, CIVD, haemorrhage in many places: brain, adrenal, skin like Schwarztmann Sanarelli syndrome (due to injection of dead meningococcal tissue into a vein).

Due to pneumococcal: (bacteraemia).

Due to exotoxins:

Staphylococcus: After dermatitis, whitlow, genital inflammation

Streptococcus β haemolysis: pharyngitis, dermatitis.

Due to typhoid bacteria:

Related to high-dose antibiotics that dissolve bacteria.

Prevention

Intensive treatment of Gram-negative infections.

Avoid indiscriminate use of antibiotics that kill Gram-positive bacteria.

Treatment

Re-establish circulating mass and adjust the acid-base balance

Isotonic fluids can be infused, possibly with a little glucose solution for energy supply.

An alkaline solution such as sodium bicarbonate.

The volume of the infusion fluid can be very heavy depending on the weight.

During the infusion, it is necessary to monitor responses, prevent fluid retention, heart failure. If Dextran solution is a high molecular weight, forming a coating in the lumen of the blood vessel that makes the profile not stick and it stays in the lumen longer.

The vasopressors

Currently, people use Dopamine dose of 5-20 μg / kg / min very slow intravenous infusion.

Note the adjustment of acidosis when using vasopressors.

In the case of tachycardia, Dobutamine can be used instead of Dopamine. The problem of using Adrenaline and Noradrenaline depends on the school and can be combined

Dopamine with Noradrenaline when Dopamine dose> 20 μg / kg / min but systolic blood pressure <90mmHg or when the heart rate is too fast> 130 times / min.

Antibiotic

The principle is to use after blood transplants and rely on antibiotic therapy, but in the meantime, antibiotic should be used with broad-spectrum antibiotics. Must use high doses should be best used intravenously. (Note that patients with functional or functional renal impairment should be cautious with nephrotoxic antibiotics such as Streptomycin, Gentamicin).

It is necessary to master the type of antibiotic you are using, the pharmacokinetics, indications, contraindications, side effects, and complications from drugs.

Monitoring the response of antibiotics, prevention of antibiotic resistance (resistant bacteria).

The duration of using antibiotics must be reasonable, economical, but of quality

The types of antibiotics commonly used for Gr (-) infection are:

III generation cephalosporins (Ceftriaxone, Cefomic):

Well absorbed from the gastrointestinal tract, the drug is distributed throughout the body except for cerebrospinal fluid, only about 20% of the drug can cross the placenta and repair the mother, excreted in the urine. The drug works well on many intestinal bacteria such as Escherichia Colie, Klebsiella, Proteus Mirabilis, Shigella, Salmonella.

Side effects and toxicity: There is about 0.05% of allergy-like Penicillin, in addition, the drug can cause digestive disorders such as diarrhoea, nausea, vomiting, fungal infections.

Reduced leukocytes, platelets, increased liver enzymes.

Aminoglycosides: (Streptomycin, Gentamicin, Tobramycin, Amikacin):

As a bactericidal drug, the half-life depends on renal function, not absorbed orally, the drug diffuses into most organs and body fluids, in which the kidney parenchyma is higher than plasma. The drug is poorly absorbed in the eyes, prostate, does not cross the placental barrier, breast milk and the blood-brain barrier, the central nervous system and the bile.

Drug excreted in urine 65% after 6 hours, 85% after 24 hours. Point:

Gram-negative infections in the kidneys and urinary system, sepsis

Side effects and toxicity:

Hearing disorders: Toxic vestibule causes dizziness, ataxia, fibrillation of the eyeballs, tinnitus, loss of or hearing loss. In severe cases, the damage will not be restored.

Kidney toxicity: The drug is eliminated, accumulates in the renal cortex and causes acute tubular disease. This effect usually occurs in the elderly, kidney disease or a condition that causes dehydration.

Amount:

Amikacin 15 mg / kg / day in 2 divided doses.

Gentamicin 5 mg / kg / day divided 2-3 times / day.

Group Nitroimidazole: (Metronidazole):

As an antibacterial drug, rapidly absorbed nearly 80% after 1 hour, plasma concentrations when used by mouth and by injection are equivalent, the half-life is from 8 to 10 hours. The drug is attached to about 20% protein. The drug diffuses rapidly and strongly in the lungs, liver, bile, cerebrospinal fluid, kidney saliva, semen, vaginal fluid. The drug permeates the placenta and breast milk.

The drug is metabolized by the liver, the concentration is high in the liver and bile. The drug is eliminated mainly in the urine and has a small amount when excreted intact, making the urine red-brown.

Side effects and toxicity:

Urticaria, pruritus, loss of appetite, nausea, metallic taste in the mouth, stomatitis, loose stools, headache dizziness, polymorphonuclear leukopenia, neuritis and if used for a long time, it may become confused psychosis.

Quinolone group: Is a biocide including:

Generation 1: Nalidixic acid, Oxonilic acid, Pipemidic.

Generation 2: (Fluoroquinolone) Norfloxacin, Ofloxacin, Ciprofloxacin, Enoxacin, Pefloxacin, Lomefloxacin, Levofloxacin.

Generation 3: Sparfloxacin (Zagam).

Well absorbed but has an affinity for heavy metals, inhibited when used with Fe, Calcium, and some Cations. Reach high concentrations when taken 1 hour before or 2 hours after eating

Absorption: the drug is quickly and very well absorbed, almost reaching 100% of the highest concentration in plasma after 6 hours of oral administration, the half-life of 6-8 hours. The drug is distributed throughout the organization and fluids such as lungs, skin, cervix, ovary, tissue and prostate fluid, sputum. The drug is eliminated mainly by the kidneys (80%). Side effects and toxicity

Gastrointestinal disturbances, epigastric pain, nausea, headache, dizziness, drowsiness, hallucinations, confusion, convulsions.

Muscle pain, joint pain, urticaria rash.

Increased SGOT, SGPT and LDH enzymes, increased BC acid, decreased neutrophilic BC and decreased platelets.

Increased effects of Theophylline, Warfarin.

Zagam causes cardiac arrhythmias in case of QT prolongation and should not be used with Cordarone.

Contraindications:

Pregnancy, lactation, infants, the elderly over 70 years old with renal impairment, people suffering from mental illness, G6 PD enzyme deficiency.

Should not be used while driving, people working at high altitudes, using machinery.

Other measures

High-dose intravenous corticosteroids prevent permeability through capillaries.

Respiratory support with high dose oxygen, mechanical ventilation, clearance of the upper respiratory tract for the patient.

The drug increases myocardial contractility.

Fresh plasma, fresh blood can help the patient restore blood volume, prevent bleeding.

At the end of stage II, early-stage III is used Heparin to prevent blood clotting, but quite dangerous. Currently, people can take Acid Aminocaproide.

Treatment to remove the foci of infection such as cholecystectomy, the treatment of an abscess.