Lectures on infectious shock
A syndrome of acute circulatory failure due to decreased cardiac output leading to tissue and tissue hypoxia because of bacteria or toxins.
A syndrome of acute circulatory failure due to decreased cardiac output leading to tissue and tissue hypoxia due to the action of bacteria or their toxins that occurs after sepsis caused by gram (-) or (+) bacteria.
Infection: Inflammation caused by bacteria.
Bacteremia: The presence of bacteria in the blood.
Systemic inflammatory syndrome (SIRS: sydrome inflamatoire de répense systémique) with at least 2 of the following 4 conditions: (Chest 1992)
Temperature > 38 0 C or < 36 0 C.
Circuit > 90.
Respiratory rate > 20 or PaCO2 < 32 mmHg.
WBC > 12,000 or < 4,000 or presence of immature polymorphonuclear leukocytes > 10%.
Sepsis: SIRS with established infection.
Septic shock: A severe sepsis accompanied by the following symptoms:
Hypotension (maximum < 90 or mean < 60 mmHg) – Tachycardia – Tachypnea.
Signs of hypoperfusion in tissues:
Skin: Fluffy, cold limbs.
Kidney: Urinating less (<0.5cc/kg/h).
Blood urea increased; blood creatinine increased.
Na+/urinary < 20mEq/1, Na+/K+/urinary < 1.
SGOT, SGPT increase.
Blood lactate increased > 4mmol/l (36mg%), blood pH decreased.
Glucose in the blood increases.
Due to Gram (+) bacteria, the following are common, depending on the source of infection:
Skin: Staphylococci, Pneumococci.
Pulmonary respiratory tract: Pneumococci, Staphylococci.
Infective endocarditis: Streptococci, Staphylococci.
Put catheter: Staphylococci.
Genitourinary, urinary: Enterococci.
Bones and Joints: Staphylococci.
Access route unknown: Staphylococci.
Due to Gram (-) bacteria, the following infections are common:
Genitourinary tract, urinary tract (urinary catheter).
The gastrointestinal tract, hepatobiliary tract, endoscopy.
Skin and respiration.
The route of entry is unknown and the type of germ is usually:
E.Coli, Klebsiella, Serretia, Proteus, Enterobacter, Pseudomonas, Neisseria Meningitidis, Salmonella...
Caused by anaerobic bacteria (intake is usually gastrointestinal or genital): Bacteroides fragilis, Clostridium perfringens.
Lungs: Pulmonary edema, hemorrhage, Hyalin membrane formation, atelectasis, increased capillary permeability, blood clots in capillaries.
Kidney: Tubular necrosis, renal cortical necrosis.
Heart: Myocardial necrosis, congestive heart failure.
Gastrointestinal tract: Superficial ulceration of the gastrointestinal tract with bleeding.
Blood clots in the capillaries of many tissues.
Binding of white blood cells and platelets.
Liver: The liver is enlarged, congested, sometimes bleeding.
Currently, on pathophysiology, people talk about the role of Cytokines in septic shock:
From cells: Endothelial, Macrophage, Monocyte, Lymphocyte B secrete Cytokines as follows:
TNF (Tumor Necrosis Factor).
TNF (TNF a) and Interleukin 1 cause:
Lower BP, reduce pulmonary capillary pressure.
The concentration of blood.
Reduce peripheral resistance.
Increase cardiac output.
Increases ACTH and Corticosteroids.
The role of NO (nitric oxide): Causes vasodilation.
The role of antibodies in the blood.
Endotoxin on the microcirculation:
Endotoxin acts on the circular muscles of the microcirculatory system causing the arterioles and venules to close blood pooling in the microcirculationhypoxic tissuesacidosis in placearteriolar sphincters open in then the venule sphincter remains closedincreased stasisincreased osmotic pressure and cardiac output (CO) decreaseddecreased blood pressurebaroreceptor stimulationncreased catecholaminevasoconstrictionworsened shock
Endotoxin acts on the cell membrane Phospholipase releases Arachidonic Acid releasing Leukotrienes, Prostaglandins, Thromboxane, Prostacyclin.
Endotoxin acts on the adrenal gland: Secretion of Catecholamines, Corticoids.
Endotoxin acting on the central nervous system secretes endorphins, Enkephalins.
Activation of capillary endoderm:
Injury mechanism of multi-organ MOFS.
Initiated by TNF a, the capillary endoderm secretes cytokines, PAF, and NO to fight infection.
Increases permeability, thrombosis, DIC, lowers blood pressure.
Regulation of the body: Regulating between signal and response.
LBP and CD14 mediate LPS effects.
Effects of Glucocorticoids.
Anti-inflammatory molecules (IL 10-TNF receptor, IL1 receptor antagonist, Cortisol) are very high in septic shock, perhaps indicating that shock occurs due to the body's inability to regulate the inflammatory response.
Vasodilation, increase in cardiac output, decrease in peripheral resistance, decrease in central venous pressure: Manifestations of this stage are called warm shock.
Warm, lethargic skin, slow contact.
Rapid, shallow breathing, clear lungs.
High fever, chills.
Blood pressure is normal.
The central venous pressure decreased slightly.
Vasoconstriction, increased peripheral resistance, decreased cardiac output, decreased central venous pressure: Manifestations at this stage are a cold shock.
Cold, sweaty hands and feet.
Rapid pulse, low blood pressure.
Left heart failure, acute pulmonary edema, DIC.
History - Favorable factors in people
Cirrhosis due to alcoholism, cancer, smoking.
Diabetes, splenectomy, immunosuppression.
Urinary tract obstruction, hepatobiliary tract.
People in the hospital.
Long-term antibiotic treatment.
Long-term corticosteroid and immunosuppressive therapy.
Chemotherapy for cancer.
Administer fluids, place an intravenous catheter.
Urinary catheterization, endotracheal intubation, tracheostomy.
Infectious foci: Skin, respiratory tract, urinary tract, hepatobiliary tract, genital tract.
Sepsis: high fever, chills, rapid pulse, rapid breathing, increased or decreased white blood cell count.
Rapid pulse, low blood pressure (maximum blood pressure <90).
White blood cells increase or decrease, platelets decrease.
Blood culture: (+) 2 times, 2 different places (when chills, high fever).
Prothrombin level decrease, Ethanol (+).
SGOT increased, SGPT increased.
Alkaline reserve decreased, pH decreased, blood gas measurement (PaO2 decreased, PaCO2 decreased).
BUN increased, Creatinine increased, Glycemic increased, ionogram.
Pus: Culture pus to find bacteria.
X-rays and ultrasound (heart and abdomen) to find the cause.
CSF puncture (if needed).
Electrocardiogram, cardiac enzymes, BNP, D. dimer.
Hypovolemic shock due to acute diarrhea.
Stun due to anaphylaxis.
Shock due to acute myocardial infarction.
Pulmonary infarction, acute pericardial effusion, arrhythmia.
Severe malaria caused by Plasmodium falciparum.
Disseminated intravascular coagulation
Platelets < 100,000.
TP < 50%.
Fibrinogen <2g/l, ethanol test (+).
Clinical manifestations: Mucosal bleeding, internal bleeding.
Acute kidney failure
Shown by oliguria, increased BUN and Creatinine.
Being in shock reduces blood flow to the kidneys.
Acute tubular necrosis, renal cortical necrosis.
Acute respiratory failure: This is pulmonary shock (lung shock) manifested by ARDS syndrome (pulmonary edema, pulmonary hemorrhage, atelectasis, hyaline membrane formation in the lungs, blood clots in the pulmonary capillaries).
Acute heart failure: Due to Myocardial depressant factor.
Gastrointestinal bleeding: Due to peptic ulcer bleeding.
Decreased albumin/blood, decreased prothrombin/blood, mild jaundice.
Coping with complications.
Central venous catheter.
Insert a urinary catheter to monitor urine output.
Breathe oxygen through a nasal tube 6-8l/min (for SaO2 >92%).
If severe intubation and mechanical ventilation with PEEP 10-15cm H2O (when ARDS syndrome).
Treatment of shock:
Rapid regeneration for perfusion.
All must measure central venous pressure (CVP).
To restore circulating blood volume based on central venous pressure, the solution used initially is: NaCl 9% or Ringer :
Specifically: NaCl 0.9% 500-1000ml infusion in the first 30 minutes
Colloidal molecule: 300-500ml (20ml/kg/10' dose).
Noradrenaline dose used 0,2μg / kg / p à 1 ~ g / kg / p
When CVP: 8-12cmH2O without or low blood pressure, add vasopressors with: Dobutamine dose starting from 2 -20 µg / kg / min and gradually increasing when effective.
Fight acidosis with Sodium bicarbonate 8.4% or 1.4% so that pH > 7.2.
Use Corticosteroids: Solu-Medrol or Hydrocortisol 200-300mg/day.
Control blood sugar in the range <140mg%.
Anti-stress ulcer with proton pump inhibitors.
Monitor urine output to treat acute renal failure.
The goal of treatment for shock in the first 6 hours:
systolic blood pressure >65 mmHg.
Urine output >0.5ml/kg/h.
Hct >30% ( Hb >8-10g/l).
Skin: staphylococcus, pneumococcus.
Respiratory tract, lungs: Pneumococcal.
Gastrointestinal tract: Gram (-) bacteria.
After surgery: Gram (-), anaerobic bacteria.
Abortion: Gram (-), anaerobic bacteria.
Intravenous catheter placement: staphylococci.
Urinary catheterization: Gram (-) bacteria.
Intubation, tracheostomy: staphylococci, gram (-).
Alcoholism, alcoholic cirrhosis: Gram (-), anaerobic.
Poker: staphylococcus, fungus.
AIDS: Staphylococci, gram (-).
For early treatment, it is not possible to wait for the results of blood cultures and antibiograms, based on the source of infection and the circumstances of the infection to predict the causative organism to choose the appropriate antibiotic.
Use antibiotics immediately.
If gram-negative bacteria are suspected, they can start with third-generation Cephalosporins, second-generation quinolones, if severe, they can be combined with Aminoglycosides.
Caused by typhoid bacteria: ceftriaxone, 2nd generation quinolones.
Cause Bacteria Pseudomonas: ceftazidime, amikacine, Imipenem.
Due to biliary tract infection: Augmentin.
Due to postoperative, peritonitis: Augmentin + Metronidazole.
If caused by Staphylococcus Aureus: Vancomycin 500mg x 4, if more severe can be combined with Amikacin and Rifamycine (or Zyvoxide 600mg x 2 times/day intravenously, Targocid 6mg/kg/24h).
Ceftriaxone can be used in combination with fosfomycin or second-generation quinolones.
If due to pneumococcal: Augmentin, Cefuroxime.
If caused by anaerobic bacteria: Metronidazole, Clindamycin.
Infections from the community: Ceftriaxone + Aminoglycoside ±Metronidazol.
Suspected: S. Aureus or S. Pneumoniae resistant to Vancomycin + Aminoglycoside.
Suspected: Pseudomonas using Ceftazidine + Aminoglycoside.
If no response: Vancomycin + Imipenem + Clindamycin.
Infections from the hospital: usually: Klebsiella, Pseudomonas, S.aureus and multi-drug resistant, starting with: Vancomycin + Imipenem.
Specifically: If Gram(+) can use Vancomycin, Augmentin, Timentin, Tazocine in combination with Amikacin or Levofloxacine.
If Gram (-): Ceftazidine, Imipenem combined with Amikacin.
Resolve the infection:
Surgical intervention is necessary when there is an infection, abscess, bowel necrosis, biliary stone, and uterine infection, so early intervention is recommended.
Treatment of complications:
Disseminated intravascular coagulation (DIC): Transfusion of fresh blood when significant bleeding is present.
Acute renal failure: Based on CVP and blood pressure, intravenous fluids and furosemide testing can be performed, if ineffective, then dialysis.
Acute respiratory failure, acute pulmonary edema, intubation, mechanical ventilation with PEEP.
Currently, in the treatment of septic shock, one can apply in the following treatments:
Anti-endotoxin antibodies are used.
Use monoclonal antibodies.
Follow-up and prognosis
Assess for septic shock.
Monitor: Pulse, blood pressure/15 minutes, temperature, breathing rate, consciousness.
Monitoring: HC, Hct, CVP.
Monitor for signs of mucosal bleeding.
Urine output/hour/24 hours.
Blood clotting function.
Ionogram, RA, blood pH, blood lactate, blood gas.
BUN, Blood Creatinine.
Cardiopulmonary imaging, ECG.
Warm skin and extremities.
Urine output 40-50ml/hour.
CVP returned to normal, no acidemia.
Clear pulse, increased blood pressure.
Current mortality rate: 50% of causes of death are irreversible shock, pulmonary shock, DIC, acute renal failure, arrhythmia, cerebral hypoxia.
Early treatment of foci of infection.
In case of septic shock, it must be urgently active