Septic shock


I- Introduction :

Septic shock is the consequence of’acute circulatory failure, which permanently alters the’oxygenation and metabolism of different tissues and organs, in response to the body of the massive invasion by an infectious agent.

Despite the’improvement in our knowledge of the pathophysiology of sepsis over the past two decades, these serious infectious states now represent’It is still a major source of morbidity and mortality in intensive care units and its mortality remains high and still approaches 50 %.

II- Definition and classification of septic states :

The definition of septic states is based on the’intensity of the response of the’organism at the’infection.

It distinguishes sepsis "uncomplicated" of severe sepsis and septic shock, each corresponding to a clinical-biological entity precise way, Sepsis is defined as a systemic inflammatory response (or SIRS, Systemic Inflammatory Response Syndrome for) secondary to clinically or biologically documented infection.

At each stage of the’infection corresponds to a prognosis, specific epidemiological data and well-defined therapeutic measures aimed at limiting the progression and sustainability of the disease’sepsis.

♦ diagnostic criteria SIRS, sepsis and septic shock

1- SIRS two or more of the following signs :

  • Temperature > 38,3° C or < 36,0°C ;
  • Cardiac frequency > 90/me ;
  • Respiratory rate > 20/min ou PaC02 < 32 mmHg or mechanical ventilation ;
  • leukocyte Count > 12000/mm3 or < 4000/mm3 or > 10 % immature cells.

2- Sepsis SIRS + infection "clinically or microbiologically documented"

3- severe sepsis sepsis + at least one d sign’hypoperfusion or d’a dysfunction of’organ :

– circulatory function :
+ low blood pressure (NOT < 90 mmHg or PAM < 60 mmHg) ;
+ blood hyperlactataemia (lactate > 2 mmol/l ) ;

– respiratory function :
+ hypoxemia (Pa02 / FI02 < 300) ;

– higher functions:
+ presence of encephalopathy or delirium (score Glasgow < 14) ;

– renal function :
+ oligurie (urine output < 0,5 ml / kg / h despite persistent filling) ;
+ creatinine > 177 pmol/l (20 mg / l) ;

– Coagulation :
+ thrombocytopenia < 100 000/mm3 ;

– hepatic : hyperbilirubinémie > 34 pmol/l ;

4- Septic shock severe sepsis + persistence, despite appropriate vascular filling, from :
– low blood pressure (NOT < 90 mmHg, PAM < 60 mmHg),
– signs of’hypoperfusion (lactatémie > 4 mmol/l, oligurie, consciousness disorders,…).

III- pathophysiology :

Septic shock should be considered as a biological succession of’events occurring extremely quickly after the’abnormal introduction into the’organism’a foreign component d’infectious origin; among microbial antigens, likely to’activate the immune system, let's quote’endotoxine, lipopolysaccharide component of the outer membrane of Gram-negative bacteria, l’lipoteichoic acid for gram-positive bacteria; Proteins from fungi and some viral protein constituents are also susceptible to’activate the immune system.

The release of the toxin in the blood goes active phagocytic cells and driven mediator release pro-inflammatory and anti-inflammatory

immunocompetent cells and mediators pro- and anti-inflammatory

NO:monoxide’azote; PAF: factor d’platelet activation; THE Ra: antagonist of the IL-1 receptor; sTNFr: récepteur TNF soluble; TGF-B: transformine growth factor-B; BPI: bacterial/permeability-inceasing protein; Sil-2r: soluble IL-2 receptor

This succession of’events involve the immune system's defense’organization, the cellular mediators of this system and the consequences of’action of these mediators on the various bodies, in particular, the heart and vascular system, lungs, liver, kidneys, the brain and the digestive system. So, the "shock" of severe sepsis represents a failure of the cardiocirculatory system secondary to decreased vasoconstrictor tone and myocardial contractility with hypovolemia.

❖ pathophysiological consequence

1- endothelial damage :

L’endothelium is the guarantor of the quality of macrocirculation and microcirculation L’endothelium performs four main functions :

  • The regulation of vasomotor tone by synthesizing molecules vasorelaxant
  • The maintenance of blood flow through the anticoagulant surface profibrinolytic
  • The modulation of l’inflammation and’apoptosis
  • Finally, he participates in the’angiogénèse.

During sepsis, the three essential properties of endothelial cells that are thrombomodulation, regulating vasomotion and modulation of the inflammatory reaction, are major revisions

l’endothelium loses its anticoagulant and profibrinolytic properties to become frankly procoagulant and antifibrinolytic

L’suffering from’endothelium also results in a loss of the character of’adaptation of vasomotor tone : septic vessel is vasoplegic. The ship n’is more capable of’adapt your tone to local stimuli, in particular to changes in infusion rate, endoluminal pressure or oxygen supply

Lesions of the’endothelium eventually lead to the’endothelial cell apoptosis. Thus his physical integrity and barrier function are met. It becomes hyperpermeable and promotes l’interstitial edema.

2- Coagulation :

  • Side endothelial injury in sepsis lay bare the endothelium-under and allow direct contact between FT and circulating clotting factors. So, l’FT exposure leads to the formation of’an FT / factor Vila complex whose resultant is l’activation of the coagulation cascade
  • Au total, l’activation of coagulation, the failure of natural anticoagulant systems and the’marked inhibition of fibrinolysis contributes to the imbalance of the coagulation and anticoagulation balance in severe sepsis. They lead to an array of’abnormal activation of coagulation and the formation of microthrombi making the bed of’a lack of perfusion’organ.

The final consequence of this activation is the occurrence of’DIC which is an acquired syndrome secondary to systemic and excessive activation of coagulation.


Vascular failure is central in the pathogenesis of septic shock. It can be divided into two major segments :

  • endothelial dysfunction (endothelial injury, microcirculation disorders and hyperpermeability),
  • vasoplegia and contractile abnormalities muscle vascular smooth.

Septic vessels becomes hyporesponsive, L’vascular hyporesponsiveness can be defined as a less increase in blood pressure for the same dose of’agent vasopresseur


The pathophysiology of myocardial dysfunction is complex and involves proinflammatory cytokines, NO by indirect and probably irreversible action including through superoxide anions / peroxynitrite, would have a greater effect on the relaxation of myocardial contraction , impaired receptor |3- adrenergic, apoptotic phenomena and calcium abnormalities passing in particular by a decrease in the sensitivity of myocardial fibers.

this dysfunction, typically in the maximum 24 early hours, is reversible with return to normal heart function usually within seven to ten days upon healing of the’septic shock


Organic alterations observed during septic shock related to the inflammatory process and the ensuing cardiovascular dysfunction. The severity of microvascular dysfunction appears to be l’ultimate determinant of dysfunction’organs.

a- metabolic impairment :

Carbohydrate metabolism is most often changed. An initial phase d’hyperglycemia is associated with increased hepatic gluconeogenesis. It is followed by’marked hypoglycemia, associated with decreased liver function, increased secretion of’insulin and an increase in’peripheral glucose use

Increased protein catabolism may play a significant role in’appearance of multi-organ failures

b- lungs :

Two main mechanisms may explain the reduction in gas exchange

  • direct action on the cell-capillary membrane with increased permeability and edema cell-interstiel
  • a breach of regulatory mechanisms of hypoxic vasoconstriction Their clinical translation ARDS

c- splanchnic reached :

Intestinal pain seems to be very early in septic shock, mucosal perfusion abnormalities’accompanies d’increased intestinal permeability which may be responsible for’a bacterial translocation

d- neurological :

maybe the fact of’hepatocellular failure, of the’renal failure, shock and / or acute respiratory distress

IV- Diagnostic :

→ Clinical Diagnosis : clinically septic shock comprises two phases

  • hot shock corresponding to an elevated heart rate in response to a decrease of vascular resistance induced by the release of vasodilator substances with hot ends, a leaping pulse and a respected blood pressure hands an increased differential mild signs of dysfunction’organs are present( disorders of the’mood, biological renal failure, abnormal liver function, hyperglycemia
  • cold shock : corresponding to l’accentuation of tissue damage, especially myocardial with vasoconstriction ,low blood pressure and pinch, a thready pulse and cyanosis of the extremities.

Severe acidosis related to’hypovolémie, decreased tissue perfusion, the fault of the’use’02 and myocardial dysfunction

In fact the cold shock corresponds to uncorrected hypovolemia or underestimated or even heart failure

L’severity assessment is based on data from the’clinical examination indicating l’existence d’visceral failure and d’vital distress : NOT<90mmhg, not responding to the filling, tachycardia > 140 B/min , polypnoea > «30 cycle/min, and / or Sa O 2 < 90% despite the’oxygen, disturbance of consciousness , cyanose, sweats and click signs of diffusion of the’infection

→ Diagnostic paraclinique :

  • Laboratory tests

L’analysis of biological parameters can find: blood lactate > 2meq/l, Fo2< 60mmhg, paint it < 130mmol/l, hematocrit < 30%, leucocytes <4000/mm3, creatinine > 20mg / l

The search for the’infection is essential for diagnosis. All samples for microbiological purposes must be carried out before starting the’antibiotic, and this without delaying the’administration. Must perform 2 or more blood cultures

  • morphological examination

Chest radiograph : can guide a worm infectious pneumonitis

L’Abdominal ultrasound : look for signs of’angiocholite, d’obstruction on the urinary tract or peritonitis

L’ASP can highlight calculations (renal or biliary) or pancreatic calcifications

abdominal CT can guide worm acute pyelonephritis ,a renal abce or para-renal, or intra-abdominal

Brain CT and’MRI looking for’affection neuroméningée L’echocardiography may show valve vegetation

  • hemodynamic exploration
  • The pose of’a radial catheter : continuously tracks the change in PA
  • A central venous catheter which allows the follow-up of the PVC as well as the’administration of vasoactive therapies
  • L’echocardiography: transthoracic or transesophageal confirms the volume disorders, the presence’ventricular dysfunction and guides the etiological diagnosis
  • The SWAN-GANZ catheter measures pressures in the right cavities and the’pulmonary artery

V- Treatment :

The treatment’a patient in septic shock proceeds under supervision : d’an ECG, measure of’pulse oximetry, Monitoring blood pressure, a central venous catheter that allows monitoring of PVC as well as’administration of vasoactive therapies, a catheter SWAN-GANZ when the hemodynamic situation remains unstable, regular measurement of blood gases, the measure of l’acid-base balance and the lactate / pyrivate ratio allows’evaluate l’tissue oxygenation
– antibiotic treatment : Empirical must be directed against the greatest number of germs that justifies the use of’a double or even a triple association allowing’bring several advantages: broadening the spectrum d’activity, obtaining’antibacterial synergy with increased bactericidal speed, prevention or limitation of the risk of selection or’emergence of mutant or resistant strains
– L’oxygen : is essential, its administration up to’for the job of’mechanical ventilation
– A daily intake of 200 g de glucose, often associated with’insulin, can cover the immediate energy needs
– Correction of the’acidosis by administration of bicarbonate for PH <7,20
– Corticosteroid therapy in patients with severe septic shock requiring high doses of l’vasoactive agent : hemisuccinate d’hydrocortisone 200 at 300 mg / j, the duration of treatment is 5 days in case of clinical response , Beyond 72 hours l’absence of hemodynamic response justifies the’discontinuation
– hemodynamic therapy

Resuscitation should be started immediately in any patient with low blood pressure or elevated lactate to the top 4 mmol/l, and this even before’admission of the patient to the intensive care unit.

The objectives are :

  • a central venous pressure (PVC) between 8 and 12 mmHg ;
  • mean arterial pressure (PAM) greater than or equal to 65 mmHg ;
  • diuresis to 0,5 ml / kg / hour ;
  • saturation 02 venous blood (Sv02 measured in l’right atrium) better than 70 % or greater 65 % in mixed venous.

→ The vascular filling

  • Constitutes l’initial step , its main objective is to’optimize the preload of the left ventricle in order to’increase transport d’oxygen by increasing cardiac output

The fluid loading may be performed by two types of solutes :

crystalloid (isotonic or hypertonic) and colloids (natural or synthetic)

Blood transfusion is performed for threshold d’hemoglobin between 8 and 10 g/dl

Filling should be continued until’to’obtaining’a PVC > 8 mmHg and d’a PAM > 65 mmHg.


  • Their goal is to restore perfusion pressure, d’ensure cardiac output allowing transport of’sufficient oxygen
  • Due to’great inter-individual variability, l’gradual increase in their dosage is recommended in order to’get a NO 90 PAM mmHg or two 60 to 65mmhg
  • dopamine : dose 5 10&/kg/mn: effect B leading to an increase in volume d’systolic ejection and cardiac output, dose ranging from at 10 at 50 &/kg / min vasopressor effects
  • norepinephrine : powerful vasopressor agent used in cases of refractory shock dopamine
  • L’adrenaline : and has effects 3 adrenergic increases the vasoconstrictor tone and cardiac output
  • La dobutamine : properties 3 1 powerful agonists has been recommended to treat myocardial depression

at dopexamine :a main adrenergic type action (3 2 has been proposed for the treatment of’congestive heart failure



Known as physiological inhibitor of thrombin, the system of protein C has anticoagulant properties, fibrinolytic, anti-inflammatory and anti- apoptotiques.

Dr Lamara's course – Faculty of Constantine