SIRS

Systemic Inflammatory Response Syndrome

is an inflammatory state affecting the whole body, frequently a response of the immune system to infection, but not necessarily so. It is related to sepsis, a condition in which individuals both meet criteria for SIRS and have a known or highly suspected infection.

According to Brunner: A syndrome resulting from a severe clinical insult that initiates an overwhelming inflammatory response by the body.

Criteria for Diagnosing:

Systemic Inflammatory Response Syndrome(SIRS) o Widespread inflammatory response o Two or more of the following Temp > 38C or 36C Heart Rate > 90 bpm Tachypnea (RR > 20) PCO2 <32 WBC > 12,000 cells/mm3, < 4000 cells/mm3 or presence of >10% immature neutrophils

Pathophysiology of SIRS

The antigen-antibody reaction stimulates multiple interacting systems such as:

Complement Cascade Cytokine cascades Arachidonic Acid Metabolites Cell Mediated Immunity Humoral Immune Mechanisms Clotting Cascade

Cytokines

Are Intercellular signaling proteins or messengers More than 30 recognized Act through binding to specific receptors on the target cells triggering other cascades or its own cascade

Pathophysiology of SIRS

Pathophysiology of SIRS

TNF-

The earliest and most potent mediator in SIRS It activates neutrophils, causing the production of Interleukin-1(IL-1), Interleukin-6 (INL-6), and Interleukin -8 (INL-8). It stimulates platelet activating factors and prostaglandin, and promotes leukocyte or vessel cell wall adhesion.

Pathophysiology of SIRS

IL-1

Pathophysiology of SIRS

During an inflammatory response, it facilitates the movement of WBCs toward the injury, ischemia, or infected area It stimulates the release of arachidonic acid from phospholipids in the plasma membranes, leading to fever, hypotension, and decrease systemic vascular resistance. IL-1 also leads to muscle protein breakdown IL-1 works with other cellular immunity components to produce IL-2, which decreases blood pressure, systemic vascular resistance, and left ventricular ejection fraction. IL-2 may also increase left ventricular end diastolic volume, cardiac output, and heart rate

Pathophysiology of SIRS

IL-6

Is a key messenger that can either trigger the rest of the cascade or its arrest Stimulates the release of acute phase reactors Its serum levels are consistent with the gravity of the immune reaction

Nitric Oxide

Nitric oxide is synthesized by inducible nitric oxide synthase (iNOS) in the vascular endothelium and smooth muscle in response to pro-inflammatory cytokines NO is the vasoactive mediator responsible for the fall in systemic vascular resistance underlying the hypotension in the late stages of SIRS and septic shock

Pathophysiology of SIRS

Arachidonic Acid Cascade

Thromboxane A2

Is a potent vasoconstrictor and platelet aggregator Leads to tissue ischemia from hypoperfusion.
Capillary endothelial permeability Bronchoconstriction Activation of neutrophils

Leukotrienes leads to

Pathophysiology of SIRS

The Complement Cascade

Controls the inflammatory process

Chemotaxis Opsonization Promotion of phagocytosis

Pathophysiology of SIRS

Clotting Cascade

Fibrin is formed due to the injury of the vascular endothelium Chemical mediators stimulate the release of Hageman Factor and Thromboplastin These form clots at the site of the injury, attempting to stabilize the site Fibrinolysis is activated by the coagulation cascade, leading to mediator induced (DIC).

Pathophysiology of SIRS

Bradykinin

The activation of the Hageman Factor stimulates the release of bradykinin Bradykinin creates vasodilatation and capillary leakage, therefore volume depletion.

Pathophysiology of SIRS

Myocardial Depressant Factor

Myocardial depressant factor is a serum protein released by the hypoperfused and ischemic cells of the pancreas It decreases the velocity of contractions of myocardial cells, leading to decreased right and left ventricular ejection fractions

Pathophysiology of SIRS

Beta Endorphins

Beta endorphins are released, by the pituitary and hypothalamus, in response to hypoperfusion They cause peripheral vasodilatation, and decrease cardiac contractility

Pathophysiology of SIRS

Stages of SIRS

4 stages according to the gravity of the situation

Pathophysiology of SIRS

SIRS 1

Stages

Release of proinflammatory mediators

These mediators create a web of reactions designed to limit new damage and ameliorate whatever damage has already occurred

Pathophysiology of SIRS

SIRS 2

Stages

Pro-inflammatory and antiinflammatory mediators appear in the systemic circulation

Pro-inflammatory mediators recruit neutrophils, lymphocytes, platelets, and coagulation factors

Pathophysiology of SIRS

SIRS 3

Stages

Massive Systemic Inflammation

Progressive endothelial dysfunction occurs increasing microvascular permeability Vessels lose tone and profound vasodilatation occurs resulting in severe shock

Pathophysiology of SIRS

SIRS 4

Stages

Most patients do not make it this far --but if they do- A compensatory anti-inflammatory response occurs trying to suppress inflammation

Clinical Picture

The typical 2 or more of:

Temp. >38C or <36C HR >90 bpm RR > 20 cpm or PaCO2 < 32 mmHg WBC count >12,000 cells/mm3

Symptoms & Signs of each organ sequels

Clinical Picture

Organ Manifestations

Cardiovascular
Skin warm and flushed Widened pulse pressure Cardiac output is but SVR is Eventually C.O. declines exacerbating hypoperfusion

Clinical Picture

Organ Manifestations

Pulmonary
Hypoxemia may be masked by hyperventilation Respiratory alkalosis Pulmonary edema Respiratory failure Bronchoconstriction ARDS

Clinical Picture

Organ Manifestations

CNS
Altered mental status Confusion Irritability Agitation Disorientation Lethargy Seizures Coma

Renal
Oliguria: < 500 ml/day Metabolic Acidosis

Clinical Picture

Organ Manifestations

GIT
Impaired motility SGPT & SGOT Hyperbilirubinemia Hepatic necrosis Hypoprothrombin emia Hypoglycemia

Blood
or WBCs PT and PTT or Platelets Anemia

Diagnostic

Cytokines assay (IL-6, IL-8 & TNF) Blood Culture Serum Procalcitonin
The only lab test that differentiates

SIRS (0.5 -2 ng/dl) from Sepsis (>2 & <10 ng/dl) from MOD (>10 and often >100ng/dl)

Prognosis

Death in 60% of cases of late stages & shock in patients with no previous history of medical conditions Death rate is higher if MOD develops & is dependant on no. of organs affected
3 organs 85% 4 organs 95% 5 organs 99%

Medical Management

Identification and Elimination of the cause Potential routes of further infection are removed Fluid replacement

Nursing Management

Strictly adhere with aseptic technique like hand washing Nurse continuously monitor the patients Vital signs Intake and output Nutritional status

Thank You

By: Nica Marie Lumba