L2 Systemic inflammatory response syndrome (SIRS)

first 10 pages LS related, skipped some

Which chemical substance will phagocytic cells release in response to destroying the pathogen ?

Lytic enzymes

• it also potent enough to damage healthy cells near the area of injury

Suggest the possible cause of generalised inflammation (5)

✓ Mechanical tissue trauma: burns, crush injuries, surgical procedures

✓ Abscess formation: intraabdominal, extremitie
✓ Ischemic or necrotic tissue: pancreatitis, vascular disease, MI
✓ Microbial invasion: bacteria, viruses, fungi, parasites
✓ Endotoxin release: gram-negative and gram-positive bacteria

Describe the pathophysiology of Multiple organ dysfunction syndrome (MODS)

• Systemic inflammatory response syndrome (SIRS) triggered the release of proinflammatory cytokines,

• which cause peripheral vasodilation and increased capillary membrane permeability, also endothelial injury and dysfunction.

• Capillary leak caused a maldistribution of circulation blood volume, leading to hypotension, interstitial edema, pulmonary edema.

• Lastly, it result in circulatory failure and distributive shock

• The poor organ perfusion and oxygenation contributed to MODS

Explain, and what are the cause of Multiple organ dysfunction syndrome (MODS)

• poor organ perfusion and oxygenation contributed to MODS

Explain, and what are the cause of circulatory failure and distributive shock

Capillary leak leads to:

• Interstitial edema and hypotension as fluid shifts out of the circulation

  • Lead to lactic acidosis caused by anaerobic metabolism

• Pulmonary aedema, then causing hypoxia and increase RR

  • lead to acute respiratory distress syndrome (ARDS)

Describe the consequence of SIRS

• It triggers the release of proinflammatory cytokines,

• which cause peripheral vasodilation and increased capillary membrane permeability, also endothelial injury and dysfunction.

• Also microemboli formation, which consume the platelets and clotting factors, thrombin clots in microcirculation.

Explain how does SIRS affect the heart, leading to cardiovascular dysfunction

myocardial depression occurs and is accompanied by decreased SVR, increased heart rate, and ventricular dilation. These compensatory mechanisms help maintain CO.

Heart failure develops, characterized by ventricular dilation, decreased diastolic compliance, and decreased systolic contractile function.

Myocardial depression is exacerbated by myocardial hypoperfusion from a low CO state and persistent lactic acidosis.

Explain how does SIRS affect the lung, leading to pulmonary dysfunction

• Lungs are frequent and early target organs, usually the first one

ARDS (actue respiratory distress syndrome) is the pulmonary manifestation of MODS.
Not all patients with ARDS develop secondary MODS.

Patients with ARDS who develop SIRS or sepsis concurrently with acute respiratory failure are at the greatest risk for MODS.

ARDS associated with MODS often within 24 to 72 hours after the initial insult.

Refractory hypoxemia caused by intrapulmonary shunting associated with pulmonary oedema.

Explain how does SIRS affect the hematologic system, leading to disseminated intravascular coagulation (DIC)

• Endotoxins (pathological cause) stimulate endothelial cells to release tissue factor which active coagulation cascade.

• Fibrin binds to platelet plugs that have adhered to damaged endothelial cells, forming a stable fibrin clot.

• These clots form throughout the microvasculature & cause additional injury and ischemia to distal tissues.

• The excessive clotting triggers the fibrinolytic system to release fibrin degradation products, which are potent anticoagulants, furthering the bleeding.

• The bleeding is characterized by low platelet and

  fibrinogen levels; prolonged PT, aPTT, and

  thrombin time; and elevated fibrin degradation

  products and D-dimers.

Explain how does SIRS affect the endocrine system, leading to hypermetabolic state

• Increased in resting energy consumption

  ➢Extensive protein catabolism & Fat catabolism

• Extensive catecholamine (hormone) release ➢↑ Glycogenolysis (Glycogen are converted to glucose) ➢↑ Insulin resistance

• Glycogen is depleted
  ➢↑ Gluconeogenesis, amino acids are converted to glucose ➢↑Fatty acids are mobilized as fuel

As a result, the increased catecholamines and Glucocorticoids causing hyperlycaemia & insulin resistance

Explain how does SIRS affect the hepatic system, leading to liver dysfunction

• Due to hepatic hypoperfusion, damaged hepatocytes, ischemic hepatitis,

• Hepatic cell death and Liver fails to metabolize drugs and waste product

• Result in liver failure

• (70% hepatic cell damage will increase liver enzymes)

Explain how does SIRS affect the GI tract, leading to GI dysfunction

Healthy probiotics are decreased in a SIRS state, and pathogenic organisms (e.g., Staphylococcus, Pseudomonas ) proliferate.

Hypoperfusion damage the normal GI mucosa barrier by decreasing mesenteric blood flow, leading to hypoperfusion of the villi, mucosal edema, ischemic necrosis, sloughing of the mucosa, and malabsorption.

Ischemic events and the absence of feedings can disrupt the normal metabolism of the gastric or intestinal lumen and the normal protective function of the gut barrier.

Explain how does SIRS affect the CNS

Major / common problem: hepatic encephalopathy

Explain how does SIRS affect the kidney, leading to renal dysfunction

• Hypoperfusion of kidney, in addition to reperfusion of it, worsening the damage of kidney tissues. Kidney ischemia reperfusion injury.

• Result in acute kidney injury (AKI)

List the manifestations of cardiovascular system in response to SIRS (6)

Massive vasodilation

↓ SVR, BP
↓ MAP
↑ HR, stroke volume ↑ CO

Biventricular failure

List the manifestations of respiratory system in response to SIRS (6)

Severe dyspnea
• Tachypnea
•↓SaO2, PaO2
• Bilateral fluffy infiltrates on chest x-ray

• Pulmonary hypertension

• Refractory hypoxemia

List the manifestations of hematologic system in response to SIRS (5)

↑ Bleeding times, ↑ PT, ↑APTT
↓ Platelet count (thrombocytopenia)

↑ Fibrin split products ↑ D-dimer

List the manifestations of endocrine system in response to SIRS (2)

Hyperglycemia → hypoglycemia

List the manifestations of hepatic system in response to SIRS (5)

↑ Liver enzymes (ALT, AST, GGT)
↑ Serum NH3
↓ Serum albumin,

Jaundice

Hepatic encephalopathy [more in L3]

List the manifestations of GI system in response to SIRS (5)

Mucosal ischemia
• ↓Intramucosal pH
• Potential translocation of gut bacteria
Hypoperfusion → ↓ peristalsis, paralytic ileus (ie no bowel sound)
Mucosal ulceration
GI bleeding

List the manifestations of CNS system in response to SIRS (5)

Acute change in neurologic status
Fever
Hepatic encephalopathy

Seizures

Confusion, disorientation,

delirium

List the manifestations of renal system in response to SIRS (2)

Decrease Urine output

Increase Creatinine

Suggest the nursing management for cardiovascular dysfunction due to SIRS (5)

• Volume management (Crystalloids: Lactated ringer sol, NS, Colloids: Gelofusine)

• Vasopressors (e.g. adrenaline, noradrenaline, vasopressin)

• Continuous ECG monitoring

• Circulatory assist devices (e.g. Intra-Aortic Balloon Pump (IABP))

• Venous thromboembolism prophylaxis (e.g. Intermittent Pneumatic Compression (IPC))

Suggest the nursing management for respiratory dysfunction due to SIRS (2)

Optimize O2 delivery and minimize O2 consumption

Mechanical ventilation

Suggest the nursing management for DIC due to SIRS (3)

• Observe for bleeding from obvious and/or occult sites

• Replace factors being lost (e.g., platelets)

• Minimize traumatic interventions (e.g., IM injections, multiple venipunctures)

Suggest the nursing management for hypermetabolic state due to SIRS (2)

• Monitor blood glucose level

• Provide continuous infusion of insulin and glucose to maintain blood glucose 6.0 -10.0 mmol/L.

Suggest the nursing management for liver dysfunction due to SIRS (2)

• Maintain adequate tissue perfusion

• Careful use of drugs metabolized by liver, e.g. pandol

Suggest the nursing management for GI dysfunction due to SIRS (4)

• Stress ulcer prophylaxis : Antacids, Proton pump inhibitors

• Auscultate bowel sounds at least every 4 hours, and monitor for abdominal distention.

• If a NG tube is present, measure drainage and check for occult blood.

• Enteral feedings

  ➢ Stimulate mucosal activity
  ➢ Provide essential nutrients & optimal calories

Suggest the nursing management for CNS dysfunction due to SIRS (2)

• Evaluate for hepatic encephalopathy

• Optimize cerebral blood flow
  ↓ Cerebral O2 requirements, Prevent secondary tissue ischemia

Suggest the nursing management for renal dysfunction due to SIRS (2)

Diuretics
✓Loop diuretics (e.g., furosemide [Lasix])
✓May need to increase dosage due to ↓GFR

Continuous renal replacement therapy

What is the pathophysiology of cellulitis ?

Bacteria release their toxins in the subcutaneous tissues, most common infectious cause of limb swelling

Suggest the signs s/s of cellulitis (3)

• Acute onset of swelling

• Localised redness, + pain

• Fever & chills

Suggest the treatment / management for cellulitis (4)

• Incision & Drainage (I&D) of a skin abscess

• Antibiotics

• Mapping of the red area to monitor if the infection is getting better or worse

• Elevate the affected area 3-6 inches above heart level

What is the pathophysiology of necrotizing fasciitis ?

• pathogens enter the tissue through an open wound and spread rapidly in the extracellular space between the subcutaneous tissue & the fascia.

• a rapid and progressive inflammatory infection of the soft tissue.

Suggest the treatment / management for necrotizing fasciitis (4)

• Radical surgery

• Necrotic tissue excision

• Broad-spectrum antibiotics (pre-op) —> specific antibiotics after C/ST

• Local and systemic infection must be completely controlled before wound closure is addressed

How to conduct rapid sequence intubation (RSI) ?

• Sedation first, then muscle relaxant

  • Sedation controls agitation, aids in mechanical ventilation provided amnesia during neuromuscular blockage.

  • Muscle relaxant facilitate endotracheal intubation, relax muscles for surgical procedures, terminate laryngospasm, eliminate chest wall rigidity, and provide for ease of mechanical ventilation if undicated.

What are the implications of the following laboratory findings in shock ?

• Arterial blood gases

  • Respiratory alkalosis

Found in early shock secondary to hyperventilation.

What are the implications of the following laboratory findings in shock ?

• Arterial blood gases

  • Metabolic acidosis

Occurs later in shock when lactate accumulates in blood from anaerobic metabolism.

What are the implications of the following laboratory findings in shock ?

• Lactate level increase

Usually increases once significant hypoperfusion and impaired oxygen utilization at the cellular level have occurred. By-product of anaerobic metabolism.

What are the implications of the following laboratory findings in shock ?

• RBC (concentration) normal

Remains within normal limits in shock because of relative hypovolemia and pump failure and in hemorrhagic shock before fluid resuscitation.

What are the implications of the following laboratory findings in shock ?

• RBC concentration decrease

Hemorrhagic shock after fluid resuscitation when fluids other than blood are used.

• haemodilution

What are the implications of the following laboratory findings in shock ?

• RBC concentration increase

Non-hemorrhagic shock caused by actual hypovolemia and hemoconcentration.

What are the implications of the following laboratory findings in shock ?

• WBC increase

Infection, septic shock.

What are the implications of the following laboratory findings in shock ?

• Creatine kinase increase

(an enzyme found mainly in the heart, brain, and skeletal muscles that helps supply energy to cells)

Trauma, myocardial infarction in response to cellular damage and/or hypoxia.

What are the implications of the following laboratory findings in shock ?

• Creatinine increase

Indicates impaired kidney function caused by hypoperfusion as a result of severe vasoconstriction.
Is more sensitive indicator of renal function than BUN.

What are the implications of the following laboratory findings in shock ?

• Increased glucose

Found in early shock because of release of liver glycogen stores in response to sympathetic nervous system stimulation and cortisol. Insulin insensitivity develops.

What are the implications of the following laboratory findings in shock ?

• Decreased glucose

Occurs because of depleted glycogen stores with hepatocellular dysfunction possible as shock progresses.

What are the implications of the following laboratory findings in shock ?

• Liver enzymes (ALT, AST) increase

Elevations indicate liver cell destruction in progressive stage of shock.

What are the implications of the following laboratory findings in shock ?

• Fibrin split products (FSP) increase

• Fibrinogen level, platelet count decrease

• aPTT & PT, INR increase

• Thrombin time increase

• D-dimer increase

Acute DIC can develop within hours to days after an initial

assault on the body

Test	Pathway	Key Clotting Factors	Primary Drug Monitored	Common Pathologies
PT / INR	Extrinsic + Common	VII, (I,II,V,X)	Warfarin	Liver disease, Vitamin K deficiency
aPTT	Intrinsic + Common	XII,XI,IX,VIII, (I,II,V,X)	Unfractionated Heparin	Hemophilia A/B, Lupus anticoagulant

Thrombine time: Measures the clotting time of a sample of plasma to which thrombin has been added

D-dimer: waste product when fibrin is being broken down

What are the implications of the following laboratory findings ?

• Amylase / Lipase

Pancreatitis if lipase level > 800 IU/L

• Normal range: 0-160

What are the implications of the following laboratory findings ?

• Elevated troponin

AMI

Pulmonary embolism

aortic dissection

sepsis

What are the implications of the following laboratory findings ?

• Liver enzymes increase

Hepatocellular injury, primary biliary cholangitis, ….. L3

Which laboratories findings should we focus on if we suspect an acute DIC ? (7)

• Fibrin split products (FSP) increase

• Fibrinogen level, platelet count decrease

• aPTT & PT, INR increase

• Thrombin time increase

• D-dimer increase

Under what situation, Hb 9g/dL is considered normal ?

In patients with chronic kidney disease (CKD), esp. those not undergoing dialysis, Hb levels may be lower due to decreased erythropoietin production.

• Hb levels around 9 may be common

• Treatment might not be initiated unless there are s/s (e.g. SOB, fatigue) or the level drops further