ARDS and SIRS

1
ARDS and SIRS
2
ARDS

• Non-cardiogenic (low pressure) pulmonary edema
• An acute inflammatory lung injury in response to
  a variety of insults
• Acute inflammatory phase
• Cytokine activated neutrophils and monocyes
  adhere to alveolar epithelium releasing
  inflammatory mediators and proteolytic enzymes
• This damages the alveolar capillary membrane,
  increasing the permeability and causing alveolar
  edema
• Alveolar collapse occurs from reduced surfactant
• Hypoxemia/respiratory failure occur from loss of
  functioning alveoli and V/Q mismatch
• Fibroproliferative phase
• Progressive pulmonary fibrosis
• Pulmonary hypertension

3
ARDS

• Diagnosis
• Severe hypoxemia (PaO2/FiO2 lt200)
• Bilateral diffuse infiltrates on CXR
• Normal or only slightly elevated PCWP (lt18)
• Acute lung injury is the precursor to
  ARDScriteria for diagnosis is the same except
  there is a lesser degree of hypoxemia (PaO2/FiO2
  lt300)

4
ARDS

• Direct pulmonary causes
• Infection
• Pulmonary trauma
• Near drowning
• Toxic gas inhalation
• Oxygen toxicity
• Gastric aspiration

• Indirect causes
• Sepsis
• Non-thoracic trauma
• Burns
• Hemorrhage
• Multiple transfusions
• Post arrest
• Bowel infarction
• Anaphylaxis
• Pancreatitis
• Uremia, toxins, eclampsia
• Drugs

5
ARDS

• Prognosis
• Mortality is high (50)
• Determined by precipitating condition and
  increased with increasing age and associated
  sepsis
• Cause of death is multi organ failure
• Clinical features
• Acute inflammatory phase
• Lasts 3-10 days
• Hypoxemia and multi organ failure
• Progressive breathlessness, tachypnea, cyanosis,
  hypoxic confusion, lung crepitations (frequently
  misdiagnosed as heart failure)
• Fibroproliferative phase
• Lung scarring and pneumothoraces are common
• Secondary and systemic infections are common in
  both phases

6
ARDS

• Investigation/Monitoring
• Vital signsurine output
• Hemodynamic monitoring
• ABGs
• Microbiology to ID infections early
• Radiology
• Serial CXR shows progression of infiltrates
• CT scans demonstrate consolidation,
  pneumothoraces, pneumatoceles, and fibrosis

7
ARDS

• Management
• ID and treat precipitating cause
• Mild disease O2, diuretics, CPT, NIV
• Severe disease mechanical ventilation
• Protective lung ventilation strategy
• Avoid oxygen toxicity
• Avoid excessive fluid loading
• General measures nutrition, sedation, infection
  control
• Additional measures NO, prone positioning,
  bronchoscopy, ECMO, chest drainage

8
SIRS

• An inflammatory response to infective and
  non-infective conditions
• The inflammatory response seen with sepsis isnt
  always due to infectionblood cultures are
  positive in lt25 of cases of sepsis
• Leading cause of multiple organ failure, ARDS,
  acute renal failure, and late death following
  trauma

9
SIRS

• Pathophysiology
• Initial cytokine release activates polymorphs,
  endothelium, platelets, complement and
  coagulation pathways
• Activated white cells adhere to and damage
  vascular endothelium, allowing fluid and cells to
  leak into the interstitial space
• Microcirculatory thrombosis impairs tissue oxygen
  delivery
• Vasodilation follows the release of inflammatory
  mediators (NO) from the damaged vascular
  endothelium
• Systolic and diastolic myocardial dysfunction is
  due to reduced coronary perfusion and the
  negative inotropic effects of NO and other
  inflammatory mediators
• Impaired tissue oxygen utilization is caused by
  sepsis-mediated cellular enzyme inhibition

10
SIRS

• Clinical features of septic shock
• Fever
• Tachypnea
• Tachycardia
• Oliguria
• Metabolic acidosis
• Elevated WBC
• CNS signs agitation, confusion, coma
• Pulmonary hypoxia/cyanosis, ARDS
• Hemodyanamic low BP, high CO, bounding pulses
  (dilated shock) or peripheral shutdown
  (vasoconstricted shock)
• Renal tubular necrosis, oliguria
• GI splanchnic ischemia, ileus, GI bleed, liver
  dysfunction
• Hematologic coagulation disorders, DIC, low
  platelet count, meningococcal rash
• Other rhabdomyolysis, peripheral edema

11
SIRS

• Sites of underyling infection
• Meninges
• Sinuses
• Ears
• IV lines
• Lungs
• Endocarditis
• Abdominal
• UTI
• GI
• Toxic shock
• Joint/bone
• Chest infection is the most common source of
  sepsis

12
SIRS

• Management
• ID and tx the cause
• Routine blood tests, C-reactive protein, plasma
  lactate, coagulation profile, ABGs, cultures
  (blood, sputum, wound)
• General urinalysis, CXR, EKG
• Specific depends on suspected underlying cause
• ATB determine the most likely causitive
  organisms and cover for thosechange once
  organism is IDd
• General measures
• Oxygen, respiratory support, nutrition,
  prophylaxis against stress ulcer and
  thromboemboli
• Monitor VS, sat, ABG, biochemical profiles

13
SIRS

• Fluid, vasopressor, inotropic support
• Early in septic shock, widespread vasodilation
  causes hypotension and relative hypovolemia
• The reduction in LV afterload increases the CO
  but inappropriate distribution causes regional
  ischemia
• Fluid administration increases the BP and
  restores organ perfusion
• As sepsis progresses, toxic myocarditis impairs
  myocardial fx, reducing the COnow all those
  fluid can cause pulmonary edema
• Vasopressors (Levophed) an increase SVR and BP
  without fluid administration, but CO may fall as
  SVR increases if myocardial performance is
  impaired
• Inotropes (dopamine, epi) increase contractility
  and can be used to maintain CO

14
SIRS

• Additional measures
• Activated protein C modifies microcirculatory
  thromboemboli and prevent organ ischemia
• Steroid therapy adrenocortical insufficiency is
  common in severe sepsis
• Antiinflammatory therapies are ineffective
• Sepsis prevention
• HANDWASHING and other infection control
• Microbiological monitoring
• Prophylactic antibiotics for some invasive
  procedures
• Prompt management of infection

15
SIRS

• About 20 of central venous catheters become
  infected and lead to sepsis
• Usually caused by poor insertion technique or
  poor line care
• Commonest organisms are S aureus, S epidermidis,
  E coli
• Infected lines should be removed and the tip
  cultureda new line is placed in a different
  siteATB
• Prevention of line infection strict aseptic
  insertion technique, firmly secured cannula,
  closed systems, change infusion sets regularly,
  change lines every 5-8 days