Acute Renal Failure

System inflammatory response syndrome and sepsis for surgery patients

System inflammatory response syndrome (SIRS) -

Sepsis — SIRS + septic site

• Systemic Inflammatory Response Syndrome Criteria (ACCP/SCCM Consensus)

– Temperature >38°C or <36°

– Heart rate >90 bpm

– Respiratory Rate>20 or PaCO₂<32mmHg

– WBC>12,000/μl or <4,000/μl

• Sepsis: 2 or more-

– Tachycardia >90bpm

– Rectal temp>38°C or <36°C

– Tachypnea(>20bpm)

• With 1 or more

– Alteration in mental status

– Hypoxemia (PaO₂<72mmHG at FiO₂0.21)

– Elevated plasma lactate

– Oligouria

Sepsis
classification by ethiology:-

• Gram (+)

• Gram (-)

• Aerobic

• Anaerobic

• Mycobacterial

• Staphylococcus

• Streptococcus

• Mixt-sepsis

Sepsis
classification by primary focus:-

• Post-traumatic:

– burn

– wound

• Lung

• Angiogenic

• Cardiogenic

• Abdominal:

– Biliary

– Pancreatic

– Intestinal

– Peritoneal

– Appendicular

• Soft-tissue inglammation

• Urological etc

Sepsis
classification by development with a time (stages):-

• Toxemia

Sepsis

Severe sepsis – sepsis + organ dysfunction

Septic shock – sepsis + hypotension

(Multiple organ dysfunction)

• Severe Sepsis

– Tachycardia >90bpm

– Rectal temp>38°C or <36°C

– Tachypnea(>20bpm) or PaCO₂<32mmHg

– Hypotension despite fluid resuscitation

– Presence of perfusion abnormalities: lactic acidosis, oligouria, alteration in mental status

• Mediators of Sepsis

– Lipospolysaccharide (gram-negative bacteria)

– Lipoteichoic acid (gram-positive bacteria

– Peptidoglycan

– Cytokines

• IL-1 – mediates systemic effects of infection

• IL-6 – effects liver function

• TNF-α- potentiates the activation of neutrophils and macrophages

• IL-8 – regulates neutrophil function, mediates lung injury in sepsis

– Complement

– Nitric Oxide

– Lipid Mediators: Chemotaxis, Cell activation, Vascular Permeability

Phospholipase A2

PAF

Eicosanoids

– Adhesion Molecules

• Selectins

• Leukocyte Antigens

• Circulatory Manifestations

– Vasodilation

– Tachycardia

– Increased Cardiac Output

– Depressed Myocardial Function

– Increased Delivery

– Decreased Extraction

– Downregulation of catecholamine receptors

– Increased local vasodilating substances

• Nitric oxide

• Prostacyclin

• Decreased Oxygen

• Low pH

• Increased anaerobic metabolism

• Shunting

• Pulmonary Dysfunction

– Endothelial Injury

– Interstitial Edema

– Alveolar Edema

– Neutrophil entrapment

– Injury Type I pneumocyte

– Hyperplasia Type II pneumocyte

– Continued Neutrophil, monocyte, leukocyte and platelet aggregation

– GI

• Ileus

• Malabsorption

• Overgrowth of bacteria, Translocation

– Liver

– Renal

– CNS

• Organisms

– Lower Respiratory Tract Infections (25%)

– Urinary Tract Infections (25%)

– Gastrointestinal Infections (25%)

– Soft Tissue Infections (15%)

– Reproductive Organs (5%)

• Risk Factors

– Extremes of Age (<10 and >70 years)

– Pre-existing Organ Dysfunction

– Immunosuppression

– Major Surgery, Trauma, Burns

– Indwelling Devices

– Prolonged Hospitalization

– Malnutrition

– Prior Antibiotic Treatment

• Principles for Management of Sepsis

– Early Recognition

– Early and Adequate Antibiotic Therapy

– Source Control

– Early Hemodynamic Resuscitation and continued support

– Drotrecogin Alpha (Apache II>25)

– Tight Glycemic Control

– Ventilatory Support

• Drotrecogin-alpha/Recombinant Human Activated Protein C

– Reduced levels of anti-inflammatory mediators

– Activated Protein C

• Inhibits thrombosis

• Decreases inflammation

• Promotes fibrinolysis

– Side Effect: Bleeding

– PROWESS study group

• Lower mortality rate (24.7 vs. 30.8%)

• Steroids???

– Older trials used high doses

– Recent trials suggest low dose, with taper and tight glycemic control may improve outcome

– Vasopressor-dependent shock

– Cosyntropin Stim Test-Relative Adrenal Insufficiency (<9mcg/dL)

• Experimental Therapies

– Dopexamine- beta 2 adrenergic and dopaminergic effects, NO alpha adrenergic activity

– Vasopressin- reduces inducible NO synthase, upregulates endogenous catecholamine receptors

– Phosphodiesterase Inhibitors-ionotropic agents with vasodilating actions

– Nitric Oxide Inhibitors- N-monomethyl-l-arginine

ARDS :-

• Frequent Complication in Sepsis(40%)

• Adult Respiratory Distress Syndrome

– Oxygenation abnormality: PaO₂/FiO₂ ratio less than 200

– Bilateral opacities on CXR

– PAOP <18mm Hg or no evidence of L atrial hypertension

• Frequent Complication in Sepsis(40%)

• Adult Respiratory Distress Syndrome

– Oxygenation abnormality: PaO₂/FiO₂ ratio less than 200

– Bilateral opacities on CXR

– PAOP <18mm Hg or no evidence of L atrial hypertension

– Frequency of ARDS in sepsis 18-38%

– 16% patients die w/irreversible respiratory failure

• Pathophysiology

– Injury to Alveolocapillary unit

– Exudative Phase

• Endothelial injury, immune cell infiltration, pneumocyte and endothelial injury and necrosis

– Proliferative Phase

• Organization of exudate, myofibroblast proliferation

• Conversion of exudate to fibrous tissue

– Fibrotic Phase

• Remodeling of fibrosis, microcystic honeycomb formation and traction bronchiectasis

• Management

– Lung-Protective Strategy-Reduction of Barotrauma

– TV 5ml/kg

– Longer inspiratory time

– Peak Inspiratory Pressure<35-40cmH₂O

– Permissive Hypercapnea

– PEEP

Acute Renal Failure

• Increases Mortality in ICU 30%

• Physiology

– Glomerular Filtration dependent on perfusion pressure (MAP 60-80mmHg)

– Less than 60mmHG

• Decreased flow

• Arterial dilation in pre-glomerular arterioles (prostaglandins)

• Constriction of post-glomerular arterioles (angiotensin II)

• As Renal Perfusion Falls

– Increased reabsorption in proximal tubules

• 90% water is reabsorbed (normal is 60%)

– Decreased fluid to the distal tubules

• Loss of potassium elimination

– Tubular cells dependent on aerobic respiration

• Ascending loop is most sensitive to ischemia

Date: 2015-12-11; view: 896