Septic Shock differentiation/treatment

• - Normal host response to infection
• - Pro/ anti inflammatory mediators released
• - Vasodilate tissues to allow more blood
• - Balance of mediators guides tissue repair/healing
• - Inflammation is intended to be local and contained

• There has to be a homeostasis between inflammation and fibrinolysis
• When inflammation increases coagulation also increases
• Imbalance between inflammation and fibrinolysis predisposes towards sepsis

• - Disruption of pro/ anti inflammatory equilibrium
• - Characterized by systemic inflammation and tissue injury

• - Endothelial damage causig vasodilation (NO released)
• - Microvascular dysfunction
• - Increased microvascular permeability (tight junctions loosen up, causing 3rd spacing of fluids, plasma into tissues, causes low BP )
• - Impaired tissue oxygenation (due to microvascular thrombi)
• - Organ injury

• 1. Infection
• 2. Disruption of pro/anti inflammatory equilibrium
• 3. systemic inflammation and widespread tissue injury
• 4. Endothelial dysfunction and microvascular thrombosis
• 5. Hypoperfusion and ischemia of vital organs
• 6. Acute Organ dysfunction (severe sepsis)
• 7. Death :(

Presence of pathogens in normally sterile body fluids (blood, urine, csf, and for the most part lower respiratory tract)

• Temperature: > 38 C or < 36 C (hypothermia worst prognosis)
• Heart Rate: > 90 bpm (excluding any other causes)
• Respiratory Rate: > 20 bpm or PaCO2 < 32mmHg
• WBC: > 12000 cells/ml or < 4000 cells/ml OR > 10% immature forms of wbc (bands)

Sepsis: Infection + >/= 2 SIRS criteria

Severe Sepsis: Infection + >/= 2 SIRS criteria + organ dysfunction

Septic Shock: Infection + >/= 2 SIRS criteria +/- organ dysfunction + hypothension despite fluid resuscitation

Pathological process induced by a microorganism

• Fever
• - Core temp > 38.3
• Hypothermia: < 36

• Heart Rate
• > 90 bpm or 2 SD > the normal value for age

• Tachypnea:
• - > 30 bpm

Altered mental status

Significant edema or positive fluid balance: > 20 ml/kg over 24 hrs

Hyperglycemia in the absence of diabetes: Glucose >100 mg/dl

Leukocytosis: WBC count > 12,000

Leukopenia: WBC < 4,000

Normal WBC with > 10% immature forms

Increased plasma C reactive protein: if it is > 2 SD the normal value (< 1 mg/dl) Eg: >17 mg/dl

Increased plasma procalcitonin: > 2 SD the normal value ( < 0.01 ng/ml) Eg: >10 ng/ml

• Arterial hypotension
• - SBP < 90 mmHg
• - MAP < 70
• - SBP down more than 40 mmHg (adults)
• - SBP > 2 SD below normal for age (pediatrics)

• Mixed venous oxygen saturation: > 70%
• - Children usually are 75-80% thus not used as a sign or sepsis in newborn or children

• Increased Cardiac Index (mostly late sepsis)
• > 3.5 L/min/m*m in adults
• - Children normally 3.5-5.5 L/min/m*m thus not to be used as sign of sepsis

• --Hyperlactatemia: > 3 mmol/L
• Normal: 0.5-1.5 mmol/L

-- Decreased capillary refill

--Mottling: irregular pattern of patches or spots (poor skin perfusion in CHF pt.)

• 3rd spacing of fluids causes tissue edema
• leads to compression of capillary beds
• deformed red blood cells plug capillary lumens
• Causes: low no. of functional capillaries, low oxygen extraction

• Endothelial injury releases endogenous vasodilators
• - Prostacyclin, nitric oxide
• Vasopressin deficiency
• Systolic and diastolic ventricular dysfunction
• Hypovolemia

• -Early sepsis: low CO and low SVR
• -Late Sepsis: after vol. resuscitation hyperdynamin CO and SVR continues to be low

• Edothelial injury in the pulmonary vasculature
• Pulmonary edema accompanied by ventilation-perfusion mismatch and arterial hypoxemia
• Acute respiratory distress syndrome !

• Intubated/sedated pts develop bacteria overgrowth of upper GI tract
• Pathogens can aspirate into lungs-- nosocomial pneumonia
• Endothelial abnormalities lead to translocation of bacteria and endotoxin into the systemic circulation

• Liver ischemia due to hypoperfusion
• Liver makes clotting factors: if not making any then super anticoagulated (high INR and aPTT)
• Dysfunctional reticuloendothelial system: decreased clearance of bacteria and byproducts that have entered the venous portal system from gut.

• Acute renal failure- common
• Acute tubular necrosis is most common
• Potential causes:
• systemic hypotension
• cytokine release (TNF)
• direct renal vasoconstriction
• activation of neutrophils by endotoxin

• Altered sensorium
• peripheral neuropathy
• microvascular thrombi in brain? microabscesses??

• Physical exam
• Procedures: CXR, LP, CT
• Labs: Chem 12, CBC with differential, coags, lactate, ABG
• Assessment of catheters
• cultures

• Lungs, abdomen, and bloodstream are most commonly infected.
• 90% of sepsis caused by bacteria.
• Fungi sometimes possible
• Community versus nosocomial

• 1. Coagulase-negative staph
• 2. Staph aureus
• 3. enterococci
• 4. Candida species
• 5. E. coli
• 6. Klebsiella
• 7. enterobacter
• 8. pseudomonas
• 9. serratia
• 10. viridans strep

• Initial resuscitation (within 6 hrs)
• Infection issues: diagnosis, abx therapy, source identification and control
• Hemodynamic support
• Adjunctive therapy
• supportive therapy