APR - created from Mind Map

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Inflammation

SIRS

CARS

Sepsis

Septic shock

MODS

Metabolism

MOF

Presentation

Characteristics

Neuroendocrine response

Hormonal response

Dolor (pain)

Calor (heat)

Rubor (redness)

Tumor (swelling)

Functio laesa (loss of function)

Hypermetabolism

Hypercatabolism

Hyperglycaemia

Luid accumulation

Cortisol

Catecholamine

Glucagon

aldosterone

ADH

Activation of SNS

Incr. glucagon release

HPA axis

Pathophysiology

Continued inflammation

Th-1 response - hyper metabolism

Risk factors

Criteria diagnosis

Inflammation in sites remote from primary site of injury

inadequate/ delayed resuscitation

Persistent inflammatory/infectious focus

Baseline organ dysfunction

Age >65

Immunosuppression

Alcohol abuse

Malnutrition

invasive instrumentation

Balances SIRS

Th-2 response

Life threatening organ dysfunction

Incr. lactate levels

Includes

Causes

Pathogensis

Presentation

Renal system

Respiratory system

Hepatic system

Gastro-intestinal system

Hepatologic and cardiac presentation later

Primary

Secondary

Direct from injury

Remote from initial injury

Excessive production of mediators

GUT hypothesis

Disruption of GUT barrier function

Translocation of enteric bacteria

Hypermetabolic

High cardiac output

Low O2 consumption

High venous oxygen saturation

Lactic academia

Protein

CHO

Lipid

Energy

Micronutrient

Vitamins

+APP

-APP

Immune function

Result

LBM loss

-N balance

External sources + endogenous production

Incr. gluconeogenesis

Insulin (diminished + resistance)

Ketones

N saving effect lost

Hypermetabolism

Incr. need for A, E, B6, C, D

Dear. Fe, Zn, Se

Iron depleted

Incr. requirements

Stress (B2, B6, C, B5)

Immune dysfunction (A, D, E, B6, C, B5, folic acid)

Wound healing (A, B2, C, Zn)

Prevent oxidative damage (C, E)

Medication

Malabsorption

Failure to correct SIRS

Immunocompetence