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The Critically Ill Patient: Surgical Intensive Care
Dr. Thomas Dr. Thomas VanderLaanVanderLaanDr. Melanie Dr. Melanie WalkerWalker
Huntington Memorial HospitalHuntington Memorial HospitalPasadena, CaliforniaPasadena, California
Outline
Recognizing Critical IllnessThe Stress Response
Systemic ReviewClinical ManifestationsTreatment
Multiple Organ Dysfunction and FailurePrevention
Metabolic Response to Critical Illness
Responses are similar regardless of cause (injury, illness, infection)Adaptive reactions serve to promote recovery following injuryCosts?
DebilityOrgan dysfunction syndromesDeath
Importance of Metabolic Response
Treatment decisions:Support?Suppress?
Goals:Decrease debilityPromote recovery
Response to Injury
Change in:Energy TemperatureO2 Consumption
Minutes Hours Days Weeks
Early LateCatabolism Anabolism
INJURY
The Physiology of Injury: Early Phase
Increased glucose levelNormal glucose productionIncreased free fatty acid levelsLow insulin concentrationDecreased core temperature
Increased levels of catecholamines and glucagonIncreased blood lactateDecreased oxygen consumptionDecreased cardiac output
The Physiology of Injury: Late Phase
Increased blood glucose levelIncreased glucose productionNormal or slightly high free fatty acid levelsNormal or slightly high insulin levelsIncreased cardiac output
High normal catecholamines and glucagonNormal blood lactateIncreased oxygen consumptionIncreased body temperature
Stress Response: The Wound
Source of mediatorsPainInflammatory cells
Other Contributing FactorsNecrotic or devitalized tissuesAbscessInflammationForeign materialDryingHypoperfusion
Stress Response: Hypovolemia
CausesHemorrhageGastrointestinal lossInsensible loss (“third spacing”)
ResponsesSympathetic nervous systemHormonal response
Stress Response: Hypovolemia
ResuscitationCrystalloidColloidBlood products
End-points of ResuscitationClinical improvementHemodynamic stabilityChemical or medication maximums
Stress Response: Pain
Pain…Limits mobility causing:
Deep venous thrombosisIleus (silent bowel)
Limits cough causing:AtalectasisPneumonia
Stress Response: Pain
TreatmentMedications
NarcoticsNon-steroidalsLocal anesthetic agents
Routes of deliveryOral IMIVEpiduralPatient-controlled analgesia
Stress Response: Inflammation and Infection
FeverCauses physiologic stress to patient
Tachycardia increased work on the heartTachypnea increased respiratory effortMalaiseAgitation
Search for sourceTreat with antipyretics
Inflammatory Syndromes
Systemic Inflammatory Response Syndrome (SIRS)SepsisSevere SepsisSeptic Shock
Systemic Inflammatory Response Syndrome
Two or more of the following:Temperature > 38°C (100.4°F) or < 36°C (96.8°F)Heart rate > 90 beats per minuteRespirations > 20 per minuteWBC > 12,000 / mm3 or < 4,000 mm3
Sepsis and Severe Sepsis
SepsisMeets criteria for SIRSClinically likely source of infection
Severe SepsisMeets criteria for sepsisAlso has impaired cardiovascular performance requiring fluid resuscitation
Septic Shock
Meets criteria for Severe SepsisAlso has impaired cardiovascular performance requiring inotropic support
Inflammation and Infection
TypesPrimary related to primary injurySecondary complication of therapy
Inflammation and Infection
SignsFeverTachycardiaWidened pulse pressureLeukocytosisGlucose intoleranceFluid retentionHypoxemiaIleusThrombocytopeniaAgitation
Inflammation and Infection: Treatment
1. Search for sourceCulturesX-raysEndoscopies
2. Empiric broad spectrum antibioticsSurgery
Drain abscessDebride necrotic tissueBiopsy
3. Change all catheters
Inflammation and Infection
PreventionSterile techniqueChange catheters regularlyKeep all access sites clean and dryProphylactic antibiotics in high risk patients
Iatrogenic Factors
Prolonged bed rest causes:Pulmonary complicationsDeep venous thrombosisSkin breakdown and ulcers
Food deprivationStarvation makes the metabolic response worseLimit to 3-4 days maximum
Invasive devices (catheters)Potential source of infectionLimit duration of use
Iatrogenic Factors
Sleep deprivation causes:ConfusionDisorientationPsychosisAnxiety
Treatment for sleep deprivation:ReorientationSedative / hypnotic medications
Manifestations of the Stress Response
HypermetabolismRelated to severity of injuryResponse dependent on age, sex, body sizeTemperature sensitive but not dependent
Alterations in Metabolic Rate
100% above normalBurn of 40-100% body surface
50% above normalMulti-organ failure
50% above normalSevere injury or infection
25% above normalLong bone fracture
25% above normalMild peritonitis
NoneFistula without infection
NoneNo postoperative complicationsCHANGE IN METABOLIC RATESAMPLE CONDITION
Manifestations of the Stress Response
Muscle wastingAccelerated protein breakdownIncreased urinary excretion of nitrogen
Why does skeletal muscle break down?
Provides amino acids for protein synthesisProvides precursors for glucose production
Alanine = urea + glucoseProvides precursors for ammonia productionProvides fuel for rapidly dividing cells
Manifestations of the Stress Response
Altered carbohydrate metabolismCritical illness causes
Increased glucose productionIncreased glucose uptakeIncreased glucose turnoverDecreased glucose utilization
Altered Carbohydrate Metabolism
Glucose productionHydrolysis of glycogen stored in liverCori cycle
Lactate glucose (very inefficient)
GluconeogenesisAlanine glucose
Altered Carbohydrate Metabolism
Glucose intolerance / Insulin resistanceHigh insulin levelsDecreased glucose utilizationReceptor defect
Stress Response: Mediators
Can have good and bad effectsMade by different types of cells
Endocrine, Autocrine, ParacrineSpecific receptors
Alter behavior of cellsAffect other receptors
Types of Mediators
HormonesInflammatory mediatorsGrowth factors
Injury: Hormones Released
ACTHCortisol AldosteroneGrowth hormoneProlactinHistamineSerotonin
EpinephrineNorepinephrineDopamineGlucagonReninAngiotensin II
Injury: Decreased Production or No Change
InsulinEstrogenTestosteroneThyroxineT3
Thyroid stimulating hormoneFollicle stimulating hormoneLuteinizing hormone
Sources and Targets of Inflammatory Mediators
Cytokinesproteins that are secreted by a cell for the purpose of altering either its own functions (autocrine effect) or those of adjacent cells (paracrine effect)
Interleukinscytokines that are produced by leukocytes and other cell types
Tissue Necrosis Factor α
Helps control local infection by:Helps control local infection by:•Inducing acute phase proteins•Stimulating white blood cells
Resulting in
•Removal of infectious agent•Immunity
Systemic release is harmful:Systemic release is harmful:•Edema •Hypoproteinemia•Neutropenia
Resulting in
•Multiple organ failure•DIC•Death
Interleukin-6
Huge number of sources and target cellsPrimarily involved in stimulating the production of acute phase proteins in the liver Induces formation of antibodies and T cellsCan inhibit the growth of some cells such as human fibroblasts and endothelial cells as well as leukemia, lymphoma and breast carcinoma cell lines
Stress Response: Central Nervous System
Afferent (incoming) signalsTell body that there is an injury
Efferent (outgoing) signalsHelps to make necessary metabolic changes
Stress Response: The Gut
Can complicate the response to critical illness
Source of gram negative bacteriaThese are the predominant infective organisms in the ICU
The Normal Gut
Has tight, intracellular junctions that do not leak contentsHas a rich supply of immune cellsHas (healthy?) liver and spleen as back-up if necessary
The Gut During Illness
mucosal barrierimmune functionfluid and electrolyte loss
The Gut and Bacteria
Altered permeability of cellshost defensesnumber of bacteria
THIS MEANS TROUBLE!
Enteral Feedings During Severe Illness
Preserve mucosal integritySome advice on enteral feeding…
Complication Rates
96Fasciitis
132Catheter sepsis
92Empyema
132Intra-abdominal abscess
3111Pneumonia
PARENTERAL FEED (%)
ENTERAL FEED (%)
SEPSIS FROM:
Multiple Organ Dysfunction or Failure?
DysfunctionMeans the organ is incapable of maintaining homeostasis
FailureMeans the organ cannot meet minimal demands and is not considered viable
Basic Criteria: Pulmonary System
DysfunctionHypoxia requiring intubation for 3 to 5 days
FailureAdult respiratory distress syndrome requiring advanced ventilator settings
(PEEP > 10 cm H20 and FiO2 > 0.5%)
Basic Criteria: Hepatic System
DysfunctionHugh serum bilirubinLiver function tests that are twice normal values
FailureClinical jaundiceTotal bilirubin > 8 – 10 mg %
Basic Criteria: Renal System
DysfunctionOliguriaAbnormally high creatinine
Failuredialysis
Basic Criteria: Gastrointestinal System
DysfunctionIleusIntolerance of enteral feeds
FailureStress ulcersAcalculous cholecystitis
Basic Criteria: Hematologic System
DysfunctionClotting times (PT / PTT) 125% of normalPlatelets < 50,000
FailureDisseminated intravascular coagulopathy (DIC)
Basic Criteria: Central Nervous System
DysfunctionConfusionMild disorientation
FailureProgressive coma
Basic Criteria: Cardiovascular System
DysfunctionDecreased ejection fraction
FailureRefractory cardiogenic shock
What Causes Organ Failure?
First EventFirst Event
Tissue TraumaInfection
Shock
Inflammatory Response Macrophages
Recovery Amplified Immune Response
Organ Failure Death
InfectionEndotoxemia
Ischemia
Second EventSecond Event
Prognosis of Multiple Organ Dysfunction Syndrome
1005
72-1004
85-1003
50-602
301
30
Mortality (%)Number of failing systems
Prevention of Multiple Organ Failure
Resuscitative Phaseaggressive volume resuscitation in early phase
Operative Phasetimely management of soft tissue injury and necrotic tissuesearly fixation of long bone and pelvic fractures
Prevention of Multiple Organ Failure
ICU PhaseEarly nutritional supportAppropriate use of antibioticsSpecific organ supportTimely surgery for any ‘missed’ injuries
Other Factors That Can be Controlled
Body oxygenationTissue perfusionPain, anxietyBody temperatureAcid-base balanceNutrient supplyGut integrityWound repair and closure