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