Therese M. Duane

The Many Faces of Shock 1

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The ABC’s of Shock and Trauma

Therèse M. Duane, MDAsst Professor of SurgeryDivision of Trauma/Critical Care

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Objectives

To understand the pathophysiologyof shockTo appreciate how shock influences the presentation and outcome of the trauma patientTo discuss the role of a systematic approach to the trauma patient

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History

1900’s: Influence of WW I / WW II1940’s: Tissue anoxia defined as cause1970’s: Swan Ganz catheter

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Definitions

Oxygen Delivery=– cardiac output x– (Hb g/dL x %sat x 1.36 cc/g) – + (Po2 x .003cc of O2 /mm Hg/dL )

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Importance of Hemoglobin

What is the ideal H/H for the critically ill patient?Consider complications of transfusion:– transmission of infection– immunosuppression– transfusion reactions– cost

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Transfusion Oxygen Support

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Importance of Hemoglobin

Why is there no improvement in pt outcomes with increased H/H?Possibly because of impaired oxygen extraction from:– decreased sensitivity of vascular alpha

adrenergic receptors– inflammatory mediated microvascular

obstruction

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Effects of transfusion on oxygen transport

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Hemodynamics

Cardiac performance determined by:– preload– afterload– contractility– heart rate

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Hypovolemic Shock

Causes– external or internal bleeding– gastrointestinal losses– third space losses

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Classification of Hemorrhage

Over 40ObtundationCardiovascular Collapse

IV.

30-40Supine Hypotension OliguraIII.

20-25Orthostatic HypotensionII.

15TachycardiaI.

% Volume Loss

Clinical SignsClass

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Hypovolemic Shock

Compensated– CO maintained– low wedge and CVP

Uncompensated– CO decreases– low wedge and cvp– elevated SVR

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Hypovolemic Shock

Crystalloids– +low cost and well tolerated– - exits vasculature quickly

Colloids– +remains intravascular longer– - cost and risk of infection transmission

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Influence of Catheter Size on Infusion Rate

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Endpoints of Resuscitation

Abramson et al 1993– 100% survival if lactic acid levels

normalized within 24 hours– 78% survival between 24-48 hours– 14% survival > 48 hours

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Comparison of the three end points

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Septic Shock

Infectious causes– cholangitis– pneumonia– peritonitis– pyelonephritis– meningitis

Inflammatory causes– crush injuries– burns– pancreatitis– anaphylaxis

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Septic Shock

Presentation– hyper or hypothermic– tachycardic– tachypneic– leukocytosis or leukopenia– thrombocytopenia– DIC

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Septic Shock

SG parameters: compensated– CO increased– low wedge pressure– decreased SVR

SG parameters: uncompensated– CO decreased– high SVR– low oxygen

consumption

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Septic Shock

Complement Cascade– C3a, C5a– increases vascular permeability,

vasodilation, chemotaxisPlasma Kinins– Bradykinin– increases vascular permeability,

vasodilation, edema

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Cytokines

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Cardiogenic Shock

Presentation– c/o chest pain, diaphoresis, confusion– appearance may by ashen or cyanotic with

cool skin and mottled extremities– JVD and pulmonary rales– 3rd and 4th heart sounds

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Cardiogenic Shock

Swan Ganz findings:– A-V O2 difference > 5.5 ml/dc– CI < 2.2 L/min/m2

– wedge > 15mmHg

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Mortality Among Study Patients

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Cardiogenic Shock

Strengths of Hochman paper– prospective randomization– outcomes similar for revascularized study

and non-study population Weaknesses of Hochman paper– lack of statistical power to detect 9%

difference in mortality at 30 days– small sample of pts > 75 years

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Cardiogenic Shock

Recommendations– early revascularization with CABG or

angioplasty– further study into revascularization in pts

older than 75 years

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Neurogenic Shock

Causes– traumatic cervical spinal cord transection– spinal anesthesia– acute gastric dilation– drugs

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Neurogenic Shock

Presentation– hypotensive– bradycardic– pink, warm skin– obvious neurologic deficits

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Neurogenic Shock

Swan parameters– CO may be low or normal– decreased SVR– decreased PVR– decreased CVP

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Neurogenic Shock

Treatment– R/O other causes of shock– hemodynamic stabilization– control spine

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Role of Steroids

NASCIS II trial– randomized, controlled, double blinded– methylprednisolone vs naloxone vs

placebo– treatment for 23 hours– blunt trauma pts only– outcomes at 6 weeks and 6 months

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Role of Steroids

NASCIS III– treated pts with methylprednisolone or

tirilazad mesylate– treatment to 23 or 48 hours– blunt trauma pts only– functional independence measure– outcomes at 6 weeks and 6 months

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Role of Steroids

Shortcomings of NASCIS II– creation of subgroups based on data– some subgroup sizes too small– outcomes not correlated clinically

Shortcomings of NASCIS III– no placebo group– subgroups based on data

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Role of Steroids

Important findings of NASCIS– overall mortality rates similar between pts

treated with steroids and control group– FIM significantly improved in overall

function, self care, and sphincter control

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Role of Steroids

Recommendations for treatment of spinal cord injuries after blunt trauma:– within 3 hours of injury treat with 23 hours

of high dose methylprednisolone– within 3-8 hours of injury treat with 48

hours of this steroid– beyond 8 hours of injury do not administer

steroids

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Four Stages Care of Trauma Patient

Primary surveyResuscitationSecondary survey with diagnostic evaluationDefinitive care plan

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Primary SurveyA - airway with C-spine protectionB - breathingC - circulationD - disability:– neurologic disability

E - exposure / environment control:– completely undress the patient but prevent

hypothermia It is designed to identify all immediate life threatening injuries!

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ResuscitationSimultaneously with primary surveyAirway is secured; ventilation is performedIntravenous lines are established and fluid resuscitation with balanced fluid solution is doneGross bleeding is controlledNeurologic deficit is identifiedPatient is exposed

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The Secondary SurveyDetail physical examination from head to toesIdentify life threatening and occult injuriesTests: – CBC– basic chemistries – ABG,XRs:

• Lat C-spine• AP CXR,pelvic film• blood for type and cross match

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After Secondary Survey

Re-exam the patientRe-check the vitals signsPrioritize the injuriesDefinitive plan

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Airway Management

Protecting, providing, and maintaining airwayFailure to obtain an airway- a common cause of preventable deathCause: simple injuries; intoxicationThink airway-with sudden deterioration

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Risks for Airway Problems

Injuries to the head or neck that cause obstruction or have an altered level of consciousness (injury, alcohol, drugs)GCS < 8 requires definitive airwayFacial injuries Neck injuries (tracheal, vascular )

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Identification of airway problem

Talk to the patientListen for abnormal airway:stridor, snoring, gurgling- all suggest supraglotic injuriesDysphonia or pain on speaking implies obstruction at laryngeal level

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Airway ManagementRule #1:Always assume that patient has neck injury– maintain immobilization in neutral position– avoid: hyperextension,hyperflexion or

rotation of the neckRule #2Lack of neurologic deficit does not exclude cervical spine injury

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Airway Management

Chin lift, jaw thrust, suction:– airway secured- oral or nasal airway:

no spontaneous ventilation-ventilatewith bag

– spontaneous breathing- supply oxygenAirway at risk: Endotracheal intubationFailed orotracheal intubation: surgical airway

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Breathing

Airway patency does not assure adequate ventilationLung function, chest wall, diaphragmExpose;auscultate, palpateIdentify pulmonary pathology

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Tension Pneumothorax: Diagnosis

Respiratory distress, subcutaneous emphysema, hypotension, distended neck veinsTracheal deviation away from the affected sideDecreased breath sound on the affected side

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Tension Pneumothorax: Treatment

Needle decompression

Tube thoracostomy

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Flail Chest

Two or more ribs fractured in at least two places with paradoxical movementAssociated lung contusion underestimated on CXRRespiratory failure may not be immediate

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Breathing: Pitfalls

Dyspneic or tachypnic patient: think problem with airwayIn a ventilated patient, vigorous bagging or positive pressure ventilation may compromise ventilationCXR after intubation

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CirculationExam the pulses:– a SBP of 60 - palpable carotid pulse– a SBP of 70 - palpable femoral pulse– a SBP of 80 - palpable radial pulse

Assume: hypotension from hemorrhageControl external bleeding before restoring circulationManual compression; avoid blind clamps

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The Treatment: Initial StepIntravascular replacementIn adults: initial bolus 2 litersIn children: 20 cc/kg/body weightBlood and blood product- type specific or O-negativeAdjunct: Pneumatic antishock garmet (PASG)- buckled into place around the legs, pelvic fracturesRelease them gradually

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Assessment of Organ Function

Level of consciousnessTemperatureSkin colorPulse rate and character

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Circulatory Management

Control hemorrhageRestore volumeReassess

Caution:– elderly– athletes– children– medications

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Disability

Baseline neurologic evaluationGCS scoringPupillary response Observe for deterioration

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Disability

Glascow Coma Scale– eye (1-4)– verbal (1-5)– motor (1-6)– worst: 3 best: 15

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Exposure/Environment

Disrobe patient– necessary to completely evaluate patient

for all injuries– log roll patient to look at back and spine

Maintain normothermia– necessary to avoid problems with

coagulopathy

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Adjuncts to primary survey

Vital signsPulse oximeter and CO2Urinary and gastric catheters unless contraindicatedLaboratory valuesPlain filmsECG

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Secondary survey

Head to toe examFinger in every orificeReevaluate hemodynamicsDetermines subsequent work up and interventions– FAST, CT’s, Angio, OR

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Case Presentation50 years old male, found in the parking lot. Unknown mechanism or history. Brought to ER. Hemodynamically unstable. 2 chest tubes, 6 uPRBC, 4 Liters of crystalloid BP 120s.To the CT scan: Unstable againTo OR emergently What might one find?

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Damage control…

Temporary closure

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Conclusions

Shock is fundamentally a deficiency in tissue oxygen perfusionHypovolemic shock is the most commonly encountered form in the trauma patientA systematic approach is vital to provide efficient and effective care

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