SHOCKJuly 12, 2001.

Rob Hall and Dr. John King

Case

• 16yo male, riding bike then swerved into traffic and was struck by a truck

• A: gurgling, stridor, facial trauma• B: RR 35, sat 85%, subQ air on R, abrasion

over sternum, dec AE on R, wheeze• C: diaphoretic, HR 145, BP 70/50, +JVD• secondary: pelvic #, femur #, large scalp

laceration, skin looks red

Case

• Ddx of shock in this patient– hemorrhagic: hemothorax, abdomen, pelvis #,

femur #, scalp laceration– obstrucitve: tension pneumo/hemothorax– cardiogenic: cardiac tamponade– anaphylactic: the patient was stung by a bee,

lost control of bike and was struck by a car

“ Shock is the transition between illness and death”

Definition of Shock

• Shock is the clinical manifestations of the inability of the circulatory system to adequately supply tissues with nutrients and remove toxic waste

Classification of Shock

• Quantitative– hypovolemic, hemorrhagic, obstructive,

myocardial dysfunction

• Qualitative– sepsis, anaphylaxis, neurogenic,

dyshemoglobinemia, cellular poisons

Classification of Shock

• Pre - heart– hypovolemia, venous pooling

• Heart– contractility, arrythmias, mech obstruction

• Post - heart– loss of vascular tone, inability to deliver to

tissues, inability of tissues to utilize

Etiological Classification

• S - septic

• S - spinal (neurogenic)

• H - hypovolemic/hemorrhagic

• O - obstructive (PE, pthrx, hthrx, ct)

• O - other (CN, CO, HS, MetHb)

• C - cardiogenic

• K - anaphylaCTic

Pathophysiology

• FOUR unifying features of shock– intracellular calcium overload– intracellular hydrogen ion– cellular and interstitial edema– catabolic metabolism

Shock Treatment Goals

• FOUR goals of treatment– oxygenation– ventilation– volume replacement– vasopressor support

Approach to Undifferentiated Shock

• Targeted history– septic: fever, immunocompromised– hypovolemic: vomiting, diarrhea, abdo pain– hemorrhagic: trauma, bleeding (UGI, LGI, PV),

abdo pain (AAA)– obstructive: chest pain, trauma– other: environmental exposures– cardiogenic: chest pain– anaphylatic: allergic reactions

Approach to Undifferentiated Shock

• Investigations– labs– ECG– CXR– ABG– urine

Septic Shock

Definitions:Consensus conference on definitions for sepsis: Critical Care

Medicine 2000. Volume 28 (1): 232 - 235

• Sepsis– clinical response to infection manifested by two

or more of the following as a result of infection• temp > 38 or < 36

• HR > 90

• RR > 20 or PaC02 < 32

• wbc > 12 or > 10% bands

Definitions Continued

• Septic Shock– sepsis induced hypotension or the requirement

for vasopressors or inotropes to maintain BP despite adequate fluids in the presence of…

• lactic acidosis

• oliguria

• acute alterations of mentation

Early versus Late Septic Shock

Warm/Early Cold/Late

Temp 38 - 40 < 36 or > 40

Skin warm cool

Physical bounding pulseswide pulse pressure

thready pulsenarrow pulse pressure

Labs Prerenal failureMild resp alkalosis

Renal failureLactic acidosis

Management of Septic Shock

• Fluids– boluses of NS or RL

• Pressors– dopamine, norepinephrine– consider after 3 boluses of crystalloid

• Antibiotics– broad spectrum empiric coverage

New Approaches to Septic Shock

• Vasoactive mediators– vasopressin, nitric oxide

• Coagulation Cascade– protein C, protein S, antithrombin III

• Inflammatory mediators– anti TNF antibodies, anti LPS, TFPI

Vasopressin and Sepsis

• Tsuneyoshi et al. Crit Care Medicine 2001.– Prospective study N=16– No control– Improved hemodynamic parameters– No effect on mortality

Antithrombin III and Sepsis

• Human Trial control AIII Fourrier 1993 50%

28% (NS) Diaz 1994 31%35% (NS) Baudo 1998

46% 50% (NS) Eisele 199841% 25% (NS)

Protein C and Septic Shock

• Bernard et al. NEJM 2001.– RCT 1690 patients– mortality in placebo 30.8%– mortality in tx grp 24.7%– ARR of 6.1% p=0.005– serious bleeding 3.5% vs 2% in control (p=.06)– conclusion: decreased mortality, increased

bleeding

IVIG in Septic Shock

• Cochrane Database of Systematic Reviews. Alejandria mm et al– 23 RCTs for total of 6991 patients– overall IVIG RR of death 0.92 (.86,.99)– anti-endotoxin monoclonal Ab RR 1.03 (.8,1.2)– polyclonal IVIG RR 0.6 (0.47,0.76)– conclusion: polyclonal IVIG promising

adjunct, no evidence for monoclonal antibodies

Neurogenic Shock

• Spinal Shock– initial loss of spinal cord function following

SCI including motor, sensory, and sympathetic function

• Neurogenic Shock– loss of sympathetic autonomic function due to

spinal cord injury

Neurogenic Shock

• Hypotension and bradycardia (relative)

• Due to unopposed parasympathetic function

• Arterial and venous dilation, bradycardia

• Management– iv fluid– atropine– vasopressors

Hemorrhagic Shock

Hemorrhagic Shock Classification

Class I Class II Class III Class IV

Volume <750ml 750 – 1500 1500-2000 > 2000

% < 15% 15-30% 30-40% > 40%

HR < 100 100 - 120 120 – 140 > 140

PP N or incrd decreased decreased decreased

BP normal normal decreased decreased

LOC anxious anxious confused lethargic

Hemorrhagic Shock

• Management– ABCs, vascular access, crystalloid bolus X 2,

blood transfusion prn– controversies

• NS versus RL

• crystalloid versus colloid

• immediate versus delayed

• small versus large volume resuscitation

• Optimal endpoints of resuscitation

End Points of Resuscitation

• Base Deficit– used as an approximation of tissue acidosis– “an increasing base deficit in a stable appearing

patient should be concerning for ongoing hemorrhage”

– retrospective evidence• Rutherford EJ 1992. Retrospective review of 3791

patients. Largest study.

End Points of Resuscitation

• Lactate Levels– used as an indirect measure for oxygen debt,

hypoperfusion, and the severity of shock– lots of animal and human data showing

correlation with mortality in shock– prospective trials: correlation with mortality– “normal serum lactate levels is a suitable end

point of resuscitation

Colloids

• Albumin, protoplasm protein fraction, hydroxyethylstarch, gelatin, dextran

• Advantages– less fluid required, more volume in vascular

space, potential to draw fluid in from tissues

• Disadvantages– expensive, allergic reactions, coagulopathies

Colloids

• Cochrane Database of Systematic Reviews. BMJ 1998: 317:235-40.– Objective: effect of albumin on mortality– Study: 30 RCTs total 1419 patients– Results: RR of death 1.46 hypovolemia, 2.40

burns, 1.69 hypoalbuminemia– Pooled RR of death 1.68 (1.26,2.23)– Conclusion: albumin increases mortality

Colloids

• Cochrane Database 2000. Colloids versus crystalloids for fluid resuscitation.– Albumin: 18RCTs RR1.52 (1.08,2.13)– HES: 7 RCTs RR 1.16 (0.68,1.96)– Gelatin: 4 RCTs RR 0.50(.08,3.03)– Dextran: 8 RCTs RR 1.24 (.94,1.65)– Conclusion: No evidence that albumins reduce

risk of death in trauma, burns, or surgery

Colloids - summary

• There is NO evidence that colloids decrease mortality in the resuscitation of critically ill patients.

• There IS evidence that colloids increase mortality in the resuscitation of critically ill patients.

Hypertonic Saline

• Advantages– less volume, stays in vascular space, draws

fluid

• Disadvantages– hypernatremia, hyperosmolarity, seizures,

coaguulopathy, anaphylactoid rxns with dextran

Hypertonic Saline

• Animal evidence – improved hemodynamics and mortality

• Human evidence– Wade et al 1997: HS and HSD in trauma– Metanalysis of 8 RCTS of HSD and 6 HS– HS (7.5% saline): no difference in mortality– HSD (+6%dextran): decreased mortality in 7/8

trials overall 3.5%; trend only ---> Not stat sign

Hypertonic Saline

• Cochrane Database 2001. Alderson P.– Objective: effect on mortality– Study: metanalysis of 8 RCTs– Results: pooled RR of 0.88 (0.74, 1.95)– Conclusion: there is a trend toward reduction

in mortality with HSD although not statistically significant

Hypertonic Saline - Conclusions

• There is evidence of TRENDS toward lower mortality in resuscitation with hypertonic saline but statistical significance has not been demonstrated …………

• More RCTs are needed………..

Controlled Fluid Resuscitation

• Rationale: early, aggressive fluid resuscitation with large volume dislodges soft clots and dilutes clotting factors leading to increased hemorrhage and mortality

Bickell et al and Controlled Fluid Resuscitation - “here

piggy,piggy”

Bickell et al 1990The Detrimental Effects of Intravenous Crystalloid after

Aortotomy in Swine. Surgery 110: 529-36.

• Objective: does rapid volume replacement inc mortality?

• Study: 16 pigs, 8 controls (no fluid), 8 tx (RL 80 ml/kg )

• Results Mortality Hemorrhage

• Controls 0/8 783 ml

• RL tx grp 8/8 2142ml

• Bickell et al 1992. HSD vs RL after Aortotomy

• HSD tx grp 5/8 1340ml

Bickell et al. NEJM 1994.Immediate versus Delayed Fluid Resuscitation for

Hypotensive Patients with Penetrating Torso Trauma

• Study: 598 patients SBP<90, odd/even day randomization, immediate fluids vs none until OR

• Immediate fluids - mortality 110/303 (38%)• Delayed fluids - mortality 86/289 (30%)• Statistically significant p = 0.04• Conclusion: delayed fluid resuscitation reduces

mortality in hypotensive patients with penetrating trauma

Controlled Fluid Resuscitation

• Cochrane Database 2001. Kwan I. Timing and volume of fluid administration for patients with bleeding following trauma.– 3 RCTs for early vs delayed fluids– 3 RCTs for large vs small volume– NO evidence for early or large volume fluid

replacement and trends toward increased mortality

Controlled Fluid Resuscitation - Conclusions

• There is evidence (limited) that early, large volume aggressive fluid resuscitation increases mortality in penetrating trauma.

• Further study needed on penetrating trauma without immediate access to OR and for blunt trauma

Obstructive Shock

Cardiogenic Shock

Cardiogenic Shock

• Definition– decreased cardiac output and evidence of tissue

hypoxia in presence of adequate intravascular volume

• Criteria– hypotension (SBP < 90), cardiac index < 2.2

L/min/m2, PCWP > 15 mmHg

Cardiogenic Shock

• Management– small fluid boluses– invasive monitoring– vasopressors

• norepinephrine

• dopamine

• dobutamine

Cardiogenic Shock

• Dobutamine: beta adrenergic

– positive B1 ionotrope; may drop BP b/c of vasodilation

– SBP 70 - 100 without signs of hypoperfusion a/f fluids

• Dopamine: dopaminergic, beta , alpha adrenergic

– SBP 70 - 100 with signs of hypoperfusion after fluids

• Norepinephrine

– alpha agonist

– SBP < 70 after fluids

Cardiogenic Shock

• Thrombolysis– GISSI (N=280) 30day mortality– streptokinase 70.1%– medical mx 69.6%

– NO trial has shown reduction mortality with cardiogenic shock with thrombolysis

Cardiogenic Shock

• Intra-Aortic Balloon Pump– Gusto I: early IABP + lysis showed trend

towards lowere 30d and one year mortality– SHOCK trial: IABP + lysis mortality 17%

versus medical mx alone 32%– ongoing research

Cardiogenic: the SHOCK trial Hochman JS et al. Early revascularizationin AMI + cardiogenic shock: NEJM 1999; vol 341 (9): 625-34.

• RCT of AMI + cardiogenic shock– 152 early revascularization (PTCA or CABG)

or 150 initial medical mx only (lysis initially, some had PTCA/CABG after 52hrs)

– End Point early revasc. Med Mx stats– 30d mort 46.7% 56% p=.11– 6mo mort 50.3% 63.1% p=.027

Cardiogenic Shock:the SHOCK trial

• Hochman JS. One year survival following early revascularization for cardiogenic shock. JAMA 2001.– Early revascularization survival 46.7%– Initial medical mx survival 33.6%– Statistically significant p<0.03– NOTE: sub group analysis only shows

mortality difference in age < 75yo

Cardiogenic Shock:the SHOCK trial

• Conclusions …….– Patients with AMI complicated by cardiogenic

shock, especially those < 75yo, should undergo emergent revascularization (PTCA or CABG)

Anaphylactic Shock

• Constellation of allergic signs and symptoms– hives, conjunctivitis, rhinitis, upper airway

edema, wheezing/SOB, hypotension ---> cardiovascular collapse

Anaphylactic Shock

• Management– airway management– epinephrine and benadryl– racemic epinephrine and ventolin nebs– ranitidine and steroids– fluids +/- vasopressors for hypotension

Anaphylactic Shock

• Mild– subQ epinephrine: 0.3 - 0.5 ml 1:1000 epi

• Moderate– im epinephrine: 0.3-0.5 ml 1:1000 epi

• Severe– iv– 1ml of 1:10,000 q 30seconds to effect– or 10 ml of 1:100,000 infused over 10 min

Conclusions

• Shock is the transition between illness and death

• Shock has many different causes but the end result is the same

• The diagnosis and management of shock is essential knowledge in emergency medicine