Shock • Shock - the rude unhinging of the

Undifferentiated Shock: Making a Difference

machinery of life

-SD Gross 1872

Matthew Strehlow, MD, FACEP Associate Clinical Professor, EM/Surgery Director, Clinical Decision Unit Stanford University

Shock

Epidemiology

• Shock - inadequate tissue perfusion • Cryptic Shock - inadequate tissue

• 1 million patients with shock will present to US EDs each year

perfusion without hypotension

• Up to 50% mortality rate • Majority of patients in ICUs with shock were initially seen in the ED

Matthew Strehlow MD

Kaiser 2012

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OUTLINE •Early vs delayed recognition of shock

Early vs delayed recognition of shock

•Recognizing shock •How vital are vital signs? •Detecting cryptic shock •The role of ultrasound in shock

No difference in mortality! Annane et al. Lancet 2007 Matthew Strehlow MD

Kaiser 2012

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Early Recognition

Early Recognition Sebat et al. Crit Care Med Nov 2007

Sebat et al. Crit Care Med Nov 2007

Results

• Interventions • Educational program • Rapid recognition and response

Time to treatment predicted mortality Mortality rate decreased 40% to 12%

system

Early Interventions

Delayed Interventions

• Traumatic shock • Golden hour • Cardiogenic shock • Early fibrinolysis or catheterization • Septic shock • Early goal-directed therapy • Early antibiotics

• Cardiogenic shock • Vasopressors • Inotropes • Septic shock • ICU based “goal-directed therapy” • Steroids

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Early recognition of shock is the most critical feature in saving patients’ lives!!!

Recognizing Shock

Case 1

Low BP in the Field

•

35 yo male motorcycle driver in a solo MVC Initial EMS vital signs: HR 80, BP 85/50 Initial ED vital signs: HR 90, BP 120/70

Lipsky et al. J Trauma Nov 2006

• 1-year prospective observational study • 1028 patients normotensive in the ED • 71 (7%) were hypotensive in the field

• •

Are this patient’s initial VS in the field concerning? Matthew Strehlow MD

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Low BP in the Field: Increased Injury

Low BP in the Field

Rate of Emergency Therapeutic Operation

• Outcomes

37%

40%

1. Emergency therapeutic operation

30% 20%

a. Within 6 hours of ED arrival

11%

10%

2.Mortality

0%

Normotensive

Hypotensive OR = 4.5 (95%CI=2.7-7.6)

Low BP in the Field:

Hypotension is a Late Median SBP vs Mortality

Mortality Rate 140.0

8%

6%

6% 4%

117.5

Median SBP 95.0 90 72.5

3%

2%

50.0

0%

Normotensive

0

Hypotensive OR = 2.3 (95%CI=0.8-6.9)

Matthew Strehlow MD

Parks et. al, Am J Surg 2006 Kaiser 2012

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40

Mortality (%)

60

80

65% 5

Mortality Increases if SBP 100) • sensitivity (95% CI) = 12% (5-24) • specificity (95% CI) = 96% (88-99)

Brasel et. al, J. of Trauma 2007

Vital Signs in Trauma:

Case 1: Update

• A low BP in the field is predictive of injury

• 35 yo M motorcycle driver in a solo MVC • Episode of hypotension during transport

even if initial ED BP is normal

and improved in ED

• A single low blood pressure below 105-110 mmHg predicts injury

Can we detect cryptic shock and predict the severity of injury in trauma patients?

• A normal HR means nothing!!! Matthew Strehlow MD

Kaiser 2012

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Predicting injury severity in Trauma

Base Deficit • Also termed “negative base excess” • Base deficit is the amount of acid that

• Base deficit • Lactate • Non-invasive

must be remove from the body to return the pH to 7.4

• -2 to 2 normal • ≥6 significantly abnormal

monitoring of regional perfusion

Non-invasive Monitoring of Regional Perfusion

Lactate

• Sublingual capnometry (SlCO2) • Muscle tissue oxygen saturation (StO2) • Transcutaneous tissue oxygenation and

• Marker of oxidative stress (anaerobic metabolism)

• Rapidly removed from body • Normal level 0.5 to 1.5 mEq/L • ≥2 abnormal • ≥4 significantly abnormal (lactic acidosis)

capnometry (PtcO2, PtcCO2)

• Renal doppler resistive index OSI Inc. homepage accessed July 2007

Matthew Strehlow MD

Kaiser 2012

Prometheus Medical homepage accessed July 2009 8

Base Deficit & Lactate Blood Loss

SLCO2

Base Deficit

Lactate

None

47

0.5

2.0

Mild to Moderate

54

3.3

4.1

Severe

66

8.1

base deficit & Lactate • Predictors of Mortality • Base deficit •

ROC (0.87, .77-.98)

•

ROC (0.80, .69-.91)

•

ROC (0.82, .70-.96)

• Lactate • SLCO2

4.8

Baron et al. J of Trauma Jan 2007

Baron et. al, J Trauma 2004

Traumatic Shock: •

Case 1 Follow-up • 35 yo M motorcycle driver in a solo

MVC with episode of hypotension during transport and improved in ED Base deficit 12 Grade IV left kidney laceration OR emergently for nephrectomy Discharged day 10

Elevated initial base deficit and lactate help predict:

• • • •

• • Mortality

Cryptic shock (i.e. bleeding)

Matthew Strehlow MD

Kaiser 2012

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Case 2

Differential Diagnosis

• 67 yo man with altered mental status • HR 120, BP 75/45, RR 48, SaO2 96%

• LV failure • Hemoperitoneum • Severe dehydration • Cardiac tamponade • Pulmonary embolus • Sepsis • Aortic dissection • Thyrotoxicosis • Dysrhythmia • Gastrointestinal Bleed • Abdominal infection

What is the etiology of his shock?

Question

Matthew Strehlow MD

• Anaphylaxis • Neurogenic shock • Valvular dysfunction • Medication error or OD

• ACS • Adrenal failure • Autonomic dysfunction

Reproducible Ideal Diagnostic• Test

• Simple • Rapid • Non-invasive • Readily available

According to the above study how often did ED physicians determine the correct etiology of their patients in shock? 25% 45% 65% 85%

• • • •

pneumothorax

Organized Diagnostic

Moore et al. Acad Emerg Med 2002

•

• Tension

• Accurate • No side effects • Performed in ED

25%

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Goal-Directed Ultrasound Pros

• Non-invasive • No side effects • Readily available • Performed in ED • Rapid

Ultrasound for

Cons

Jones, Crit Care Med 2004 184 hypotensive patients randomized immediate vs delayed US (15 vs 30 min) Main outcome measures Correct diagnosis Number of diagnoses still in differential

• Accurate?

• •

• Operator dependent • Patient dependent • Training required

Jones Protocol: Challenges

Jones Protocol: Results •

• Average time 5.9 minutes • Training program for bedside

Correct diagnosis 80% (early US) vs 50% (delayed US) 30% improvement (95%CI, 16%-42%)

• •

ultrasound

• >100 non-cardiac US • >25 cardiac US • 6 hour didactic lecture and lab

• Median number of diagnoses in differential • 4 (early US) vs 9 (delayed US) (p50% reduction in diameter with inspiration

Subcostal Cardiac Matthew Strehlow MD

RV

• If yes, is tamponade

Kaiser 2012

Liver

IVC

12

3. Parasternal Long Axis Cardiac View •

IVC

What is the LV function? hyperdynamic

• • normal • moderately impaired • severely impaired

4. Apical 4 Chambered Cardiac View

RV LV

• What is the RV size? • Normal or Dilated

Matthew Strehlow MD

LV

Function judged by inspection of wall contraction and thickening during systole

Inferior Vena Cava

Parasternal Long Axis Cardiac View

RV

RV

LV

• Confirm LV function Kaiser 2012

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RV

5. Right Upper Quadrant

LV

• Is intra-peritoneal fluid present?

• Yes or No

Liver

Kidney

Anechoic collection between liver and kidney

Apical 4 Chambered Cardiac View

6. Pelvic View • Is intra-peritoneal fluid present?

• Yes or No

Bladder

Sagittal and transverse planes

Right Upper Quadrant Matthew Strehlow MD

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7. Abdominal Aorta View • Is an abdominal

aortic aneurysm present?

• Yes or No Sagittal and transverse planes to the level of bifurcation

Pelvic View

IVC

Aorta

Aorta

Jones Protocol: Summary • 7 views • 5.9 minutes to complete • Improved diagnostic accuracy in shock

• Requires training

Abdominal Aorta Matthew Strehlow MD

Kaiser 2012

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Shock and US: The Bottom Line

RUSH Protocol Perera, Emerg Med Clin N Am Feb 2010

• Critical tool in ED assessment • Improves ED physician diagnostic

• Rapid Ultrasound in SHock (RUSH) • 3 areas of focus • the “pump” • the “tank” • the “pipes”

accuracy

• Ideal protocol not yet determined

Case 2 Follow-up

Case 3

• 67 yo M with AMS and

• 70 yo female with fatigue • T 97.6, HR 90, BP 85/40, RR 16, 95% RA • 1 L NS and BP improved (100/45)

hypotension IV NS and dopamine US protocol Pericardial effusion Pericardiocentesis VS improved Admitted to ICU

• • • • • •

Matthew Strehlow MD

Does a single low BP reading in ED medical patients have prognostic value? Kaiser 2012

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ED Hypotension: Increased

ED Hypotension Jones, Chest October 2007

•

Hypotension 0%

Prospective cohort of 4,790 ED admissions

5%

10%

15%

Sustained Episodic

• Compared mortality in: • Exposures (SBP 100)

Transient None

Mortality Jones, Chest October 2007

Examining for Signs of Shock

ED Hypotension: Increased Lowest BP

0%

5%

10%

15%

• Shock index • Poor skin perfusion • Oliguria • Altered mental status

20%

99

Mortality Jones, Chest October 2007 Matthew Strehlow MD

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Shock index in trauma pts >55 yo

Shock Index • Heart rate/Systolic blood pressure • 0.5 to 0.7 normal • ≥0.9 significantly abnormal • Increased sensitivity compared to HR

• In patients >55 y0 the best predictor of mortality was

• SI x Age = >49

• Overall, vital signs were a poor predictors

or BP alone, still low sensitivity for occult hypoperfusion

of mortality

Zarzaur, J Trauma 2010

Poor Skin Perfusion

Oliguria • Measure over ≥30 min • Normal • ≥1 ml/kg/hour • Reduced • 0.5 to 1 ml/kg/hour • Severely reduced • 4.5 sec • cool to touch • Predictive of • organ failure Lima A, et al. Crit Care Med 2009 Matthew Strehlow MD

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Examining for Signs of Shock

Case 3: Update • The patient’s BP remains stable but given

• Shock index • Poor skin perfusion • Oliguria • Altered mental status

her increased mortality risk a further evaluation is conducted

• CXR - left lower lobe infiltrate • Lactate - 9.0

How should we interpret this patient’s elevated lactate?

Elevated Lactate, Higher Mortality

Elevated Lactate, Higher Lactate

Mortality Risk Relative to Lactate Level

• Marker of cellular

30%

• Higher levels are

18%

hypoxia

associated with increased mortality

Shapiro N et al Ann Emerg Med 2005;45:524-28

Matthew Strehlow MD

• Patients with lactate >4 without hypotensive septic shock

24%

• Mortality rate 26.5% • Independent predictor of 28-day

12% 6% 0%

mortality

0-2.5

2.5-4

>4 Howell et al. Intensive Care Med 2007 Mikkelsen et al. Crit Care Med 2009

Lactate Level (mmol/L) Kaiser 2012

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Factors That May Elevate Lactate

Lactate Clearance Effect of Lactate Clearance on

• Lactate decrease by 10% at 6 hours predicted

• • Less vasopressors Increased survival

70%

Mortality Vasopressors

53% 35% 18% 0%

Decreasing Not Decreasing

Inadequate Oxygen Delivery

Disproportionate Oxygen Demands

Inadequate Oxygen Utilization

Volume depletion or Profound dehydration

Hyperthermia

Systemic inflammatory response syndrome

Significant blood loss

Shivering

Diabetes mellitus

Septic shock

Seizures

Total parenternal nutrition

Profound anemia

Strenuous exercise

HIV infection

Prolonged carbon monoxide exposure

Drugs such as metformin, salicylate, antiretroviral agents, isoniazid, propofol, cyanide

Trauma

Nguyen et al. Crit Care Med 2004;32:1637-42

Thiamine deficiency

Severe hypoxemia

Lactate: The Bottom Line

Case 3 • 70 F with pneumonia and elevated lactate

• Elevated lactate portends a worse prognosis

• Sepsis “code” activated • Early Goal-Directed Therapy initiated • Patient is admitted to ICU and within 1

in hypotensive and normotensive patients

• Serial lactates can help monitor response to therapy

hour hypotensive on vasopressors

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Summary • • •

Vital signs HR and BP are late findings A single low BP increases mortality risk Base deficit and lactate BD predicts mortality/injury in trauma Lactate predicts mortality in septic shock Ultrasound Assists in diagnosing the undifferentiated hypotensive patient

• •

Defer no time, delays have dangerous ends -William Shakespeare

• • •

Special Thanks Sarah Williams, associate residency director Laleh Gharahbaghian, Director Ultrasound Stanford University School of Medicine J. Christian Fox, Director of Ultrasound UC Irvine School of Medicine

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Early Identification of Shock in Critically Ill Patients Matthew C. Strehlow,

MD

a,b,

*

KEYWORDS  Shock  Hypotension  Lactate  Base deficit  Evaluation

In the eighteenth century the French surgeon Le Dran coined the term choc for soldiers suffering from severe traumatic injuries and heavy blood loss. Shock began appearing in the medical literature in the nineteenth century, and in 1872 the venerated trauma surgeon Samuel D. Gross defined shock as ‘‘the rude unhinging of the machinery of life.’’1 Over the centuries the term shock became synonymous with hypotension. The misconception that hypotension is necessary to define shock persists, despite evidence and international consensus recommendations to the contrary. More appropriately, shock is defined as a life-threatening condition characterized by inadequate delivery of oxygen and nutrients to vital organs relative to their metabolic demand. Inadequate oxygen delivery typically results from poor tissue perfusion but occasionally, may also be caused by an increase in metabolic demand.2 In the setting of persistent inadequate oxygen delivery, cells are unable to produce adenosine triphosphate (ATP) to power vital functions. Cells transition to anaerobic metabolism to continue production of ATP, generating lactic acid, which accumulates in the cell and is transported into the blood. The accumulation of lactic acid in the cell is compounded by an increase in production of its precursor, pyruvate, via the stress response.3 Increased production of lactate accounts for most elevation in blood levels, but a reduction in lactate metabolism also occurs.4,5 Systemically, the stress response is intended to release energy stores and augment perfusion to vital organs. Receptors in large arteries detect a decrease in wall tension, activating a hormonal response via the hypothalamus-pituitary-adrenal axis and a neurogenic response through sympathetic stimulation. The resultant increase in circulating levels of epinephrine, norepinephrine, corticosteroids, renin, and glucagon

The author has no financial interests to disclose. a Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, 701 Welch Road, Building C, Palo Alto, CA 94304, USA b Emergency Department, Stanford University Hospital and Clinics, Stanford, 701 Welch Road, Building C, Palo Alto, CA 94304, USA * Department of Surgery, Division of Emergency Medicine, Stanford University School of Medicine, 701 Welch Road, Building C, Palo Alto, CA 94304. E-mail address: [email protected] Emerg Med Clin N Am 28 (2010) 57–66 doi:10.1016/j.emc.2009.09.006 0733-8627/09/$ – see front matter ª 2010 Elsevier Inc. All rights reserved.

Matthew Strehlow MD

Kaiser 2012

emed.theclinics.com

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Strehlow

elevates the heart rate and produces vasoconstriction of peripheral arteries. As a whole, cardiac output is augmented, blood pressure elevated, and increased glucose and fatty acids are available to cells as energy precursors. Counteracting these effects is the build-up of toxic metabolites and inflammatory mediators. Endogenous toxic metabolites derived from damaged cells and exogenous toxins can cause cellular dysfunction, myocardial depression, and vasodilation. Inflammatory mediators are released from the up-regulated immune system, leading to further organ dysfunction and microischemia. The corresponding acidemia potentiates cellular and organ dysfunction. If the imbalance between oxygen delivery and demand persists, compensatory mechanisms fail, blood pressure and cardiac output decrease, and multiple organ dysfunction syndrome (MODS) develops. Once MODS develops, mortality is high and it is challenging to reverse the cycle of cellular death and dysfunction. Despite the high prevalence and morbidity of shock, the lack of a widely accepted definition and clear diagnostic criteria have limited the development of robust epidemiologic data. Estimates suggest that more than 1.2 million emergency department (ED) visits annually are for patients in shock.6,7 Mortality for patients in shock varies depending on the cause, but common causes of shock including sepsis, trauma, and cardiac failure have mortality ranging from 20% to 50%.8–10 ED patients with persistent hypotension incur the highest rate of death, but mortality is also substantial in those with cryptic shock, or shock without overt hypotension. In patients with presumed septic shock without hypotension, for example, mortality ranges from 18% to 27%.11,12 EARLY DETECTION OF SHOCK

Early recognition and, correspondingly, early intervention before the onset of multiple organ dysfunction have been demonstrated to decrease morbidity and mortality in critically ill patients. The ‘‘golden hour’’ of trauma care has been a tenant for emergency practitioners for decades and more recently the ‘‘golden hour’’ for medical patients is being hailed as imperative to improving outcomes.13 Goal-directed therapy, attempted for years in the intensive care unit (ICU) with variable results, when implemented within the first 6 hours of presentation to the ED improved absolute mortality by 16% in the original study by Rivers.14 Evidence has continued to accumulate and more recently a meta-analysis reported that an early, quantitative resuscitation strategy in patients with severe sepsis and septic shock significantly reduced mortality. In contrast, the same investigators concluded that equivalent strategies initiated later in the patient’s course were not effective.15 Although most recent research has focused on septic shock, studies of alternate causes of shock have also shown that early intervention is a critical factor in determining outcomes. Sebat and colleagues16 described a 5-year process of implementing an early recognition and rapid-response strategy for patients with all forms of shock. Mortality was reduced by a factor of 3 (40%–12%). Although results of this magnitude are difficult to replicate, they suggest that reducing time to recognition is a critical aspect of caring for patients in shock. In contrast to the mortality reductions seen with strategies that target early recognition and intervention, care decisions in later stages of shock, such as choice of vasopressor, administration of steroids, and implementation of tight glycemic control, have proven to have minimal if any effects.17–21 HISTORY AND PHYSICAL EXAMINATION

Emergency providers are frequently presented with the undifferentiated patient and must be intimately familiar with the elements of history, physical examination, and Matthew Strehlow MD

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Early Identification of Shock

diagnostic testing that may suggest early shock, before the onset of significant organ dysfunction (Box 1). Vital-sign abnormalities have long been the cornerstone of shock recognition. Traditionally, a patient was deemed to be in shock when tachycardic, tachypneic, and possessing a systolic blood pressure (SBP) less than 90 mm Hg. Current evidence suggests that traditional vital signs are insensitive markers of early hypoperfusion. Advanced trauma life support (ATLS) teaches that decreased blood pressure is a marker of hemorrhage that is already moderate to severe. Despite this, a SBP of less than 90 mm Hg is still used as a screening criterion for the activation of trauma patients. Recent evidence supports ATLS teaching that a SBP less than 90 mm Hg is a late and insensitive finding of hemorrhage and shock.22–27 Parks and colleagues26 performed a retrospective evaluation of the National Trauma Database. They evaluated a cohort of trauma patients with a median initial SBP of 90 mm Hg; mortality in these patients was 65% and the base deficit 20. Lipsky and colleagues28 determined that patients who were hypotensive (2 seconds) Pale or cool skin Narrowed pulse pressure Oliguria Lactic acidosis Elevated base deficit Late signs Decreased mental status Weak or absent central pulses Central cyanosis Hypotension Bradycardia a

Early signs of shock are frequently seen in later stages and late signs such as altered mental status may present early depending on the cause and the patient.

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Strehlow

In nontrauma patients systemic hypotension is likewise a late finding of critical illness and mortality ranges from 20% to 60% for common causes of hypotensive shock.29,30 A single episode of hypotension (