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TABLE11.1 DEFINITIONS

Systemic inﬂammatory response syndrome(SIRS)

Sepsis • SIRS criteria in response to known or suspected

Severe sepsis • Sepsis with organ dysfunction, hypoperfusion, or

Septic shock • Sepsis with hypotension despite appropriate

Denitions

• Two or more of the following:

• Temperature >38°C or<36°C

• Heart rate >90 beats perminute

• Respirator y rate >20 breaths per minute or

PaCO2 <32mmHg

• White blood cell count >12,000/ cu mm, <4000/

cu mm, or >10% immature (band) forms

infection

hypotension.

uid resuscitation and perfusion abnormalities.

gram- positive bacteria in the last decade in the United States.46 Statistics from the year 2000 showed grampositive bacteria were the cause of 52.1% of sepsis cases, gram- negative bacteria accounted for 37.6%, polymicrobial infections for 4.7%, fungi for 4.7%, and anaerobes for 1%.46 Globally, however, gram- negative organisms continue to be predominant. A prevalence study of ICU infections conducted in 2007 involved 1,265 ICUs across 75 countries found that of patients considered to be infected, 70% had positive blood cultures— 62% with gram- negative organisms, 47% with gram- positive organisms, and 19% with fungi.49 Opportunistic fungal infections are emerging as the most rapidly growing cohort due to a rise in the number of immunocompromised patients, with Candida species being the most common opportunistic mycotic species worldwide.50 Candida infections

also carry a crude mortality rate ranging from 46% to 75% as inclusion criteria for major clinical trials on sepsis47 (see Table 11.1). Asecond consensus group revisited these denitions in 2001, but ultimately no changes were made.48 ey dened the systemic inammatory response syndrome (SIRS) as a constellation of symptoms seen in many disease processes and when SIRS is found in conjunction with a conrmed or suspected infection, it is termed sepsis (Figure11.1).

in part due to a delay in treatment and inadequacy of the

selected therapeutic regimens.

e source of infection in a majority of sepsis cases is respiratory in origin (33%– 64%), followed by genitourinary (14%– 32%), gastrointestinal (20%– 23%), bone or joint (7%), and so tissue (5%).

49,51

In studies of severe sepsis in children within the United States, main etiologies of infection were identied to be respiratory infections or primary bacteremia with staphylococcal organisms as the most

CAUSES

Sepsis can be caused by any pathogen, including bacterial, fungal, and viral sources. e microbial causes of sepsis haveevolved epidemiologically over time with rates of gram- negative bacteria as the historically predominant causative organism declining and surpassed by

common causative agent, followed by fungal infections. ere are also seasonal and regional variations in incidence, causes, and mortality of sepsis.54 Danai etal. showed that the most pronounced seasonal variations occurred with respiratory sepsis, which paralleled the incidence of viral pneumonia, with the greatest increase in rate and fatality occurring between summer and winter.

52,53

Temp < 36

°C or > 38 °C

Heart rate >

RR > 20 or

< 32

PaCO

WBC < 4k

or > 12k

86 PART III.SHOCK

SIRS and

infection

Sepsis with organ dysfunction, hypoperfusion,

or hypotension

Figure11.1 Systemic inammatory response

syndrome (SIRS), sepsis, and severe sepsis.

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PRESENTATION

Early identication and recognition of sepsis and septic shock is crucial in the implementation of goal- directed therapy and improved patient outcomes. Due to the multiple etiologies of sepsis, clinical presentations can be variable and depend on the source of infection and pathogen involved. Based on the criteria put forth by the North American and European Consensus Committee in 2001, diagnosis of sepsis can be made by clinical parameters and laboratory values indicating infection and organ dysfunction (see Box 11.1).

A hallmark of septic shock is the systemic immune response triggered by the invading pathogen, which causes a cascade of hormonal, proinammatory, and

BOX 11.1 CLINICAL DIAGNOSTIC CRITERIA FORSEPSIS

Infection (documented or suspected) and some of the

following:

General variables

• Fever (core temperature > 38.3°C)

• Hypothermia (core temperature <36°C)

Organ dysfunction variables

• Arterial hypoxemia (PaO

• Acute oliguria (urine output < 0.5 mL/ kg/ hr or 45mmol/L

for at least 2 hours)

• Creatinine increase > 0.5mg/ dL

• Coagulation abnormalities (INR > 1.5 or aPTT > 60 sec)

• Ileus (absent bowel sounds)

• Thrombocytopenia (platelet count < 100,000/ mcL)

• Hyperbilirubinemia (plasma total bilirubin < 4 mg/ dL

[70mmol/ L])

Tissue perfusion variables

• Hyperlactatemia (> mmol/ L)

• Decreased capillary rell or mottling

WBC, white blood cell; SBP, systolic blood pressure; MAP, mean arterial blood pressure; SvO2, mixed venous oxygen saturation; INR, international normalized ratio; aPTT, activated partial thromboplastintime

(Levy MM, et al. 2001 SCCM/ ESICM/ ACCP/ ATS/ SIS International Sepsis Denitions Conference. Crit Care Med. 2003. 31(4):1250– 6. With kind permission from Springer Science and Business Media.)

/ FiO2<300)

• Heart rate > 90/ min or 2 SD above the normal value

forage

• Tachypnea

• Altered mentalstatus

• Signicant edema or positive uid balance (> 20 mL/ kg

over 24hours)

• Hyperglycemia (glucose > 120 mg/ dL [> 7.7mmol/ L]) in

the absence of diabetes

Inammatory variables

• Leukocytosis (WBC count > 12,000/mcL)

• Leukopenia (WBC count < 4000/mcL)

• Normal WBC count with > 10% immatureforms

• Plasma C- reactive protein > 2 SD above the normalvalue

• Plasma procalcitonin > 2 SD above the normalvalue

Hemodynamic variables

• Arterial hypotension (SBP < 90 mm Hg, MAP < 70, or an

SBP decrease >40 mm Hg in adults)

• SvO

>70%

• Cardiac index > 3.5 L/ min/ m

anti- inammatory mediators that ultimately leads to alterations in cellular metabolism, tissue hypoperfusion, and organ dysfunction distant from the initial site of infection.

Tumor necrosis factor α (TNF- α), interleukin 6 (IL-6), and IL- 1 are proinammatory cytokines that have been implicated in the SIRS response and pathogenesis of multiorgan failure in septic shock.

55,56

Systemic infusions of TNF- α and IL- 1 have been shown to reproduce symp- toms of SIRS and septic shock in both human and animal models. Furthermore, high or persistently elevated serum levels of TNF- α, IL- 6, and IL- 1 were associated with sep- tic shock, the development of multiorgan failure, higher severity of acute respiratory distress syndrome (ARDS), and higher mortality rates.

57– 62

Studies also suggest that TGF- β inhibits the inducible form of nitric oxide synthase (iNOS), producing relatively high levels of nitric oxide (NO) during acute infection, which is postulated to be a mechanism of vasodilation and refractory hypotension in septic shock.

MECHANISM OFVASOPLEGIA

63– 65

e innate immune response to bacterial cell wall components, particularly endotoxin, has been used as the basis of

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many animal models of gram- negative sepsis. Presence of endotoxin has been correlated with the severity of septic shock, multiple organ failure, cardiac depression and mor-

66,67

tality. TNF- α, IFN- γ) induce iNOS, resulting in the overproduc-

Endotoxin and inammatory cytokines (IL- 1β,

tion of NO in multiple cell types including endothelial, vascular smooth muscle, and hepatocytes. is is a central mechanism to the vascular hyporesponsiveness, vascular injury, and multiorgan dysfunction observed in septic

68– 70

shock.

Under normal circumstances endogenous vasoconstrictors such as angiotensin II and norepinephrine bind to receptors on vascular smooth muscle cells (VSMCs) and cause the release of intracellular calcium and inux through voltage- gated channels, resulting in depolarization of the VSMC membrane, activation of the actin- myosin complex, and vasoconstriction.

71,72

Membrane hyperpolariza-

tion through activation of ATP- sensitive potassium (K

ese include alterations in coagulation, microcirculation, and cellular bioenergetics that ultimately lead to tissue dysoxia and oxygendebt.

Renal Manifestations ofSepsis

More than 50% of patients with septic shock also have acute renal failure, which carries an increased mortality rate of 70% compared with 45% in patients with acute renal failure alone.79 Systemic arterial vasodilation in sepsis and septic shock causes activation of the renin- angiotensinaldosterone system (RAA) and local down- regulation of iNOS that results in renal vasoconstriction and renal hypoperfusion.79 ere is also direct tissue injury from inammatory cytokines, reactive oxygen species, inltration of tissue by neutrophils and macrophages, and compromise of the microvasculature due to microthrombi.

)

insults lead to renal ischemia and acute tubular injury.

AT P

79,80

ese

channels causes inhibition of voltage- gated calcium channels and vasodilation unresponsive to vasoconstrictors.71 During septic shock, various mediators including lactate, nitric oxide, and decreased ATP concentrations activate these potassium channels causing hyperpolarization of the membrane and vasoplegia.

71,73

Another mechanism of vascular hyporesponsiveness in septic shock is the depletion of circulating vasopressin. Refractory hypotension during circulatory shock, including septic shock, activates the arterial baroreex (see previous section), which leads to increased secretion of vasopressin, norepinephrine, and angiotensin II through autonomic regulation.74 Landry et al. demonstrated that patients with septic shock have markedly lower levels of plasma vasopressin compared to patients with cardiogenic shock despite ongoing hypotension due to a impaired baroreex- mediated secretion,75 and exogenous low dose infusions of vasopressin had norepinephrine sparing eects in severe septic shock.

76,77

Alarge, multicenter randomized controlled trial comparing the mortality benet of vasopressin infusions to norepinephrine infusions in patients with septic shock found no signicant dierence in 90- day mortality, however the mortality in patients with less severe shock was improved with the use of vasopressin.

Splanchnic Circulation and Liver Perfusion

Rates of liver failure and liver dysfunction in severe sepsis range from 35% to 46% and 3% to 6%, respectively.

81,82

Aside from the liver’s metabolic role, it is actively involved in the body’s innate immune response against pathogens. Asignicant component of the liver is myeloid and lymphoid tissue housing the body’s largest reservoir of tissueresident macrophages known as Kuper cells (KCs).83 e KCs are involved in the clearance and scavenging of endotoxin and bacteria from the portal circulation and are responsible for a large part of the host response to infection. In the setting of sepsis- induced liver dysfunction, there are alterations in metabolic function promoting gluconeogenesis and glycogenolysis, transient increases in transaminase activity, and increased bilirubin levels due to intrahepatic cholestasis.

84,85

Pulmonary Manifestations ofSepsis

Sepsis is one of the most common etiologies of indirect acute lung injury (ALI) and ARDS, with incidences as high as 40%.86 Based on the American- European consensus conference on ARDS, ALI is distinguished from ARDS

CLINICAL SEQUELAE:MALDISTRIBUTION OFBLOODFLOW

Mechanisms of multiorgan failure in septic shock are complex and multifactorial, arising from eects of the inammatory cascade extending beyond the initial site of infection.

based on PaO2/ FiO2 ratio ≤ 300 compared to PaO2/ FiO2 ratio ≤ 200, respectively, but both have diagnostic criteria that include acute onset, radiographic evidence of bilateral inltrates, and pulmonary capillary wedge pressure of ≤18 mmHg.87 More recently the Berlin criteria further straties severity of ARDS based on degree of

88 PART III.SHOCK

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hypoxemia, which was found to be predictive of mortality:mild (200mmHg < PaO2/ FIO2 ≤ 300mm Hg), moderate (100mmHg < PaO2/ FIO2 ≤ 200mmHg), and severe (PaO2/ FIO2 ≤ 100mmHg).88 Mortality rates for ARDS have decreased over the last two decades and range between 30% and 60%, with most deaths caused by sepsis rather than respiratory failure.

89– 91

e pathogenesis of ALI is attributed to loss of the alveolar- capillary barrier integrity due to endothelial and epithelial injury. Increased permeability causes an inux of protein- rich uid and inammatory cells into airspaces disrupting the normal alveolar infrastructure and promoting the formation of hyaline membranes and brin deposition.92 Inammatory cytokines including TNF- α, IL- 1, IL- 6, and IL- 8 are found in the serum and bronchoalveolar lavage (BAL) uid of ARDS patients and are thought to be involved in the up- regulation of adhesion molecules promoting inux of erythrocytes and inammatory cells into the alveolar space across the disrupted epithelial- endothelial barrier.

93– 95

Neutrophils are considered to be the dominant leukocytic component of BAL uid in ARDS patients and are implicated in the produc-

shock, with high CO, warm skin, tachycardia, and hypotension, and (2)“cold” shock, with low CO, cold skin, thready pulse, and hypotension. to undervolume resuscitated septic shock.

106

Cold shock was later attributed

107

Patients with sepsis- induced cardiac dysfunction have a higher rate of mortality compared with those without, 70% versus 20%, respectively.

108

Parker et al. characterized hemodynamic variables among survivors and nonsurvivors of septic shock and found that initial mean cardiac indices and heart rate were elevated and systemic vascular resistance indices were reduced in both groups; however, survival was better if the heart rate was less than 95 beats per minute, and the SVRI was greater than 1529 dyne/ sec/ cm5 × M2.withing 24hours of initiating treatment.

107

Parker et al. also described initially depressed le ventricular ejection fraction and le ventricular dilation in survivors of septic shock that normalizes within 1 to 2 weeks.

109

Similar reversible changes were also seen in the right ventricle function of septic shock survivors.

110

Myocardial depression by cytokines such as TNF- α, IL- 1 and IL- 6, and nitric oxide is considered to be the main contributor to myocardial dysfunction insepsis

tion of elastases, collagenase, and matrix metalloproteinases contributing to alveolar injury.

92,96

Sepsis and Coagulation

Cerebral Manifestations ofSepsis

Altered cognition is a common manifestation of sepsis and has been seen in up to 70% of bacteremic patients, with accompanying electroencephalographic (EEG) changes in more than 80% of those patients.

97,98

e presentation of sepsis- associated encephalopathy (SAE) can be variable and can range from mild confusion and delirium to coma. Several mechanisms have been described to contribute to the presentation of SAE, including altered cerebral microcirculation due to decreased density of perfused microvas-

Derangements of coagulation are very common in sepsis and septic shock, with the most extreme manifestation being disseminated intravascular coagulation (DIC).

111

Tissue factor (TF) plays a central role in initiating the extrinsic coagulation pathway, resulting in brin deposition in tissue microvasculature that contributes to multiorgan dysfunction in sepsis. Plasma levels of TF and TF expression are up- regulated in sepsis.

112– 116

Impairment of anticoagulant pathways in sepsis is attributed to altered expression of protein C, protein S, thrombomodulin, antithrombin, and TF pathway inhibitor.

117– 119

culature, dysfunction of cerebral autoregulation, loss of the blood- brain barrier integrity, and inammatory mediators that disrupt neurotransmission and cause neuronal apopto-

99– 103

sis.

ere are no specic treatments for SAE, and most therapies are targeted toward appropriate treatment of sepsis and supportive care. ough SAE may be reversible in some cases, critical illness and severe sepsis in particular have been associated with long- term cognitive impairment and disability that can persist for years.

104,105

BIOMARKERS OFSEPSIS

e two main markers used clinically in sepsis are arterial lactate concentration and procalcitonin. e importance of measuring arterial lactate concentration in sepsis is discussed in the section “Evaluation of Perfusion.” Procalcitonin is a 116– amino acid peptide involved in calcium homeostasis and has been explored as a serum marker that is able to dierentiate sepsis from other noninfectious causes of

Cardiac Manifestations ofSepsis

Early observations of sepsis- induced cardiac dysfunction were characterized by two distinct presentations:(1)“warm”

SIRS. Studies have correlated high plasma procalcitonin concentrations in patients with sepsis.

120,121

To date, metaanalyses have shown conicting results regarding the diagnostic utility of procalcitonin due to heterogeneity of study

DISTRIBUTIVESHOCK 89

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populations and study selection criteria. meta- analysis by Wacker etal. analyzed data from 30 studies that included 3,244 patients and showed procalcito-

122– 124

A recent

BOX 11.2 INITIAL RESUSCITATION

A. Initial Resuscitation

nin to have a mean sensitivity of 0.77 (95% CI 0.72- 0.81) and specicity of 0.79 (95% CI 0.74- 0.84) in identifying patients with sepsis.

124

Currently recommendations do not include procalcitonin in diagnostic criteria for sepsis, though it may be a helpful marker in conjunction with other serum markers.

TREATMENT

e treatment of sepsis is outlined in the Surviving Sepsis Campaign (SCC) International Guidelines for Management of Severe Sepsis and Septic Shock. It centers

1. Protocolized, quantitative resuscitation of patients with

sepsis- induced tissue hypoperfusion (dened in this

document as hypotension persisting after initial uid

challenge or blood lactate concentration ≥ 4mmol/ L).

Goals during the rst 6 hours of resuscitation:

a) Central venous pressure 8– 12mmHg

b) Mean arterial pressure (MAP) ≥ 65mmHg

c) Urine output ≥ 0.5 mL/ kg/ hr

d) Central venous (superior vena cava) or mixed venous

oxygen saturation 70% or 65%, respectively (grade1C).

on early diagnosis and implementation of uid resuscitation, antibiotic therapy, and hemodynamic support in a protocolized manner.

125

Institutional participation in sepsis

2. In patients with elevated lactate levels targeting

resuscitation to normalize lactate (grade2C).

care bundles is associated with improved survival and more timely and appropriate antibiotic administration, though it cannot be determined whether this is due to an increased awareness of sepsis or due to specic recommendations within the bundle.

126,127

Early administration of antimicrobials within the rst hour of documented hypotension in septic patients improves survival, and every hour of delay is associated with an increase in mortality.

128

e SCC recommends initial resuscitation endpoints be modeled aer the protocol that Rivers etal. used as intervention in their study of early goal- directed therapy, which was associated with a mortality benet in patients presenting to the emergency department with septic shock. tions for initial resuscitation and hemodynamic support are

129

e recommenda-

outlined in Boxes 11.2 and11.3.

ere are caveats to these guidelines, as some of these recommendations are controversial and in contrast to wellestablished evidence. Current guidelines recommend an aggressive uid challenge of at least 30 mL/ kg of crystalloid to aim for the following targets:a CVP of 8– 12mmHg, a mean arterial pressure (MAP) ≥ 65 mmHg, urine output ≥ 0.5 mL/ kg/ hr, mixed venous oxygen saturation (MVO2) of 65% or superior vena cava oxygen saturation (ScVO2) of 70% and normalization of serum lactate. a guideline for adequate uid resuscitation is problematic,

125

Use of CVP as

as it correlates poorly with patient volume status (see section “Evaluation of Perfusion”). Additionally, ScVO2 is a controversial indicator of tissue perfusion, ScVO2 does not necessarily correlate with MVO2 and cardiac output, and in shock ScVO2 can be consistently higher than MVO2.

130,131

Overresuscitation is also problematic, and careful attention to uid overload is required, as higher positive uid balance

and CVPs were associated with increased mortality rates in patients with septic shock, ALI, and renal failure.

18,132,133

Despite the limitations, there are currently no good alternatives to the SCC guidelines. Studies in the last 15–20years of direct pharmacological interventions that aim to treat sepsis have been disappointing (steroids, activated protein C, TNF- α, dichloracetate) and their routine use is discouraged. Newer adjunctive therapies that are not part of the SCC guidelines may warrant further extensive investigation and include the following.

Beta Blockade

Beta blockade is thought to exert various eects on immunologic, metabolic, and cardiac alterations in septic shock, though evidence of mortality benet from prospective trials is lacking. A retrospective study by Macchia et al. showed a lower 28- day mortality rate in septic patients previously on chronic beta- blocker therapy, 17.7%, compared with those untreated, 22.1%.

134

Further randomized studies

are required before its routine use is to be recommended.

MethyleneBlue

Methylene blue is a chemical dye that inhibits iNOS and the eector enzyme of NO, guanylate cyclase, both important mediators of refractory vasodilation in sepsis. Small, randomized prospective clinical trials of methylene blue infusions in patients with septic shock demonstrated improved mean arterial blood pressure and reduced vasopressor

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BOX 11.3 HEMODYNAMIC SUPPORT

G. Fluid Therapy ofSevereSepsis

1. Crystalloids as the initial uid of choice in the resuscitation of severe sepsis and septic shock (grade1B).

2. Against the use of hydroxyethyl starches for uid resuscitation of severe sepsis and septic shock (grade1B).

3. Albumin in the uid resuscitation of severe sepsis and septic shock when patients require substantial amounts of

crystalloids (grade2C).

4. Initial uid challenge in patients with sepsis- induced tissue hypoperfusion with suspicion of hypovolemia to achieve a

minimum of 30 mL/ kg of crystalloids (a portion of this may be albumin equivalent). More rapid administration and greater

amounts of uid may be needed in some patients (grade1C).

5. Fluid challenge technique be applied wherein uid administration is continued as long as there is hemodynamic improvement

either based on dynamic (e.g., change in pulse pressure, stroke volume variation) or static (e.g., arterial pressure, heart rate)

variables(UG).

H. Vasopressors

1. Vasopressor therapy initially to target a mean arterial pressure (MAP) of 65mmHg (grade1C).

2. Norepinephrine as the rst- choice vasopressor (grade1B).

3. Epinephrine (added to and potentially substituted for norepinephrine) when an additional agent is needed to maintain

adequate blood pressure (grade2B).

4. Vasopressin 0.03 units/ minute can be added to norepinephrine with intent of either raising MAP or decreasing

norepinephrine dosage(UG).

5. Low- dose vasopressin is not recommended as the single initial vasopressor for treatment of sepsis- induced hypotension, and

vasopressin doses higher than 0.03– 0.04 units/ minute should be reserved for salvage therapy (failure to achieve adequate

MAP with other vasopressor agents)(UG).

6. Dopamine as an alternative vasopressor agent to norepinephrine only in highly selected patients (e.g., patients with low risk

of tachyarrhythmias and absolute or relative bradycardia) (grade2C).

7. Phenylephrine is not recommended in the treatment of septic shock except in circumstances where (a)norepinephrine is

associated with serious arrhythmias, (b)cardiac output is known to be high and blood pressure persistently low, or (c)as

salvage therapy when combined inotrope/ vasopressor drugs and low- dose vasopressin have failed to achieve MAP target

(grade1C).

8. Low- dose dopamine should not be used for renal protection (grade1A).

9. All patients requiring vasopressors have an arterial catheter placed as soon as practical if resources are available(UG).

I. Inotropic Therapy

1. Atrial of dobutamine infusion up to 20 micrograms/ kg/ min may be administered or added to vasopressor (if in use) in

the presence of (a)myocardial dysfunction as suggested by elevated cardiac lling pressures and low cardiac output, or

(b)ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and adequate MAP (grade1C).

2. Not using a strategy to increase cardiac index to predetermined supranormal levels (grade1B).

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requirements compared with controls, however without clear mortality benets.

135,136,137

resistant to catecholamines. It has been suggested that vasopressin

145,146

and methylene blue

147

may be eective in treat-

ing this hypotension. However there are no randomized

Nitroglycerin

While it may be counterintuitive to use vasodilator therapy in the setting of septic shock, nitroglycerin may be able to reverse microvascular dysfunction and ultimately restore tissue oxygenation in target organs. Studies surrounding nitroglycerin administration have been conicting, with initial data reporting improved sublingual microvascular blood ow in septic shock patients aer volume resuscitation and subsequent data showing no dierence.

138,139

trials and this evidence remains anecdotal.

Discontinuation of angiotensin system antagonists prior to cardiac surgery has been associated with an increased risk of perioperative ischemic events,

148

and these drugs should

therefore be continued prior to cardiac surgery.

ere has been concern about an increased incidence of hypertension if RAA system antagonists are discontinued before surgery. is concern may be unfounded, as a recent randomized trial demonstrated

149

: 526 patients undergoing same- day and ambulatory surgery were randomized to either withholding or continuing ARB/ ACE- I prior to sur-

SUMMARY

Sepsis and septic shock cause severe alterations in the function of every organ system and are associated with high mortality. Current therapy focuses on early, rapid resusci-

gery. e authors found no dierence in the incidence of perioperative hypertension dened as Stage 1 hypertension (systolic blood pressure [SBP] ≥140 mmHg or diastolic blood pressure [DBP] ≥90mmHg) or Stage 2 hypertension (SBP ≥ 160 or DBP ≥ 100mmHg).

tation using protocolized bundles. Most direct intervention have failed to demonstrate a benet. Nonconventional therapies such as beta blockade or nitroglycerin may warrant further evaluation.

ANTIHYPERTENSIVE- RELATED VASOPLEGIA

Preoperative continued use of the renin- angiotensinaldosterone (RAA) system antagonists such as angiotensinconverting enzyme inhibitors (ACE- I) or angiotensin II receptor blockers (ARB) has been associated with intraoperative hypotension. Multiple studies, a meta- analysis,

143

have found that preoperative continu-

140– 142

including

DISTRIBUTIVE SHOCK INLIVER FAILURE

Liver failure and hepatic cirrhosis is associated with a vasodilatory and maldistributive shock similar to that which has been observed in septic shock. Hepatic cirrhosis is associated the elevated levels of endotoxin fragments, IL- 10,

151

inammatory markers, cytokines such as IL-6,

152

and TNF.

153,154

e level of inammatory markers

150

as well as bacterial

and of bacterial DNA fragments directly correlates with the severity of liver disease and with outcome.

151,152

e resultant inammatory state has signicant consequences, as described in this section.

ation of RAA system antagonists will result in increased incidence of intraoperative hypotension. e underlying mechanism for this hypotension may be the inability of endogenous vasoconstrictor systems to counteract the vasodilatory eects of anesthetics if renin- angiotensin system antagonists are present. Alarge retrospective study found that particularly patients undergoing noncardiac surgery who chronically used antagonists of the renin- angiotensinaldosterone system and diuretics prior to surgery were at increased risk of hypotension (MAP < 70mmHg, periods with a 40% decrease in systolic blood pressure, periods with a 50% decrease in systolic blood pressure, and vasopressor boluses) compared with patients on diuretic therapy only.

144

ere was, however, no dierence in rates of renal failure or postoperative myocardial infarction between the groups.

Hypotension caused by antagonists of the renin-

angiotensin- aldosterone system can be severe and is oen

SPLANCHNIC VASODILATION

Vasoplegia and specically splanchnic vasodilation occurs resulting in a vasoplegic and maldistributive state. e degree of vasodilatory state correlates with the severity of liver failure (Figure 11.2). Portal hypertension seen in cirrhosis is the result of not only increased intrahepatic resistance to portal blood ow but also splanchnic vasodilation and pooling of blood in the splanchnic circulation. Activation of the sympathetic and renin- angiotensin- aldosterone system will result in a compensatory peripheral vasoconstriction and cardiac hyperdynamic state similar to septic shock. e resultant renal arterial vasoconstriction will cause a decrease in glomerular ltration rate (GRF) with retention of uid and possibly hepatorenal syndrome (HRS).

155

HRS is considered a reversible decrease in GRF that leads to

e

92 PART III.SHOCK

MELD

1250

SVRI

Correlation of SVRI and preOP MELD

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45 40 35 30 25 20

15 10

5 0

0250 500750 1000

Figure11.2 Correlation between Systemic Vascular Resistance Index

(SVRI) and Model of Endstage Liver Disease (MELD) score in patients with cirrhosis. SOURCE:Reprinted from Wagener G., etal. Vasopressin deciency

and vasodilatory state in end- stage liver disease. J Cardiothorac Vasc Anesth,

2011;25(4):665–70, with permission from Elsevier.

uid and sodium retention. Hepatorenal syndrome type 2 is dened as a slowly progressive deterioration of renal function (increase of serum creatinine to more than 1.5 mg/ dL) despite diuretic withdrawal and uid administration in the absence of nephrotoxic insults. Usually, HRS type 2 is seen as a natural progression of hepatic cirrhosis and ascites and may be amenable to treatment with vasopressin or vasopressin analogues. Hepatorenal syndrome type 1 is dened as a rapidly progressive deterioration of renal function (doubling of serum creatinine within 2 weeks) usually in conjunction with acute on chronic liver failure. ere is oen a precipitating event such as surgery or infection that leads to a rapid collapse of renal and hepatic function. e average survival of patients with HRS type 1 is months compared with 6months in patients with HRS type2.

Hepatic cirrhosis, as for septic shock,

with low endogenous vasopressin levels.

156

is associated

156

Low endogenous vasopressin levels are likely due to depletion of pituitary vasopressin stores and may cause further deterioration of vasomotor tone. Cirrhotic patients with low endogenous vasopressin levels were exquisitely sensitive and responded with an increase of blood pressure when receiving low dose exogenous vasopressin. Exogenous vasopressin administration results in decreases of portal venous pressure and ow, a consequence of splanchnic vasoconstriction, which is considered benecial in cirrhosis. Vasopressin and vasopressin analogues such as ornipressin or terlipressin have been used to treat hepatorenal syndrome in conjunction with albumin administration and diuretic withdrawal.

158,159

REPERFUSION SYNDROME

Distributive shock that is commonly experienced aer cardiopulmonary bypass or liver reperfusion.

POSTCARDIOTOMY VASOPLEGIA

Postreperfusion syndrome during cardiac surgery is dened as profound loss of vascular tone and hypotension aer separation from cardiopulmonary bypass. It has been reported to occur in up to 22% of all cardiac surgeries.

160,161

of this profound vasoplegia is thought to be an inammatory reaction caused by exposure to foreign surfaces, heparin anticoagulation and surgical trauma among others. As a result, cytokines levels are increased.

162

is will cause hyperpolarization of the endovascular membrane through the activation of inducible NO synthase and ATP- dependent potassium channels.

163

Multiple studies found that preoperative use of reninangiotensin- aldosterone system antagonists some studies beta blockers

161

) increases the risk. However this

160,161,164

does not necessarily translate into poor outcomes, and interestingly, studies have suggested that the preoperative use of ACEIs reduces the risk of acute kidney injury ischemia.

166

Other risk factors for cardioplegia aer cardiopul-

165

and myocardial

monary bypass include low le ventricular ejection fraction, prolonged cardiopulmonary bypass, and hypothermia.

Similar to other causes of vasoplegia, hypotension aer cardiopulmonary bypass is oen catecholamine resistant and vasopressin or its analogues

167

are eective in reversing the vasodilatory state. One of the rst descriptions of vasopressin use for treatment of vasoplegia was in patients undergoing implantation of ventricular assist devices who developed profound postcardiotomy shock.

168

In this randomized trial, vasopressin increased MAP and decreased norepinephrine dose. e vasoconstrictor eect was more pronounced in patients with low endogenous vasopressin levels, evidence that vasoplegia aer cardiopulmonary bypass is at least in part due to inadequately low endogenous vasopressin levels. ese ndings were conrmed in a larger trial of vasopressin use in patients undergoing general cardiac surgery.

Methylene blue has also been used to treat postcardiotomy shock in addition to catecholamines. Methylene blue inhibits guanylate cyclase and therefore counteracts NO-

157

induced vasodilation. Guanylate cyclase is also directly activated by IL- 1

170

and free radicals,

171

and methylene blue could

oset vasodilation mediated by these inammatory products.

POSTREPERFUSION SYNDROME AFTER LIVER TRANSPLANTATION

Postreperfusion syndrome aer liver transplantation is dened as hypotension following reperfusion of the transplanted liver gra.

172

It is most commonly dened as a decrease of mean arterial blood pressure by more than 30% within 5 minutes aer reperfusion, lasting for at least

e cause

(and in

160,161

169

DISTRIBUTIVESHOCK 93

https://t.me/medicina_free

1minute. a reported incidence of 25% kines such as IL- 6 and TNF as well toxins, acid, and potassium postreperfusion syndrome. e most consistent risk factor is prolonged cold ischemic time. retrospective study of intraoperative cardiac arrest found that more than one- third of all cardiac arrests were due to postreperfusion syndrome. postreperfusion syndrome required more intraoperative blood transfusions and had longer duration of ventilation, length of ICU stay, and length of hospital stay aer transplantation. during the anhepatic phase decreases the risk. domized trial of dierent reperfusion techniques found that portal vein ush without vena caval venting had the lowest incidence of postreperfusion syndrome, however this technique was associated with higher potassium levels. other agents

173,174

Postreperfusion syndrome is common, with

176

from the gra have been implicated as a cause of

179

e use of a temporary portocaval shunt

181

Prophylactic use of phenylephrine,

184

has been suggested to prevent postreperfu-

173

to 50%.

173,177

178

175

Release of cyto-

Alarge, single- center

Patients who experience

173,180

182

atropine,

Aran-

183

and

BOX 11.4 CLINICAL CRITERIA FORDIAGNOSING

ANAPHYLAXIS

Anaphylaxis is highly likely when any one of the following

three criteria are fullled:

1. Acute onset of an illness (minutes to several hours)

with involvement of the skin, mucosal tissue, or both

(e.g., generalized hives, pruritus or ushing, swollen lips-

tongue- uvula) and at least one of the following:

a. Respiratory compromise (e.g., dyspnea, wheeze-

bronchospasm, stridor, reduced PEF, hypoxemia)

b. Reduced BP or associated symptoms of end- organ

dysfunction (e.g., hypotonia [collapse], syncope, incontinence)

2. Two or more of the following that occur rapidly after

exposure to a likely allergen for that patient (minutes to

several hours):

a. Involvement of the skin- mucosal tissue (e.g.,

generalized hives, itch- ush, swollen lips- tongue- uvula)

sion syndrome but have not been tested in well- done trials.

b. Respiratory compromise (e.g., dyspnea, wheeze-

bronchospasm, stridor, reduced PEF, hypoxemia)

ANAPHYLAXIS

Anaphylaxis is an acute immunological reaction that causes release of mediators from mast cells resulting in profound vasodilation. While rare, anaphylactic shock can be fatal in about 1% of cases

185

by causing profound multiorgan failure.In the United States, anaphylaxis causes about 0.5 deathsper million.

186

Most commonly, anaphylaxis is dened as an immunoglobulin E (IgE)– mediated reaction, however nonimmunological responses can cause a massive release of mediators by mast cells and basophils as well. Classically,

c. Reduced BP or associated symptoms (eg., hypotonia

[collapse], syncope, incontinence)

d. Persistent gastrointestinal symptoms (e.g., crampy

abdominal pain, vomiting)

3. Reduced BP after exposure to known allergen for that

patient (minutes to several hours):

a. Infants and children:low systolic BP (age specic) or

greater than 30% decrease in systolicBP*

b. Adults:systolic BP of less than 90mmHg or greater

than 30% decrease from that person’s baseline

anaphylaxis occurs when antigens interact with specic IgE that is bound to mast cells and basophils. Previous exposure to the antigen is necessary to form specic IgE receptors that are bound to either mast cells or basophils. Repeated contact of the antigen with IgE can lead to degranulation of the cells mediated by high- anity IgE receptors (FcεRI, or Fc epsilon RI). A massive release of histamine, proteoglycans,

PEF, peak expiratory ow; BP, blood pressure.

*Low systolic blood pressure for children is dened as less than 70mmHg from 1month to 1year, less than (70mmHg + [2 x age]) from 1 to 10years, and less than 90mmHg from 11 to 17years.

Reprinted from Sampson HA, Muñoz- Furlong A, Campbell RL, etal. Second symposium on the denition and management of anaphylaxis:summary report— second National Institute of Allergy and Infectious Disease/ Food Allergy and Anaphylaxis Network symposium. Ann Emerg Med. 2006;47(4):373– 80. With permission from Elsevier.

serotonin, and serine proteases will lead to the clinical picture of anaphylaxis. Systemic release of histamine will cause profound vasodilation and ushing mediated by H1 receptors and tachycardia, pruritis, and bronchospasm mediated by H2 receptors.

187

On average, anaphylaxis occurs about 5 to 30 minutes aer exposure to the antigen. e diagnosis is clinical and can be based on the criteria dened by the SECOND symposium on the denition and management of anaphylaxis

188

(Box 11.4).

First response should be removal of the suspected allergen, followed by administration of epinephrine either intramuscularly or intravenously (in much lower doses) if intravenous access is immediately available. Epinephrine is the ideal rst- line agent, because the alpha- 1 agonistic action will counteract the vasodilatory state and shock,

94 PART III.SHOCK

https://t.me/medicina_free

beta- 1 agonistic action will augment cardiac output, and beta- 2 agonism will treat bronchoconstriction. Delay in administering epinephrine has been recognized as contributing to the risk of death in anaphylactic shock.

189

patients who chronically take beta- blocking agents, epinephrine may cause hypotension. Glucagon can be given to these patients to maintain vascular tone and cardiac output independent of the sympathetic- adrenergic system.

190

In case of severe respiratory symptoms (stridor or respiratory arrest) the patient should be tracheally intubated without delay, as increasing upper airway edema may impede an easy intubation at a later time. Generous intravenous uid administration will aid in maintaining adequate blood pressure and perfusion.

Antihistamines such as diphenhydramine can be administered, but this should not delay administration of epinephrine. ese may relieve hives and itching but do not treat the life- threatening symptoms of anaphylaxis. Glucocorticoids should be administered as an adjunct to epinephrine, but it will take hours before their onset. ere has been a lack of evidence that glucocorticoids aect outcome in anaphylactic shock, and they should not replace or delay the administration of epinephrine.

192

Concomitant with the treatment, a blood sample should be obtained to determine serum tryptase levels and conrm the diagnosis of anaphylaxis. Tryptase is released from mast cells during anaphylaxis and has a longer plasma half- life (approximately 2 hours

193

) than histamine (approximately

10 minutes).

e prognosis is usually good as long as epinephrine is rapidly administered. Aer recovery, the identity of the triggering agent should be conrmed and patients should be educated on how to avoid the agent and how to selfadminister epinephrine in case of a recurrence.

having had at least one crisis and the frequency is estimated at about 6.3 in 100 patient years.

194

It can also occur in

patients with primary adrenal insuciency even if they

receive glucocorticoid replacement if the mineralocorticoid requirements are not met.

195

Patients present with shock, fever, nausea and vomiting, and acute abdominal pain. Because infection and trauma can be precipitating factors and the symptoms are nonspecic and oen similar to those seen with septic shock, patients with Addisonian crisis are oen misdiagnosed. e delay in diagnosing Addisonian crisis signicantly contributes to the mortality in patients with adrenal insuciency.

Specic ndings on physical exam (for example hyperpigmented skin due to chronic adrenocorticotropic hormone [ACTH] hypersecretion) may hint at the presence of decompensated chronic primary adrenal insuciency. Secondary adrenal insuciency (a rare cause of Addisonian

191

crisis) will however cause pale skin due to low levels of ACTH. Treatment should not be delayed until specic laboratory tests such as serum cortisol levels and ACTH stimulation test are completed, especially if the patient is hemodynamically unstable. If Addisonian crisis is suspected, treatment should consist of 100 mg intravenous hydrocortisone, followed by 400– 500 mg during the rst 24 hours, in addition to supportive therapy (aggressive uid administration, electrolyte and glucose control, and other critical care interventions).

197

In patients without a diagnosis of primary adrenal insuciency 4 mg of intravenous dexamethasone can be given, because it does not interfere with the serum cortisol assay.

198

If diagnosed and treated rapidly, the prognosis of Addisonian crisis is good but also depends on the precipitating trigger. Most studies found that patients with chronic adrenal insuciency can have a normal quality of life and life expectancy, if they

196

receive adequate hormonal replacement. However a recent

ADDISONIANCRISIS

population- based study in Sweden reported a mortality rate more than twice as high in patients with Addison disease as compared with the general population. e excess mor-

Addisonian crisis is a rare but potentially life- threatening acute disease, most oen caused by an acute exacerbation

tality in this study was mostly attributed to cardiovascular disease, malignancies, and infections.

199

of (frequently undiagnosed) primary adrenal insuciency. Other less frequent causes of Addisonian crisis are bilateral adrenal infarction or patients with primary or secondary adrenal insuciency who abruptly withdraw from steroids (Figure 11.3). Commonly, stress, acute infections, or trauma may cause an exacerbation of adrenal insuciency, resulting in complete failure of the glands to produce adrenal mineralocorticoids, glucocorticoids, androgens, and catecholamines. Acute Addisonian crisis is rare, but almost 50% of patients with primary adrenal insuciency report

CASE- BASED LEARNING DISCUSSION

1. What are the clinical signs indicating that this patient

is in shock? How do you assess the severity of shock in this patient?

2. What is your dierential diagnosis for the cause of

shock in this patient? What is most likely predominant

DISTRIBUTIVESHOCK 95

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