Shock Shock

Dr.Tarek T.El-sefi ASS.Lecturer CRITICAL CARE

Definition of Shock
A clinical state in which blood flow is inadequate for tissue requirements or oxygen utilization is impaired. There is either insufficient oxygen delivery, maldistribution of oxygen delivery or impaired utilization

At cellular level..
Shock is a state of acute nutritional
insufficiency of oxygen and other essential substrates, resulting in cellular anoxia, cellular dysfunction and eventually cell death

Physiology of Perfusion
Dependant on 3 components of circulatory system:
*Pump *Fluid *Container

Causes of Inadequate Perfusion

Inadequate pump
Inadequate preload Poor contractility Excessive after load Inadequate heart rate Hypovolemia

Inadequate fluid volume

Inadequate container

Excessive dilation Inadequate systematic vascular resistance

Changes in Afterload and Preload

Peripheral vasoconstriction
peripheral vascular resistance

afterload
blood pressure.

Changes in Afterload and Preload

Peripheral vasodilation

peripheral vascular
resistance

afterload
blood pressure.

Changes in Afterload and Preload

fluid volume
preload

contractility (Starlings Law) blood pressure. cardiac output.

Changes in Afterload and Preload

fluid volume preload contractility
(Starlings Law)

blood pressure.

cardiac output.

Maintenance of Fluid Volume

Renin-Angiotensin-Aldosterone system:
Works through kidneys to regulate balance of Na+ and water.

Renin-Angiotensin-Aldosterone
Plasma volume
Detected by

&/Or [Na+]
Via ACE (Angiotensin Converting Enzyme)

Kidney (juxtaglomerular apparatus)

Releases

Renin
Converts

Angiotensin II Angiotensin I Angiotensinogen

Renin-Angiotensin-Aldosterone
vasoconstriction
Angiotensin II thirst ADH (anti-diuretic hormone) Adrenal cortex
Releases

PVR

Fluid volume

BP!

Aldosterone

Na+ reabsorption

Container
Vasculature is continuous, closed and pressurized system Blood flow dependent on PVR

Responses to Shock
Catecholamine release causes increased:
heart rate heart contractility venous and arteriolar tone preload cardiac output

Neuroendocrine response
Hypothalamic - glucocorticoid, GH & aldosterone Renal : ADH,renin and angiotensin

Responses to Shock
Normal compensation includes:
Progressive vasoconstriction Increased blood flow to major organs Increased cardiac output Increased respiratory rate and volume Decreased urine output

Cellular Response to Shock

O2 use
Anaerobic metabolism ATP synthesis Na+ Pump Function

Tissue perfusion
Stimulation of clotting cascade & inflammatory response Intracellular Na+ & water

Impaired cellular metabolism

Impaired glucose usage

Cellular edema Vascular volume

Aerobic Metabolism
6 CO2

6 O2

METABOLISM
GLUCOSE

6 H2O 36 ATP

HEAT (417 kcal)

Anaerobic Metabolism

2 LACTIC ACID

GLUCOSE

METABOLISM

2 ATP

HEAT (32 kcal)

Anaerobic? So What?
Inadequate Cellular Oxygenation

Inadequate Energy Production

Anaerobic Metabolism

Lactic Acid Production

Metabolic Failure

Cell Death!

Metabolic Acidosis

Cellular Response to Shock

Net results of cellular shock:
systemic lactic acidosis decreased myocardial contractility decreased vascular tone decrease blood pressure, preload and cardiac output

SEQUELEE OF SHOCK I.R.I.

SM., C., SK. MUSCLES *ATROPHY * WEAKNESS GUT * STRESS ULCER * ILEUS *HYPERPERMEABILITY * TRANSLOCATION *MESENTRIC L. N. ABCESS LUNGS * PRIMING OF N. IN GUT *LUNG LEUKOSTASIS

KIDNEY
*TUBULAR EPITHELIUM *SHEDDING *APOPTOSIS * NECROSIS * BACK LEAK * OBSTRUCTION * DECREASE FUNCTION

*EARLY ARDS.(SHOCK
LUNG) LIVER * CHOLESTASIS *ISCHEMIA BRAIN & PANCREASE *ISCHEMIA - INFARCTION

*GUT ISCHEMIA
*TERTIARY PERITONITIS

ATN

*ACALCULAR CHOLACYSTITIS *N. PRIMING & EARLY ARDS

*M.&N. ACTIVATION IN MUSCULAIS EXTERNA &LATE ARDS

Stages of Shock
*Compensated *Decompensated *Irreversible

Compensated Shock
#Defense mechanisms are successful in maintaining perfusion #Presentation
Tachycardia Decreased skin perfusion Altered mental status

Decompenstated Shock
#Defense mechanisms begin to fail #Presentation
Hypotension Prolonged Cap refill Marked increase in heart rate Rapid, thready pulse Agitation, restlessness, confusion

Irreversible Shock
#Complete failure of compensatory mechanisms #Death even in presence of resuscitation

DIAGNOSIS

HISTORY

CLINICAL

LAB.INV.

Shock: Signs and Symptoms

Restlessness, anxiety Decreasing level of consciousness Dull eyes Rapid, shallow respirations
Nausea, vomiting Thirst Diminished urine output

Shock: Signs and Symptoms

Hypovolemia will cause Weak, rapid pulse Pale, cool, clammy skin Cardiogenic shock may cause: Weak, rapid pulse or weak, slow pulse Pale, cool, clammy skin Neurogenic shock will cause: Weak, slow pulse Dry, flushed skin Sepsis and anaphylaxis will cause: Weak, rapid pulse Dry, flushed skin

Classification of Shock
Hypovolemic
(hemorrhage)

Cardiogenic
(myocardial infarction)

Obstructive
(pulmonary embolism)

Distributive
(septic shock)

SVR

CO

PAOP

Shock -- Classification
Four major categories
Hypovolemic Cardiogenic Extracardiac Obstructive Distributive
TYPES OF SHOCK

NB: Overlap exists

Determinants of Blood Pressure

blood pressure

cardiac output

total peripheral resistance

stroke volume

heart rate

preload

contractility

afterload

Determinants of Blood Pressure Distributive shock

blood pressure

cardiac output

total peripheral resistance

stroke volume

heart rate

preload

contractility

afterload

Determinants of Blood Pressure Hypovolemic shock

blood pressure

cardiac output

total peripheral resistance

stroke volume

heart rate

preload

contractility

afterload

Determinants of Blood Pressure Obstructive shock

blood pressure

cardiac output

total peripheral resistance

stroke volume

heart rate

preload

contractility

afterload

Determinants of Blood Pressure Cardiogenic shock

blood pressure

cardiac output

total peripheral resistance

stroke volume

heart rate

preload

contractility

afterload

Determinants of Blood Pressure Hypovolemic shock

blood pressure

cardiac output

total peripheral resistance

stroke volume

heart rate

preload

contractility

afterload

Hypovolemic Shock
#rapid fluid loss results in multiple organ failure due to inadequate perfusion. #Most often, hypovolemic shock is secondary to rapid blood loss (hemorrhagic shock).

Hypovolemic Shock
Causes
Blood loss: trauma, vascular, GIT, pregnancy related Plasma loss: burns Water loss: Vomiting, diarrhea and excessive sweating Third space loss: pancreatitis,ascites

Hypovolemic Shock
*Traumatic causes can result from penetrating and blunt trauma. *Common traumatic injuries that can result in hemorrhagic shock include the following: myocardial laceration and rupture, major vessel laceration, solid abdominal organ injury, pelvic and femoral fractures, and scalp lacerations.

Hypovolemic Shock
Vascular disorders that can result in significant
blood loss include: *Aneurysms *Dissections *Arteriovenous malformations

Hypovolemic Shock
GI disorders that can result in hemorrhagic
shock include the following: *bleeding esophageal varices * bleeding peptic ulcers *Mallory-Weiss tears

Hypovolemic Shock
Pregnancy-related
disorders include: *ruptured ectopic pregnancy. * placenta previa. *abruption of the placenta.
Hypovolemic shock secondary to an ectopic pregnancy is common. Hypovolemic shock secondary to an ectopic pregnancy in a patient with a negative urine pregnancy test is rare but has been reported.

Classification of haemorrhage severity.

Hypovolemic Shock
Lab Studies:

Initial laboratory studies should include analysis of the CBC, electrolyte levels (Na, K, Cl, HCO3, BUN, creatinine, glucose levels), prothrombin time, activated partial thromboplastin time, ABGs, and urinalysis (in patients with trauma). Blood should be typed and cross-matched.

Hypovolemic Shock
The workup for the patient with trauma and signs and symptoms of hypovolemia is directed towards finding the source of blood loss.

Hypovolemic Shock
*If a traumatic abdominal injury is suspected, a FAST (Focused Abdominal Sonography for Trauma) ultrasound exam may be performed in the stable or unstable patient in the ED. Computed Tomography (CT) scanning typically is performed in the stable patient. *If long-bone fractures are suspected, radiographs should be obtained

Hypovolemic Shock
*If GI bleeding is suspected, a nasogastric tube should be placed, and gastric lavage should be performed *Endoscopy can be performed (usually after the patient has been admitted) to further delineate the source of bleeding.

Hypovolemic Shock
*A pregnancy test should be performed in all female patients of childbearing age.

*If the patient is pregnant and in shock, surgical consultation and the consideration of bedside pelvic ultrasonography should be immediately performed in the ED.

Hypovolemic Shock
Mangment: Prehospital Care: The treatment of patients with hypovolemic shock often begins at an accident scene or at home. The prehospital care team should work to prevent further injury, transport the patient to the hospital as rapidly as possible, and initiate appropriate treatment in the field.

Hypovolemic Shock
*Prevention of further injury applies mostly to patients with trauma. *The cervical spine must be immobilized, and the patient must be extricated, if applicable, and moved to a stretcher. * Splinting of fractures can minimize further neurovascular injury and blood loss

Hypovolemic Shock
*Most prehospital interventions involve immobilizing the patient (if trauma is involved), securing an adequate airway, ensuring ventilation, and maximizing circulation(ABC approach) *Some procedures, such as starting intravenous (IV) lines or splinting of extremities, can be performed while a patient is being extricated.

Hypovolemic Shock
Emergency Department Care: (1) Maximize oxygen delivery (2) control further blood loss (3) Fluid resuscitation

Hypovolemic Shock
Maximizing oxygen delivery:
The patient's airway should be assessed immediately upon arrival and stabilized if necessary. The depth and rate of respirations, as well as breath sounds, should be assessed. If pathology (eg, pneumothorax, hemothorax, flail chest) that interferes with breathing is found, it should be addressed immediately. High-flow supplemental oxygen should be administered to all patients, and ventilatory support should be given if needed.

Hypovolemic Shock
Maximizing oxygen delivery:
o Two large bore IV lines should be started

o If central lines are obtained, a large-bore singlelumen catheter should be used

o In children younger than 6 years, intraosseous access also may be used.

Hypovolemic Shock
Maximizing oxygen delivery:
o Once IV access is obtained, initial fluid resuscitation is performed with an isotonic crystalloid, such as lactated Ringer solution or normal saline. o An initial bolus of 1-2 L is given in an adult (20 mL/kg in a pediatric patient), and the patient's response is assessed.

Hypovolemic Shock
If vital signs transiently improve, crystalloid infusion should continue and type-specific blood obtained

Hypovolemic Shock
If little or no improvement is seen, crystalloid infusion should continue, and type O blood should be given (type O Rh-negative blood should be given to female patients of childbearing age to prevent sensitization and future complications). Correct coagulopathy if present Vpressors are the last line, but commonly required

Hypovolemic Shock
Maximizing oxygen delivery The position of the patient can be used to improve
circulation; one example is raising the hypotensive patient's legs while fluid is being given or rolling a hypotensive gravid patient with trauma onto her left side which displaces the fetus from the inferior vena cava and increases circulation.

Hypovolemic Shock
Controlling further blood loss:
o external bleeding should be controlled with direct pressure o internal bleeding requires surgical intervention. o Long-bone fractures should be treated with traction to decrease blood loss.

Hypovolemic Shock
Controlling further blood loss:
*In the patient with GI bleeding, intravenous vasopressin and H2 blockers have been used. Vasopressin commonly is associated with adverse reactions, such as hypertension, arrhythmias, gangrene, and myocardial or splanchnic ischemia. *Somatostatin and octreotide infusions have been shown to reduce gastrointestinal bleeding from varices and peptic ulcer disease. These agents possess the advantages of vasopression without the significant side effects.

Hypovolemic Shock
Controlling further blood loss:
*In patients with variceal bleeding, use of a Sengstaken-Blakemore tube can be considered. These devices have a gastric balloon and an esophageal balloon. The gastric one is inflated first, and then the esophageal one is inflated if bleeding continues. *The use of this tube has been associated with severe adverse reactions, such as esophageal rupture, asphyxiation, aspiration and mucosal ulceration. For this reason, its use should be considered only as a temporary measure in extreme circumstances.

Hypovolemic Shock
Controlling further blood loss:
o all causes of acute gynecological bleeding that cause hypovolemia (eg, ectopic pregnancy, placenta previa, abruptio placenta, ruptured cyst, miscarriage) require surgical intervention.

Hypovolemic Shock
fluid resuscitation: crystalloids or colloids

Determinants of Blood Pressure Cardiogenic shock

blood pressure

cardiac output

total peripheral resistance

stroke volume

heart rate

preload

contractility

afterload

Cardiogenic Shock
Shock is characterized by primarly by myocardial dysfunction resulting in the inability of the heart to maintain adequate cardiac output

Cardiogenic Shock
Causes: o Acute Myocardial Infarction (AMI) o Myocarditis o Cardiomyopathy o Valvular disease o Arrhythmias

Cardiogenic Shock
R.A.S. Activation
CO

Catecholamine Release

Volume/ Preload

Myocardial O2 demand

SVR
O2 supply Peripheral & pulmonary edema

Impaired myocardial function

Dyspnea

Clinical Findings
Physical Exam: elevated JVP, +S3, rales, oliguria, high cvp,acute pulmonary edema Hemodynamics: dec CO, inc SVR CXR showing pulmonary congestion ECG abnormalities: ST segment elevation, pathologic Q waves new bundle branch blocks and other conduction abnormalities (ie. Nodal blocks and dysrhythmias)

Swan-Ganz Catheter
Utilized to differentiate types of shock and assist in treatment response. Probably overused by physicians. Studies documenting increased mortality in patients with catheters versus no catheters, although somewhat swayed by selection bias.

Swan-Ganz Catheter

Pulmonary Artery Catheterization

K l k j

Swan-Ganz Interpretation
Etiology
cardiogenic
hypovolemic

CO
decreased decreased increased decreased

PCWP
increased decreased decreased Increased

SVR
increased increased decreased increased

distributive obstructive

Cardiogenic shock
Management: 1)Treat reversible causes 2)Optimize pump function 3)Consider thrombolytics, angioplasty, aortic balloon counterpulsation in specific cases

Cardiogenic shock
Management: Optimizing pump function
*Invasive monitoring if available *Aggressive airway management *Judicious fluid management *Pressor agents

Drugs used in cardiogenic shock

Dopamine:
<5 renal vascular dilation 5-10 +chronotropic/inotropic (beta effects) >10 vasoconstriction (alpha effects)

Dobutamine:positive inotrope, vasodilates, arrhythmogenic at higher doses Norepinephrine (Levophed): vasoconstriction, inotropic stimulant. Should only be used for refractory hypotension with dec SVR. Vasopression: vasoconstriction VASO and LEVO should only be used as a last resort

Cardiogenic shock
Augment cardiac output by diuresis and providing inotropic support. IABP is utilized if medical therapy is ineffective.Catheterization if ongoing ischemia Cardiogenic shock is the exception to the rule that fluids is always given for hypotension as it will exacerbate cardiac shock

Intra-Aortic Balloon Pump

Cardiogenic shock
Management: Optimizing pump function (cont.)
*Morphine as needed for anxiolysis *Vasodilators as needed for afterload reduction *Short acting beta blocker, esmolol, for refractory tachycardia

Determinants of Blood Pressure Distributive shock

blood pressure

cardiac output

total peripheral resistance

stroke volume

heart rate

preload

contractility

afterload

Distributive Shock
Etiologies
#sepsis(septic shock) #anaphylaxis(anaphylactic shock) #neurologic insult(neuroginc shock)

Septic Shock
Definition: perfusion embarrassment secondary to dilated vascular bed in response to bacteria and their products circulating in the blood

Basic Definitions
Septicemia is a state of microbial invasion from a portal of entry into the blood stream which causes sign of illness. Sepsis: known or suspected infection plus systemic manifestations of infection (SIRS)

Septic Shock
Systemic inflammatory response syndrome (SIRS): The systemic inflammatory response to a wide variety of severe clinical insults manifests by 2 or more of the following conditions: Temperature greater than 38C or less than 36C Heart rate greater than 90 beats per minute (bpm) Respiratory rate greater than 20 breaths per minute or PaCO2 less than 32 mm Hg White blood cell count greater than 12,000/mL, less than 4000/mL, or 10% immature (band) forms

Septic Shock
Severe sepsis: This is sepsis + acute organ dysfunction thought to be due to sepsis:
Hypotension Oliguria Altered mental state Increased lactate level

Septic Shock
Septic shock:
Severe sepsis + hypotension refractory to fluid resuscitation

The Sepsis Continuum

SIRS Sepsis

Severe Sepsis

Septic Shock

A clinical response arising from a nonspecific insult, with 2 of the following: T >38oC or <36oC HR >90 beats/min RR >20/min WBC >12,000/mm3 or <4,000/mm3 or >10% bands

SIRS with a presumed or confirmed infectious process

Sepsis with organ failure

Refractory hypotension

SIRS = systemic inflammatory response syndrome

Chest 1992;101:1644

Septic Shock
Pathophysiology Mediator-induced cellular injury
The gram-positive and gram-negative bacteria induce a variety of proinflammatory mediators through the bacterial cell wall component

Septic Shock
Type Mediator Lipopolysaccharide Activity

Lipoteichoic acid
Cellular mediators

Peptidoglycan
Superantigens Endotoxin

Activation of macrophages, neutrophils, platelets, and endothelium releases various cytokines and other mediators

Potent proinflammatory effect Cytokines Neutrophil chemotactic factor Acts as pyrogen, stimulates B and T lymphocyte proliferation, inhibits cytokine production, induces immunosuppression Activation and degranulation of neutrophils Cytotoxic, augments vascular permeability, contributes to shock Involved in hemodynamic alterations of septic shock Promote neutrophil and macrophage, platelet activation and chemotaxis, other proinflammatory effects Enhance vascular permeability and contributes to lung injury

TNF-alpha and IL-1b IL-8 IL-6 IL-10 MIF* G-CSF Complement

Nitric oxide
Humoral mediators Lipid mediators Phospholipase A2 PAF Eicosanoids Arachidonic acid metabolites

Adhesion molecules Selectins Leukocyte integrins

Enhance neutrophil-endothelial cell interaction, regulate leukocyte migration and adhesion, and play a role in pathogenesis of sepsis

pathophysiology
sepsis Massive inflammator y response Cytokine and noncytokine Interleukins TNF thromboxane

Hypo perfusion , capillary leak and end organ failure

Vasodilatation Endothelial damage

The SEPSIS CASCADE

Balk , adapted from R Bone

Septic Shock
Causes
1)Lower respiratory tract infections
>Streptococcus pneumoniae >Klebsiella pneumoniae >Staphylococcus aureus >Escherichia coli >Legionella species >Haemophilus species >Anaerobes >Gram-negative bacteria >Fungi

Septic Shock
2)Urinary tract infections
>E coli >Proteus species >Klebsiella species >Pseudomonas species >Enterobacter species >Serratia species

Septic Shock
3) GI tract infections
E coli Streptococcus faecalis Bacteroides fragilis Acinetobacter species Pseudomonas species Enterobacter species Salmonella species

Septic Shock
Risk factors for severe sepsis and septic shock; 1)Extremes of age (<10 y and >70 y) 2)Primary diseases Liver cirrhosis Alcoholism Diabetes mellitus Cardiopulmonary diseases Solid malignancy Hematologic malignancy

Septic Shock
3)Immunosuppression
Neutropeniao Immunosuppressive therapy o Corticosteroid therapy o Intravenous drug abuse o Compliment deficiencies o Aspleniao

4) Major surgery, trauma, burns

Septic Shock
5) Invasive procedures Catheters Intravascular devices Prosthetic devices Hemodialysis and peritoneal dialysis catheters Endotracheal tube 6) Prior antibiotic treatment 7) Prolonged hospitalization 8) Childbirth, abortion 9) Other factors Malnutrition

Clinical
History Physical exam

History

Nonspecific symptoms

Systemic symptoms

Localizing symptoms

symptoms

Nonspecific symptoms include fever, chills, and constitutional symptoms These symptoms are not pathognomonic for infection and may be seen in a wide variety of noninfectious inflammatory conditions. Alternatively, they may be absent in serious infections, especially in elderly individuals

systemic symptoms
1 2
systemic inflammatory response syndrome (SIRS)

Fever is a common feature of sepsis.

Altered mental status is perhaps the most consistent clinical feature in sepsis. Mild disorientation or confusion is especially common in elderly individuals. More severe manifestations include apprehension, anxiety, and agitation

Localizing symptoms
1

head and neck infection Pulmonary infection

abdominal and GI infection pelvic and genitourinary infection

Bone and soft tissue infection

physical
Vital signs

Narrow pulse pressure and tachycardia

Peripheral vasodilatation warm shock

Stroke volume and cardiac out put decrease

Altered mental status and oliguria

Work up

Lab Studies

Imaging Studies procedures

Lab studies:CBC
WBC Elevated count not specific with infection Criteria of SIRS hg To maintain oxygen capacity to tissue goal is to maintain HCT>30% and HG>10 g/dl platelets are an acutephase reactant typically elevated in the setting of inflammation decrease in the setting of DIC

Comprehensive chemistry panel

Sodium and chloride abnormal in severe dehydration Urea and creatinine can point to severe dehydration or renal failure.

bicarbonate can point to acute acidosis

Chemistry studies
glucose hyperglycemia associated with higher mortality LFTs levels are important in evaluating for multiorgan failure potential source of sepsis Serum lactate level correlates with mortality, with a level greater than 4 mlmol/L associated with a precipitous increase.

Coagulation studies
PT and PTT Fibrinogen level decreased and fibrin split products are increased in the setting of DIC.

are elevated in DIC

Blood cultures

Blood cultures should be obtained in patients who have suspected sepsis in order to isolate a specific organism to tailor antibiotic therapy. Note, however, that blood cultures are positive in fewer than 50% of cases of sepsis.

Urinalysis and urine culture

UTI is a common source of sepsis, especially in elderly patients. obtaining a culture is important in order to isolate a specified organism Febrile adults without localizing symptoms or signs have a rate of occult urinary tract infection of 10-15%.

Gram stain and cultures Sputum specimen should be obtained if pneumonia is suspected. Abscesses should be drained promptly, and pus should be sent to the microbiology laboratory for analysis. CSF specimen should be obtained if meningitis is suspected

Imaging studies

Imaging should be performed as appropriate to search for a source of infection

Imaging studies
Chest radiography Abdominal film Abdominal ultra sound
Infiltrates are detected with a chest radiograph in about 5% of febrile adults detecting evidence of ARDS

clinical evidence bowel obstruction or perforation exists. of

acute cholecystitis

Imaging studies
Abdominal CT scan
diverticular abscess, ischemic bowel, appendicitis, perinephric abscess require urgent operative intervention

Plain film
extremities

evidence of soft-tissue gas formation; however, necrotizing fasciitis is a clinical diagnosis (eg, extreme pain, crepitus, bullae, hemorrhage, foul-smelling exudates),

Procedures
0rotrachial intubation and mechanical ventilation Intravenous excess

Intubation should be considered early in the course of sepsis in order to optimize ventilation and oxygenation

Two large-bore (16gauge) intravenous lines should be placed

A central venous (CV) catheter should be placed

Urinary catheter

Cutaneous or soft tissue abscess drainage

A soft-tissue abscess should be drained promptly in the setting of sepsis

to follow urinary output

Normal urinary output in an adult is about 0.5 mL/kg/h or about 30-50 mL/h for most adults

Superficial abscesses can be drained in the ED; however, deep abscesses should be treated in the OR for drainage

Septic Shock
MANGMENT Cardiac monitoring, noninvasive blood pressure monitoring, and pulse oximetry are necessary because these patients often require intensive care admission for invasive monitoring and support. Supplemental oxygen is provided during initial stabilization and resuscitation.

Septic Shock
1)Resuscitate the patient from septic shock using supportive measures to correct hypoxia, hypotension, and impaired tissue oxygenation. (2) Identify the source of infection and treat with antimicrobial therapy, surgery, or both. (3) Maintain adequate organ system function guided by cardiovascular monitoring and interrupt the pathogenesis of multiorgan system dysfunction .

Surviving Sepsis Campaign (SSC) guidelines for management of severe sepsis and septic shock
Dellinger RP, Carlet JM, Masur H, Gerlach H, Calandra T, Cohen J, Gea-Banacloche J, Keh D, Marshall JC, Parker MM, Ramsay G, Zimmerman JL, Vincent JL, Levy MM and the SSC Management Guidelines Committee
Crit Care Med 2004;32:858-873 Intensive Care Med 2004;30:536-555

Surviving Sepsis Campaign

Launched in Fall 2002 as a collaborative effort of European Society of Intensive Care Medicine, the International Sepsis Forum, and the Society of Critical Care Medicine Goal: reduce sepsis mortality by 25%

Key Components
Fluid resuscitation Appropriate cultures prior to antibiotic administration Early targeted antibiotics and source control Use of vasopressors/inotropes when fluid resuscitation optimized

Key Components
Evaluation for adrenal insufficiency Stress dose corticosteroid administration Low tidal volume mechanical ventilation for ARDS Tight glucose control

Therapy Across the Sepsis Continuum

SIRS Sepsis

Severe Sepsis

Septic Shock

Early Goal Directed Therapy

Antibiotics and Source Control

Early Goal-Directed Therapy (EGDT): involves adjustments of cardiac preload, afterload, and contractility to balance O2 delivery with O2 demand
Chest 1992;101:1644.

Early Goal-Directed Therapy Results: 28 Day Mortality

60 50 40
Sudden CV Collapse

49.2%

P = 0.01*
33.3%

Mortalit y

30
20 10 0

21% vs 10%
p=0.02
MODS

22% vs 16%
P=0.27

Standard Therapy N=133

EGDT N=130
NEJM 2001;345:1368-77.

*Key difference was in sudden CV collapse, not MODS

Goal

Goal

Early Goal-Directed Therapy

CVP: central venous pressure MAP: mean arterial pressure ScvO2: central venous oxygen saturation

NEJM 2001;345:1368-77.

1 2

Antibiotic Choices
Given the world wide resistance issues the most effective antibiotic choices to cover gram negatives would be Fourth generation cephalosporins aminoglycoside Carbapenems aminoglycoside Pip-Tazobactam + an aminoglycoside If the incidence of MRSA is high add an anti Staphylococcal agent --Vanco, Teicoplanin

SURVIVING SEPSIS CAMPAIGN UPDATES 2012

Guide to Recommendations Strengths and Supporting Evidence

1 = strong recommendation 2 = weak recommendation or suggestion A = good evidence from randomized trials B = moderate strength evidence from small randomized trial(s) or multiple good observational trials C = weak or absent evidence, mostly driven by consensus opinion.

Fluid Resuscitation
They gave a strong 1A recommendation for the use of crystalloids like normal saline as the initial fluid resuscitation for people with severe sepsis. They further advised that the initial fluid challenge should be 1L or more of crystalloid, and a minimum of 30 mL/kg of crystalloid (2.1 L in a 70 kg or 154-pound person) in the first 4-6 hours

Fluid Resuscitation(contnd)
Incremental fluid boluses should be continued as long as patients continue to improve hemodynamically (in blood pressure, pulse pressure, or both) (Grade 1C). They weakly recommended adding albumin to initial fluid resuscitation with crystalloid for severe sepsis and septic shock (Grade 2B)

Fluid Resuscitation(contnd)
Authors strongly recommended not using hetastarches/hydroxyethyl starches greater than 200 kDa in molecular weight (Grade 1B). They did not comment on the use of lower molecular weight hetastarches or the use of gelatins; trials are ongoing to evaluate these resuscitative agents

What Pressors for Septic Shock ?

Authors strongly recommended norepinephrine (Levophed) as the first choice for vasopressor therapy (Grade 1B). Vasopressin 0.03 units / minute is an alternative to norepinephrine, or may be added to it (Grade 2A). When a second agent is needed epinephrine is their weakly-recommended vasopressor choice (Grade 2B)

What Pressors for Septic Shock ?

Dopamine was only recommended in highly selected patients whose risk for arrhythmias was felt to be very low and who had a low heart rate and/or cardiac output (Grade 2C). Dobutamine is strongly recommended for patients with cardiac dysfunction as evidenced by high filling pressures and low cardiac output, or clinical signs of hypoperfusion after achievement of restoration of blood pressure with effective volume resuscitation (Grade 1C)

Corticosteroid Recommendations

For those with vasopressor-refractory septic shock, they recommend IV hydrocortisone in a continuous infusion totaling 200 mg/24 hrs a weak Grade 2C

Surviving Sepsis Campaign Statement on Glucose Control in Severe Sepsis

Consider initiating insulin therapy when blood glucose levels exceed 180 mg/dL with a goal blood glucose approximating 150 mg/dl

Neurogenic Shock
Definition: hypotension as a result of the loss of sympathetic vascular tone below the level of spinal cord injury

Neurogenic Shock

Mechanism: Loss of autonomic innervation of the cardiovascular system (arterioles, venules, small veins, including the heart)

Neurogenic Shock

Causes: 1. Spinal cord injury 2. Drugs 3. Regional anesthesia 4. Neurological disorders

Neurogenic Shock
Clinical presentation: Moderate hypotension Relative bradycardia Warm, dry skin Flaccid paralysis below level of spinal cord injury

Neurogenic Shock
Shock in the trauma patient is ALWAYS hypovolemia/hemorrhage until proven otherwise Neurogenic shock is a diagnosis of exclusion

Neurogenic Shock
Management
Alpha agonist to augment tone if perfusion still inadequate dopamine at alpha doses (> 10 mcg/kg per min) ephedrine (12.5-25 mg IV every 3-4 hour) Treat bradycardia with atropine 0.5-1 mg doses to maximum 3 mg +may need transcutaneous or transvenous pacing temporarily

Anaphalactic Shock

Anaphylactic Shock
Results from severe allergic reaction Body responds to allergen by releasing histamine Histamine causes vessels to dilate and become leaky

Anaphylactic Shock

Anaphylactic Shock
Patients with anaphylaxis develop: o Hypotention
o hives (urticaria) o Itch o wheezing and difficulty breathing (bronchospasm) o angioedema

Anaphylactic Shock Anaphylactic Shock

What are some symptoms of anaphylaxis?
First- Pruritus, flushing, urticaria appear

Next- Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness

Finally- Altered mental status, respiratory distress and circulatory collapse

Anaphylactic Shock TREATMENT

ABCs
Angioedema and respiratory compromise require immediate intubation

IV, cardiac monitor, pulse oximetry IVFs, oxygen Epinephrine Second line
Corticosteriods H1 and H2 blockers

Anaphylactic Shock TREATMENT

Epinephrine
0.3-0.5 mg IM Repeat every 5-10 min as needed Caution with patients taking beta blockers- can cause severe hypertension due to unopposed alpha stimulation For CV collapse, 1 mg IV If refractory, start IV drip

Anaphylactic Shock TREATMENT

Corticosteroids Methylprednisolone 125 mg IV Prednisone 60 mg PO Antihistamines H1 blocker- Diphenhydramine 25-50 mg IV H2 blocker- Ranitidine 50 mg IV Bronchodilators Albuterol nebulizer Atrovent nebulizer Magnesium sulfate 2 g IV over 20 minutes Glucagon For patients taking beta blockers and with refractory hypotension 1 mg IV q5 minutes until hypotension resolves

Determinants of Blood Pressure Obstructive shock

blood pressure

cardiac output

total peripheral resistance

stroke volume

heart rate

preload

contractility

afterload

Obstructive Shock

Tension pneumothorax Air trapped in pleural space with 1 way valve, air/pressure builds up Mediastinum shifted impeding venous return Chest pain, decreased breath sounds No tests needed! Rx: Needle decompression, chest tube

Obstructive Shock

Cardiac tamponade Blood in pericardial sac prevents venous return to and contraction of heart Related to trauma, pericarditis, MI Becks triad: hypotension, muffled heart sounds, JVD Diagnosis: large heart CXR, echo Rx: Pericardiocentisis

Obstructive Shock

Pulmonary embolism Virchows triad: hypercoaguable, venous injury, venostasis Signs: Tachypnea, tachycardia, hypoxia Low risk: D-dimer Higher risk: CT chest or VQ scan Rx: Heparin, consider thrombolytics

Obstructive Shock

Aortic stenosis Resistance to systolic ejection causes decreased cardiac function Chest pain with syncope Systolic ejection murmur Diagnosed with echo Vasodilators (NTG) will drop pressure! Rx: Valve surgery