dallas, tx november 2–4, 2012 sepsis recognition and treatment of severe sepsis in the pediatric...

Dallas, TX • November 2–4, 2012

Sepsis

Recognition and Treatment of Severe Sepsis in the Pediatric and

Adult Populations


Can your staff recognize sepsis?

Sepsis can be subtle until it is so obvious you can’t miss it


62 year old admitted to hospital with hip infection

• On admission– T – 38.5– RR – 24– P – 104– WBC – 19,000

• Where should he be admitted?


36 hours post admission

Urine output drops – What should be done?


48 hours post admission

Pulse oximeter drops and becomes difficult to read – what should be

done?


Modified from criteria published in: Balk RA. Crit Care Clin. 2000;16:337-352. Kleinpell RM. Crit Care Nurs Clin N Am 2003;15:27-34.

CardiovascularTachycardiaHypotension

Altered CVP and PAOP

Renal OliguriaAnuria

Creatinine

Hematologic platelets,

PT/INR/ aPTT protein C D-dimer

Hepatic Jaundice

Liver enzymes Albumin

CNSAltered consciousness

Confusion

MetabolicMetabolic acidosis

Lactate level Lactate clearance

Respiratory Tachypnea

PaO2

PaO2/FiO2 ratio

IDENTIFYING ACUTE ORGAN DYSFUNCTION AS A MARKER OF SEVERE SEPSIS


Difference between Sepsis States

Sepsis / ICD 995.91 Severe Sepsis/ ICD 995.92 Septic Shock/ ICD 785.52

Pulse ≥ than 90 beats per minute

Respiratory rate ≥ than 20 breaths

per minute

Temperature > 38.0 oC or < 36.0 oC

WBC < 4,000 or > 12,000; or bands

> 10%



per minute


WBC < 4,000 or > 12,000; or bands

> 10%



per minute


WBC < 4,000 or > 12,000; or bands

> 10%

Real or suspected infection: Real or suspected infection: Real or suspected infection:

Organ dysfunction: Organ Dysfunction

Hypotension

SIRS- Patient’s labs/vitals reflect any two of the following with an infectious or noninfectious etiology: Temp= < 96.8 or > 100.4 RR= > 20/min or PaCO2 < 32 mmHG HR= > 90 bpm WBC= <4000 or > 12,000; or > 10% bands

Sepsis- Systemic Inflammatory Response Syndrome (SIRS) with an identified source or suspected source of infection.

Severe Sepsis- Sepsis associated with organ dysfunction, hypoperfusion or hypotension. Manifestations may include lactic acidosis, oliguria, and an acute alteration in mental status.

Septic Shock- Acute circulatory failure unexplained by other causes: SBP <90 or MAP < 60, Reduction in 40 mmHg from baseline despite adequate volume resuscitation or Patients who require inotropic or vasopressor support despite adequate fluid replacement.

Definitions


“Our arsenals for fighting off bacteria are so powerful, and involve so many different defense mechanisms, that we are more in danger from them than from the invaders.

“We live in the midst of explosive devices; we are mined!”

Lewis Thomas - 1972Germs, New England Journal Of Medicine

DR 32708 3000093662 1204.5 Copyright © 2004, Eli Lilly and Company. All rights reserved.Xigris is a registered trademark of Eli Lilly and Company.


“Except on few occasions, the patient appears to die from the body's response to infection rather than from it.”

Sir William Osler – 1904The Evolution of Modern Medicine


History of Treating Severe Sepsis

Antibiotics, fluids, vasopressors - Have they been successful?

Have we searched for better treatments?


Key to Success Rapid Identification

• Nursing’s role in identifying and helping in the treatment of sepsis is more important than ever before

• Implementing protocols on the floor, ED and ICU

• Physician and coder’s working together to improve documentation


12

Hemodynamics of Sepsis

• Concept of early resuscitation– Establishing urgency – use of

Lactate– Normal 1-2 mmol– > 4 mmol with metabolic acidosis

suggests tissue hypoxia

• Fluids with a goal– The role of mixed venous

oxyhemoglobin (ScvO2)


Early Sepsis

Blood pressure 88/52 mm Hg

Pulse 108 beats/min

Stroke index 14

Cardiac index 1.6

Peak Velocity 79

CVP 5 mm Hg

SvO2 0.37


Late Sepsis

Blood pressure 88/56 mm Hg

Pulse 104 beats/min

Stroke index 50

Cardiac index 5.5

Peak velocity 65

CVP 7 mm Hg

SvO2 0.84


Microvascular Blood Flow Is Impaired in Severe Sepsis: Role of

Antithrombotics/Profibrinolytics

Venous bloodVenous blood

Arterial bloodArterial bloodSO2 - .98

SO2 - .94

SO2 - .65

SO2 - .86

SO2 - .65

SO2 - .83

SO2 - .65


Lactate Levels and SBP

Lactate

N= 529

< 2 (N=219) 2-4 (N=177) > 4 (N = 104)

SBP > 90 158/219 (72%) 116/177 (65%) 64/104 (62%)

SBP < 90 61/219 (28%) 61/177 (34%) 40/104 (38%)


Case Example – Is Action Needed?

• 29 year old male with history of Crohn’s disease is admitted from ED with perirectal abscess.

• Lactate 5.9• SI – 20 ml/m2• StO2 - .51• SpO2 - .94• BP – 92/50• HR – 81• RR – 20• T – 38.1• UO – 1 ml/kg/hr (55

ml/hr)


Sepsis often progresses when the host cannot contain the

primary infection

• a problem most often related to– characteristics of the microorganism,

• such as a high burden of infection • the presence of superantigens and other virulence

factors, • resistance to opsonization and phagocytosis, • antibiotic resistance.


Cell dysoxia

• Epithelial cells have diminished oxygen consumption– due to a depletion of nicotinamide adenine

dinucleotide (NAD)

• Concept of cell stunning or hibernation


Pathophysiology of Sepsis

What do we need to know


Immune Response Immune Response


Coagulation and Impaired Fibrinolysis In

Severe Sepsis

Reprinted with permission from the National Initiative in Sepsis Education (NISE).

Endothelium

Neutrophil

Monocyte

IL-6IL-1TNF-

IL-6

Inflammatory Responseto Infection

Thrombotic Responseto Infection

Fibrinolytic Responseto Infection

TAFI

PAI-1

Suppressedfibrinolysis

Factor VIIIaTissue Factor

COAGULATION CASCADE

Factor Va

THROMBIN

Fibrin

Fibrin clotTissue Factor


Hotchkiss, R. S. et al. N Engl J Med 2003;348:138-150

The Response to Pathogens, Involving "Cross-Talk" among Many Immune Cells, Including Macrophages, Dendritic Cells, and CD4 T Cells


How do We Identify Sepsis Now?

In absence of biomarkers, must rely on crude physical indicators


SIRS AND SEPSISSepsis is defined as an infection

plus 2 SIRS criteria

• Temperature >38°C or <36°C

• HR >90 beats/min

• Respirations >20/min

• WBC count >12,000/mm3 or <4,000/mm3 or >10% immature neutrophils

SIRSSeveresepsis

MODSSeptic shock

SIRSSeveresepsis SepsisInfection

Other

Pancreatitis

Trauma

Burns

Sepsis

Levy MM, et al. Crit Care Med. 2003;31:1250-1256.


Case Study 1


Case Study 1

• 63 year old male in MICU with CAP, pneumothorax

• Progressing well but on day 3 – Develops spontaneous pneumothorax– RLL infiltrate

• Temp increases to 39.1– P – 122– BP – 92/58 (following EGDT)

• WBC 16,500• Is SOB, requires intubation, 50% FIO2,

AMV 12/14, Vt – 500 ccs, PEEP +10• Day 4

– SpO2 - .92, PaO2 64 (P/F ratio > 100), pH 7.28, PaCO2 32, HCO3 - 17

• Sepsis is suspected with treatment rapidly started

– Has received EGDT• 4 L NS• norepinephrine (Levophed) 30 mcg• ScvO2 < 60

• Is on hydrocortisone 50 mg Q 6 hrs• Insulin to keep glucose < 150 • Platelets – 110,000


Day 5


Case Study 2: Should Drotrecogin Alfa

(Activated) Have Been Started? • 62-year-old, 150 kg female with history of

ovarian cancer– Undergoes debulking surgery

for tumor– 4 days post-op develops

wound infection– Norepinephrine at

10 µg/min– PEEP 12 cm H2O, FiO2 90%– Sedated (Ramsey – 6)

• Drotrecogin alfa (activated) (24 µg/kg/hr) started on day 5– Day 6: norepinephrine off– Day 10: off ventilator

• Respiratory failure recurs on day 15• Dies on day 24


ICU Admission Characteristics

40% are low risk

Likely to recover without ICU admission

50% are mid risk

Will benefit and usually recover due to ICU care

10% are high risk

High mortality even with ICU care


121,000

7,100

52,000

44,000

40,000

40,000

27,000

18,000

174,200

215,000

0 50,000100,000150,000200,000250,000

In-hospital CPR

Mechanical ventilation in stroke

rhEPO

CABG

Coronary angiography

Lung transplantation

Implantable defibrillators

Coronary stent

Drotrecogin alfa (activated)

tPA

Cost/QALY (dollars)

Cost-Effectiveness of Various Interventions in Critically Ill

Patients

Angus DC, et al. Crit Care Med 2003;31:1-11.


Erin K. Flatley/ Dr. Carl FlatleyIn 2002, sepsis claimed the life of Erin K. Flatley. Erin was a healthy, vibrant 23-year old graduate student in Florida. She went into the

hospital for a "routine" surgery but a post-operative infection occurred and because of the lack of recognition and prompt

treatment, it continued to advance. She died five days later. The killer was sepsis.

Stop the dying www.remembererin.com


Summary

• The bedside clinician, i.e. nurse or physician, is often the first to identify organ dysfunction as a marker of severe sepsis

• Treatments must be started rapidly to achieve benefit

• Cost issues are minimized by implementation of evidenced based practice

dallas, tx november 2–4, 2012 sepsis recognition and treatment of severe sepsis in the pediatric...

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