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A presentation to pharmacist on how to properly manage patients in the pre-stages of sepsis in regards to nutritional support
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Strategizing against
Systemic Inflammatory Syndrome
Trey Rumph
Objectives Define SIRS and Sepsis, and understand the
difference between the two Identify those at risk for SIRS or Sepsis Understand the general pathophysiology of
SIRS Understand how organ systems may be
affected by SIRS or Sepsis Understand how the use of Nutrition can help
in the ICU patient population with SIRS or Sepsis
Prevalence Leading cause of death in critically ill patients,
claiming approximately 225,000 deaths annually in the US alone
Associated with a high mortality rate ~40-50%, even with appropriate therapy
InflammationThe Role of inflammation is to contain the site of
damage, localize the response and restore tissue function.
Initiated by microbes or tissue damage
Dilation of the small blood vessels, causes leakage in those vessels and a pathway for leukocytes to get from the blood stream into the tissue in created increased blood flow to damaged area.
Causes the heat and redness associated with inflammation
Cardinal Signs:Redness Swelling Heat Pain
Infection A pathological process involving a sterile or
colonized site that becomes over run with a pathogenic paracytic microorganism
SIRS
Systemic Inflammatory Response Syndrome 1+ symptoms
*Can be observed without the identification of an infection
Sepsis Must meet criteria for Infection + >2 SIRS
criteria
Severe Sepsis Sepsis complicated by organ dysfunction,
organ hypoperfusion or hypotension
Septic Shock Persistent arterial hypotension in a septic
patient Defined: systolic arterial pressure <90 mmHg or a
reduction in systolic pressure >40mmHg from baseline
Classification system for Sepsis
PIRO System P: predisposing conditions
I: insult, the nature and extent of the
R: response, the nature and magnitude of the host
O: organ dysfunction, the degree of concomitant
this system stratifies patients based on these criteria, but it has not gone through enough clinical trails to be applicable in practice
Pathophysiology of Septic Shock Pathogenic micro-organism Body illicit a response to fight off invader
Neuroendocrine reflexes* Inflammatory Response* Plasma Protein Cascades
Complement, Intrinsic and Extrinsic Pathways, Fibrinolytic System
Innate and Humeral Immunity Response The interaction between these different
systems is what causes the body microvascular harm organ/tissue ischemia and multiple organ dysfunction/failure
Neuroendocrine reflex The response initiated by recognition of free
LPS in the body. Fever Stimulation of the bone marrow and function of
leukocytes Catabolism Breakdown of muscle proteins Rapid increase in production of acute-phase
proteins (APP) Positive
(CRP, D-dimer, Coagulation factors, Haptoglobin, Ferritin) Negative
(Albumin, Transferrin, Retinol-binding protein)
Inflammatory Response
Inflammatory Response Hyper-inflammatory state SIRS “Systemic
inflammatory response syndrome” If severe can precipitate to Early MOF (multiple
organ failure)
As time proceeds, certain aspects of SIRS begin to down-regulate (to minimize autogenous tissue injury) CARS “counter anti-inflammatory response syndrome” If severe can cause a severe immunosuppressed
state Lead to infections, local and systemic Late MOF-
associated infections
Liver The liver actively modulates inflammatory
processes by filtering, inactivating, and clearing bacteria, bacterial products (e.g., endotoxin), vasoactive substances, and inflammatory mediators.
A stimulated liver manufactures cytokines, bioactive lipid and Acute phase proteins
Early Dysfunction (1st couple of hours) Hypoperfusion “Liver shock”
Increase in LFTs Reversed with adequate treatment
Late Dysfunction Structural and functional injury May be accounted to a bacterial, endotoxin, inflammatory
mediator spillover that trigger/sustain the MOF
Gastrointestinal Tract Instigator and victim of MOF Estimated ~70% of immune system Hypoperfusion decreased function of the intestinal
epithelium as a barrier between the enteric flora and portal circulation If toxin reaches the portal system then cycle continues, and
SIRS response intensifies Mesenteric lymph nodes are last line defense to neutralize
toxin Reperfusion initiates pro-inflammatory mediators
to be made that amplify the early SIRS contributing to MOF
Bacterial overgrowth and increased release of endotoxin contribute to late sepsis-associated MOF
Gastrointestinal Tract Disuse of the gut
Leads to ileus formation, colonization of new pathogens in the normally sterile upper gut, and increased mucosal permeability and decreased local gut immunity decreased gut immunity furthers systemic
immunosuppression Additionally, gut flora disseminate via aspiration or
translocation to become pathogenic and cause late infection.
GI motility is generally decreased following: Neurologic injury Severe trauma
Gastrointestinal Tract Figure 20.1 “conceptual framework for the
role of the gut in late MOF.”
Nutritional Clinical Effects Protein, Carbohydrates and Lipids
Risks associated with overfeeding
Clinical Pearls
TPN Formulation Protein Aminosyn 15%
GOAL: attenuate the loss of lean body mass (high protein)
Normal 1.2 – 2.0 g/kg (ABW) BMI <30
Obese > 2.0 g/kg (IBW) BMI 30-40 > 2.5 g/kg (IBW) BMI > 40
During Stress the body is in an increased metabolic state and more
proteolysis is occurring, use nutrition to attenuate damage incurred by supplying enough protein to maintain the nitrogen balance.
TPN Formulation Carbohydrates Dextrose 70%
GOAL: reduce excess glucose Patients are in a catabolic state and experience glucose
intolerance
During Stress hepatic glucose production is double the normal rates
during stressed state, and the provision of glucose at a rate of 4mg/kg/min is only able to suppress 50% of the endogenous glucose production.
TPN Formulation Lipids Liposyn 20%/30%
GOAL: limit serum FFA
During Stress Insulin secretion is inhibited Lipolysis is activated Hepatic clearance of FFA increases Increased production of hepatic TG Increased hepatic TG leads to accumulation in the liver
“fatty liver”
Summary
Consequences Overfeeding Protein
Impair kidney function due to the following: Uremia Hypertonic dehydration Metabolic acidosis
Carbs Fatty Liver, mechanical ventilation
Hyperglycemia Hypercapnia
Fats Fatty Liver
Hypertriglyceridemia Fat overload syndrome
During a stress response the patient will have increase glucose circulation along with FFA mobilization increased metabolic activity (ICU patients)
Important to realize is that this therapy does Important to realize is that this therapy does not prevent catabolism it merely minimizes not prevent catabolism it merely minimizes the amount of damage that could possibly the amount of damage that could possibly incur in the patient without proper nutritionincur in the patient without proper nutrition
Clinical Pearls Tight Glycemic control (BG < 150)
No more than 3.0mg/kg/min Patients become insulin intolerant
Limit Lipids Due to increased FFA during sepsis limit lipids to <
20% of NP Ample Protein on board
To help prevent proteolysis we add between 1.2-2.5g/kg, depending on the BMI of the patient
Questions???
“The microorganisms…turn out…to be rather more like bystanders. It is our response to their presence that makes the disease. Our
arsenals for fighting off bacteria are so powerful…that we are more in danger from
them than the invaders.”-Lewis Thomas
Germs NEJM 1972;287:553-5
Table 6-1 Criteria for Systemic Inflammatory Response Syndrome
General variables Hemodynamic variables
Fever [core temp >38.3°C (100.9°F)] Arterial hypotension (SBP <90 mmHg, MAP <70, or SBP decrease >40 mmHg)
Hypothermia [core temp <36°C (96.8°F)] SVO2 >70%
Heart rate >90 bpm Cardiac index >3.5 L/min per square meter
Tachypnea Organ dysfunction variables
Altered mental status Arterial hypoxemia
Significant edema or positive fluid balance (>20 mL/kg over 24 h)
Acute oliguria
Hyperglycemia in the absence of diabetes Creatinine increase
Inflammatory variables Coagulation abnormalities
Leukocytosis (WBC >12,000) Ileus
Leukopenia (WBC <4000) Thrombocytopenia
Bandemia (>10% band forms) Hyperbilirubinemia
Plasma C-reactive protein > 2 s.d. above normal value
Tissue perfusion variables
Plasma procalcitonin >2 s.d. above normal value
Hyperlactatemia
Decreased capillary fillingbpm = beats per minute; MAP = mean arterial pressure; SBP = systolic blood pressure; s.d. = standard deviations; SVO2 = venous oxygen saturation; WBC = white blood cell count.
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