SURGERY

SYSTEMIC RESPONSE TO INJURY II

Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM

only in the degree & duration of their

OUTLINE
I. Overview of the injury – Associated
Systemic Inflammatory Response
i. The Detection of Cellular Injury
ii. High Mobility Group Protein B1
(HMGB1)
II. Central Nervous System Regulation of
Inflammatory Response
i. Communication of CNS with the body
ii. How does CNS sense inflammation
III. Stimuli of Neuroendocrine Reflex
IV. Neurohormonal Mediation of the Injury
V. Chemical Categories of Hormone
i. 3 Major Intracellular Pathways that
allows signal transduction
VI. Hormones under Pulmonary Control
VII. Hormones under Autonomic Control
VIII. Mediators of Inflammation
IX. Clinical Spectrum of Infection and
Systemic Inflammatory Response
Syndrome
X. Sequela of Injury
XI. Modifying Post- Traumatic Response
OVERVIEW OF THE INJURY- ASSOCIATED
SYSTEMIC INFLAMMATORY RESPONSE
• The inflammatory response to injury or
infection occurs as a consequence of the local
or systemic release of “pathogen associated”
or “damage associated” molecules, which use
similar signaling pathways to mobilize the
necessary resources required for the
restoration of homeostasis.
• Minor host, insults result in localized
inflammatory response that is transient & in
most cases beneficial.
• Major host insults, however, may lead to
amplified reactions, resulting in systemic
inflammation, remote organ damage, &
multiple organ failure in as many as 30% of
those who are severely injured.
• Severely injured patients who are destined to
die from their injuries differ from survivors
dysregulated acute inflammatory response.
• Sepsis, defined by a systemic inflammatory
response to infection, is a disease process
with an incidence of over 900,000 cases per
year.
• Trauma is the leading cause of mortality &
morbidity for individual under age 45.
THE DETECTION OF CELLULAR INJURY
• The detection of injury is mediated by
members of the Damage-Associated
Molecular Pattern Family.
• Traumatic injury activates the innate immune
system to produce a systemic inflammatory
response in an attempt to limit damage and
to restore homeostasis.
• 2 General Responses:
o An acute proinflammatory response
resulting from innate immune system
recognition of ligands.
o An anti-inflammatory response that
may serve to modulate the
proinflammatory phase & direct a
return to homeostasis.
• The degree of the systemic inflammatory
response following trauma is proportional to
injury severity & is an independent predictor
of subsequent organ dysfunction & resultant
mortality.

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Editor: Jacinto 1/11
 SURGERY
SYSTEMIC RESPONSE TO INJURY II
Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM
• The clinical features of the injury- mediated
systemic inflammatory response,
characterized by:
o Increase body temperature, heart
rate, respirations, and white blood
cell count, are similar to those
observed with infection.
o Systemic inflammation following
trauma is sterile.
• Mechanisms of sterile response are due to:
o Endogenous molecules that are
produced as a consequence of tissue
damage or cellular stress, as may
occur with hemorrhagic shock&
resuscitation
§ Alarmins or Damage-
associated molecular
patterns (DAMPS)
§ Pathogen-associated
molecular patterns (PAMPS)
o Both interact with specific cell
receptors that are located both on
the cell surface &intracellularly.
o Trauma DAMPS are---
“IMMUNOLOGICALLY ACTIVE” --Once
they are outside the cell, DAMPs
promote the activation of innate
immune cells, as well as the
recruitment & activation of antigen
presenting cells, which are engaged
in host defense.
High-mobility group protein B1 (HMGB1)
• DAMP with a direct link to the systemic
inflammatory response.
• Is rapidly released into the circulation within
30 minutes following trauma
• Actively secreted from immune- competent
cells stimulated by PAMPs (e.g. endotoxin) or
by inflammatory cytokines (e.g. tumor
necrosis factor & interleukin-1).
• Can be secreted by:
o Stressed nonimmune cells such as
endothelial cells & platelet.
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Editor: Jacinto 2/11
o Passive release of HMGB1 can occur
following cell death whether it is
programmed of uncontrolled
(necrosis).
• The diverse proinflammatory biologic
responses that result from HMGB1 signaling
include:
o The release of cytokines and
chemokines from macrophages/
monocytes & dendritic cells;
o Neutrophil activation and
chemotaxis;
o Alterations in epithelial barrier
function, including increased
permeability;
o Increased procoagulant activity on
platelet surfaces
• HMGB1 binding to toll like receptor TLR4
triggers the proinflammatory cytokines that
mediates “sickness behaviour”.
CENTRAL NERVOUS SYSTEM REGULATION OF
INFLAMMATORY RESPONSE
The Central Nervous System Communicates with
the body through
• Ordered systems of sensory & motor
neurons, which receive & integrate
information to generate a
coordinated response.
• CNS receives information with regard
to injury induced inflammation both
via soluble mediators as well as direct
neural projections that transmit
information to regulatory areas in the
brain.
How does the CNS sense inflammation?
• DAMPs & inflammatory molecules
convey stimulatory signals to the CNS
via multiple routes.
• Soluble inflammatory signaling
molecules from the periphery can
 SURGERY
SYSTEMIC RESPONSE TO INJURY II
Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM
reach neurons & glial cells directly
through the:
§ Fenestrated endothelium of
the circumventricular organs
(CVO)
§ Via a leaky blood brain
barrier in pathologic settings
such as may occur flowing a
traumatic brain injury.
NOTE:
Inflammatory stimuli can interact with
receptors located in the brain endothelial
cells. It generates variety of proinflammatory
mediators like cytokines, chemokines,
adhesion molecules, proteins of the
complement system
THE MAIN GOAL OF NEUROENDOCRINE
RESPONSE
• to initiate reflexes that lead to release of
substances that are directed towards the
respiration of effective circulating volume
and delivery of clinical energy substrate.
STIMULI OF NEUROENDOCRINE REFLEX
A. EFFECTIVE CIRCULATING VOLUME
• stimulate baroreceptors & stretch
receptors. Maximal responses on the
effective circulating volume has been
decreased by 30-40%. Further decrease
cannot be handled by compensatory
systems and shock follows
B. DECREASE IN OXYGEN, INCREASE IN CARBON
DIOXIDE AND HYDROGEN IONS
• chemoreceptor activation causes an
increase in heart rate and cardiac
contractility
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Editor: Jacinto 3/11
C. PAIN
• neuroendocrine responses not activated
unless the neural pathways are intact
D. EMOTION
E. DECREASE IN ENERGY SUBSTRATE
• particularly glucose
F. EXTREMES OF TEMPERATURE
• changes in core temperature activate
neuroendocrine pathway
G. WOUND
• both sterile and dirty wounds activate
neuroendocrine pathway through the
action of inflammatory responses.
NOTE:
Afferent signals to the brain plays a key role in
orchestrating the inflammatory response thru:
neurohormonal and endocrine signals injury or
infection thru a signal pathway that amplify the
stimulus
Neural circuit relaying messages of localized injury
to the brain(nucleus tractus solitarius). The brain
follows with a hormone release(ACTH,
glucocorticoids) into the systemic circulation and
by sympathetic response.
The vagal response rapidly induce acetylcholine
which are directed at the site of injury to curtail
the inflammatory response elicited by the
activated immunocytes
CHOLINERGIC ANTI- INFLAMMATORY PATHWAYS
The vagus nerve exerts several homeostatic
influence
A. Enhance gut motility
B. Reduce heart rate
C. Regulate inflammation
 SURGERY
SYSTEMIC RESPONSE TO INJURY II
Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM

ACETYLCHOLINE • Autonomic central nervous system

• the primary neurotransmitter of the • Hormonal

parasympathetic system
• reduces tissue macrophage activation NOTES:
CHOLINERGIC STIMULATION
Hormones are chemical signals released to
• directly reduces tissue macrophage modulate the function of the target cell
release of pro-inflammatory mediators
specifically TNF-a, IL-1, IL-18 & HMG-1
(high mobility group protein) but not the CHEMICAL CATEGORIES OF HORMONES
anti-inflammatory cytokine IL- 10 • Polypeptides
o cytokines, glucagon, insulin
NOTE: • Amino Acids
o epinephrine, serotonin,
Signals discharged from the vagus nerve are Histamines
precisely targeted at the site of injury or infection • Fatty Acids
o glucocorticoids,
In summary, vagal stimulation reduces heart rate, prostaglandins, Leukotrienes
increase gut motility, dilates arterioles and causes
pupil constriction, as well as regulates 3 MAJOR INTRACELLULAR PATHWAYS THAT ALLOWS
inflammation SIGNAL TRANSDUCTION

1. Receptor kinases such as insulin & insulin-

like growth factor receptors

2. Guanine nucleotide binding or G-protein

receptors & prostaglandin receptors

3. Ligand gated ion channels that permit ion

transport when activated.
NOTE:

On activation---the signal is then amplified

through the action of secondary signaling
molecules---intracellular signaling lead to protein
synthesis & further mediator
NEUROHORMONAL MEDIATION OF THE INJURY release
RESPONSE
ORMONES UNDER AUTONMIC CONTROL
A. Requires an intact CNS

B. Principal signs that start the

norepinephrine response pain and
hypovolemia HORMONES UNDER PITUITARY CONTRO

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Editor: Jacinto 4/11
 SURGERY
SYSTEMIC RESPONSE TO INJURY II
Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM
HORMONES UNDER PULMONARY CONTROL
1. CRH (Hypothalamus )
ACTH (Anterior Pituitary )
Cortisol (Adrenal Cortex)
• ACTH is synthesized & released by the
Ant. Pituitary
• Persistent elevations of serum
cortisol is associated with decrease
survival
• Most injury is characterized by
elevations in corticotrophin releasing
hormone & ACTH that are
proportional to the severity of injury.
• Pain, anxiety, ADH, Angiotensin II,
cholecysteine, VIP, catecholamine,
proinflammatory cytokines are all
prominent mediators of ACTH release
in the injured patient
• Stimulates the zone fasciculate of the
adrenal gland to increase
glucocorticoid production.
2. Cortisol and Glucocorticoid
• Cortisol is the major glucocorticoid in
humans & is essential for survival
during significant physiological stress
• Metabolically, cortisol potentiates
the actions of glucagon &
epinephrine that manifest as
hyperglycemia
• During injury, cortisol potentiates the
release of free fatty acids,
triglycerides & glycerol from adipose
tissue as a means of providing
additional energy sources
• In the liver, cortisol stimulates the
enzymatic activities favoring
gluconeogenesis, but induces insulin
resistance in muscles & adipose
tissues
• In skeletal muscle, cortisol induces
pain, protein degradation as well as
the release of lactate that serves as a
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Editor: Jacinto 5/11
substrate for hepatic gluconeogenesis
• Glucocorticoid is an effective
immunosuppressive
agent
• Decrease proinflammatory cytokine
production
(TNF-alpha, IL-1 & IL-6) and increase
the
production of the anti inflammatory
mediator, IL-10
NOTE:
Summary:
• ↑availability of glucose
• Potentiates the action of glucagon &
epinephrine
• ↑lipolysis
• ↓glucose uptake
• ↓the action of insulin
3. TRH
• TRH from the hypothalamus and TSH
from the anterior pituitary, T3 T4 from
the thyroid gland-no significant change
4. GH
• GH from the hypothalamus promotes
protein synthesis and halts breakdown of
carbohydrates and lipid stores
5. Gonadotropin (Hypothalamus ) and Sex
hormones
• no significant increase
6. Arginine Vasopressin ( Hypothalamus )
• formerly known as ADH
• stimulated by changes in effective
circulating volume
• Causes peripheral vasoconstriction
 SURGERY
SYSTEMIC RESPONSE TO INJURY II
Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM
• Preserves intravascular volume by
absorbing solute free H2O in the distal
tubules
• Causes hepatic glycogenolysis
HORMONES UNDER AUTONMIC CONTROL
1. CATHECOLAMINES
• Epinephrine (adrenal medulla) and
norepinephrine (axon terminals of
synaptic postganglionic neurons)
• The hypermetabolic state observed
following severe injury is attributed to
activation of the adrenergic system
• ↑cardiac output, ↑BP
• Both NE and EPI are ↑ 3- 4 in plasma
immediately following injury with
elevations lasting 24-48 hours before
returning toward baseline level
• In the liver, EPI promotes glycogenolysis,
gluconeogenesis, lipolysis, and
ketogenesis
• ↓insulin release, but ↑glucagon
secretion
• Peripherally, EPI ↑s lipolysis in adipose
tissues and induces insulin resistance in
skeletal muscle
2. ALDOSTERONE
• The mineralocorticoid aldosterone is
synthesized, stored, and released in the
adrenal zone glomerulosa
• ACTH is the most potent stimulant of
aldosterone release
• The major function of aldosterone is to
maintain intravascular volume by
conserving sodium and eliminating K and
H ions in the early distal convoluted
tubules of the nephrons.
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Editor: Jacinto 6/11
3. RENIN
Stimulates:
• ↑sympathetic stimulation of
juxtaglomerular cells
• ↓renal arterial perfusion pressure
• ↓delivery of NaCl to macula densa
• Acts to convert angiotensinogen I to AII
• ↑cardiac contractility, ↑ in HR,
↑vascular permeability
Effects:
o ↑BP- vasoconstriction of arteries and
veins
o ↑aldosterone- water and salt
retention
o ↑secretion of ACTH and vasopressin
o ↓water and Sodium excretion
o Hepatic Glycogenolysis
4. INSULIN
• Hormones and inflammatory mediators
associated with stress response inhibit
insulin release
• Peripheral insulin resistance following
injury, this results in stress induced
hyperglycemia and catabolic state
immediately following injury
• In healthy adult individual, insulin exerts a
global anabolic effect by promoting
hepatic glycogenesis and glycolysis
glucose transport into cells adipose tissue
lipogenesis and protein synthesis
5. GLUCAGON
Stimulates: hypoglycemia and Catecholamine
Effects:
• promote hyperglycemia by stimulating
• Glycogenolysis
• Gluconeogenesis
• Lipolysis
6. SOMATOSTATIN
• potent inhibitor of GH, TSH, insulin
 SURGERY
SYSTEMIC RESPONSE TO INJURY II
Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM
INSULIN LIKE GROWTH HORMONES
• Formerly known as somatomedins
• Stimulate proteoglycan synthesis
• ↑hepatic protein synthesis and glucose
uptake
• Promotes synthesis of skeletal muscles
MEDIATORS OF INFLAMMATION
A. CYTOKINES
• Are polypeptide hormones
• Messengers in cellular communication,
act like hormone
• Active in very low concentrations
• Stimulated by the host defense
mechanism
• Are soluble peptide molecules
synthesized and secreted by a number of
immunocytes in response to injury,
inflammation and infection
• Cause body responses such as fever,
leucocytosis, hyperventilation and
tachycardia
• Eradicate invading microorganisms and
actively promote wound healing
• Activity is primarily exerted locally via cell
to cell interaction (paracrine)
• Overwhelming production of
proinflammatory cytokines in response to
injury can cause hemodynamic instability
(i.e., septic shock) or metabolic
derangements (i.e., muscle wasting). If
uncontrolled, the outcome of these
exaggerated responses is end-organ
failure and death.
1. Tumor Necrosis Factor Alpha (Cachectin) TNF-a
• Also known as cachectin
• Produce cell death in certain tumors; may
produce hypotension that is seen in
sepsis leading to septic shock, tissue
injury and death, cause release of PGE-2
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Editor: Jacinto 7/11
causing neutrophil aggregation,
thromboxane synthesis
• Is the earliest and one of the most potent
mediators
• Produced by macrophage and kupffer
cells in the liver
• Short half life
• Is the principal mediator in the evolution
of MODS and because of its
hemodynamic metabolic effects and the
secondary effects that it stimulates
• Induces shock and metabolism
• Stimulates muscle breakdowns, cachexia,
increased catabolism and insulin
resistance
• Mediates coagulation activation, cell
migration, phagocytosis
2. Interleukins
• Interleukin-1
o Is a major proinflammatory
mediator with multiple effects
including regulation of skeletal
muscle proteolysis
o Induces fever by stimulation of
the release of prostaglandins
lessens pain perceptions,
stimulates the production of
acute phase reactants from the
liver produce mild hypoglycaemia
• Interleukin-2
o Promotes lymphocyte
proliferation, immune globulin
production, gut barrier integrity
o Acts as an immune stimulant
activates lymphokines activated
killer cells
• Interleukin-4
o Potent anti-inflammatory
properties against activated
 SURGERY
SYSTEMIC RESPONSE TO INJURY II
Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM
macrophages and downgrading
effects of IL-1, IL-6, IL-8
o Induce B lymphocyte production
of IgG4 and IgE
o Mediators of allergic and anti-
helminthic and IgE
• Interleukin-6
o Prolong activated neutrophil
survival
o Long half life
o Elicited by all immunogenic cells
o Enhances the immune system
• Interleukin-10
o Prominent anti-inflammatory
cytokine
o Reduces mortality in sepsis and
ARDS models
B. HEAT SHOCK PROTEIN (HSP)
• Are group of intracellular proteins that
are increasingly expressed during times of
stress such as burns, inflammation and
infection
• Formation require gene induction by heat
shock transcription factor
• Binds to both autologous and foreign
proteins
• Protect cells from deleterious effects of
traumatic stress
• Alert immune system of tissue damage
C. REACTIVE OXYGEN SPECIES (ROS)
• Are small molecules that are highly
reactive due to the presence of unpaired
outer orbit electrons
• Produced as by-products of oxygen
metabolism and by-products of anaerobic
metabolism
• Host cells are protected normally through
the endogenous antioxidants such as
superoxide dismutase, catalase, and
glutathione peroxidase
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Editor: Jacinto 8/11
• During stress or ischemia – enzymatic
clearance are consumed – on restoration
of perfusion – unbalanced production of
ROS – reperfusion injury
D. FATTY ACID METABOLITES
• Function as inflammatory mediators
• Fatty acid metabolites – omega 3 – anti-
inflammatory effects
• Omega 6 – effects largely due to its
conversion to eicosanoids
E. KALLIKREINS
• Kallekrein – kinin is a group of proteins
that contribute to inflammations, BP
control coagulation and pain responses
• Activated by Hageman factor of the
clotting system, stimulated by hypoxia,
and ischemia, potent vasodilators that
increase the capillary permeability,
producing edema, evokes pain sensation,
increase bronchial resistance and
enhances glucose clearance.
F. SEROTONIN
• Is a monoamine neurotransmitter derived
from tryptophan
• Found in the enterochromaffin cells, can
cause endocardial fibrosis, stimulates
vasoconstriction and bronchoconstriction,
platelet aggregation, stimulates
myocardial contractility and heart rate
G. EICOSANOIDS
• Derived by oxidation of the membrane
arachidonic acid (icosatetraenoic acid)
and secreted by nucleated cells except
lymphocytes, stimulated by hypoxic
ischemia tissue, injury, pyrogens, other
cytokines
• Not stored within the cells but generated
in response to hypoxic or direct tissue
 SURGERY
SYSTEMIC RESPONSE TO INJURY II
Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM

injury, endotoxin, norepinephrine,

vasopressin, bradykinin, AII, serotonin,
cytokine and histamine
• Prostaglandins seen in many
inflammatory conditions like arthritis and
bursitis; implicated in ARDS, pancreatitis
and renal failure
• The synthesis of arachidonic acid from
phospholipids requires activation of
phospholipase A2
Arachidonic acid broken down to:
a. Cyclooxygenase pathways
Prostaglandins
Thromboxane
b. Lipoxygenase
Hydroxy eicosatetraenoic acid (HETE)
Leukotrienes
• causes capillary leakage 10,000 times that
histamine, causes leukocyte adhesion,
bronchoconstriction and vasoconstriction,
chemotaxis and superoxide release by
neutrophils
PROSTACYCLIN
• member of eicosanoid family, primarily
produced by the endothelial cells
• Effective vasodilator and inhibit platelet
aggregation
• Early clinical studies with prostacyclin
have delivered some encouraging results
showing that infusion of prostacyclin
improved cardiac index, splanchnic blood
flow as measured by intestinal
tonometry, and oxygen delivery in
patients with sepsis. Importantly, there
was no significant decrease in mean
arterial pressure.

CLINICAL SPECTRUM OF INFECTION AND

SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME (SIRS)

• The systemic inflammatory response

syndrome (SIRS) is characterized by a
sequence of host phenotypic and
metabolic responses to systemic
inflammation that includes changes in:
o Heart rate
o Respiratory rate
o BP
o Temperature regulation, and
o Immune cell activation
PROSTAGLANDINS
INFECTION
• widespread effects
• identifiable source of microbial insult
THROMBOXANE A2 • Response manifested by two or more of
the following conditions:
• causes vasoconstriction and platelet
aggregation o Temperature: > 38°C or < 36°C
o HR: > 90beats/min
LEUKOTRIENES o RR: > 20 breaths/min

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Editor: Jacinto 9/11
 SURGERY
SYSTEMIC RESPONSE TO INJURY II
Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM

o PaCO2: < 32 mmHg or on • Decrease PR due to catabolic Reponses

mechanical ventilation
o WBC :> 12,000/mm3 or < 4,000
mm3 - 10% band forms
SEPSIS
• identifiable source of infection + SIRS
SEVERE SEPSIS
• Sepsis + organ dysfunction
SEPTIC SHOCK
• Sepsis + cardiovascular collapse (requiring
vasopressor support)
SEQUELA OF INJURY
4 Phases of Convalescence
• Long range dynamic course of surgical
patients through phases of convalescence
and into complete rehabilitation
1. ACUTE INJURY PAHASE : 1-3 days
• Loss of appetite, nausea, vomiting &
weight loss
• Feels ill, listless
• Sleeps excessively
• In civilian or multiple casualties – injury
initiates and surgery limits duration of
injury phase
• The purpose of excellence in surgical
technique is to diminish the depth and
duration of injury components in
surgical operations
2. TURNING POINT PHASE :3-5 days
• Decrease N2 urine excretion, decrease
glucagon and other hormones, increase
insulin
3. ANABOLIC PHASE
• Replacement of lost proteins, increase
appetite
• +N2 balance
• Regain muscle strength and vigor
• Increasing appetite and increase food
intake
• Reproductive function return
4. FAT GAIN PHASE
• N2 metabolism return to 0 balance gain
in weight – overnight
• Positive caloric balance
NOTE:
The purpose of the injury response is to
mobilize sored fuel (adipose tissue) and other
tissue components (primarily skeletal muscle-
derived amino acids) and transport this
substrate to the wound to support the healing
process, to immunologically active tissue to
support cellular function and replication, and
to other vital organs to optimize their function
in supporting recuperation. In short, we break
down our own tissue to ensure tissue repair.
MODIFYING POST-TRAUMATIC RESPONSE
Moderate to severe catabolism, if unchecked
and prolonged, can result in severe debilitation
and wasting, and prolonged convalescent
recovery.

1. FEEDING THE PATIENT

• Fever disappears, desire for food
• Most spectacular of the dynamic phases
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Editor: Jacinto 10/11
 SURGERY
SYSTEMIC RESPONSE TO INJURY II
Dr. Roberto Lozada, MD 10/25/2019 1:00-3:30 PM
• Providing exogenous nutrients, either
by the enteral or parenteral routes, has
become a standard of care for seriously
ill patients over the past decade.
Feeding prevents weight loss and
attenuates the protein wasting that
occurs in injured or infected patients.
• However, in spite of presumed
adequate feedings, loss of body protein
still occurs in patients with catabolic
diseases
2. WARMING THE PATIENT; MINIMIZING
THERMAL STRESS
• As previously notes, trauma and burn
patients have reset their central
reference temperature and utilize
physiological and behavioral
mechanisms to keep warm.
• Hospitals use environmental
engineering techniques to maintain a
cool working temperature (usually
around 23-25oC) for the staff and
visitors, which is undesirably cool for
most patients
• Patients who are sedated and
mechanically ventilated are unable to
utilize many of their physiological
mechanisms to maintain their internal
thermal balance
• Patients generally prefer a temp of 27-
29°C depending on their illness
3. USING MINIMALLY INVASIVE PROCEDURE
• With the introduction of laparoscopic
and thoracoscopic procedures, it has
become evident that patients no longer
sustain the postoperative discomfort
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Editor: Jacinto 11/11
and complications observed when
similar procedures were done with
open techniques
4. PROVIDING SELECTIVE NUTRIENTS
• It is known that a variety of nutrients
can modify the inflammatory response.
Compounds such as the antioxidant
vitamins, the amino acids Lglutamine
and L- arginine, w-3 fatty acids, and
ribonucleotide have all been evaluated
in animal and cell-culture studies, and
found to have modifying effects on
immunologic Reponse
• Modify catabolic response and
minimize infections
5. EPIDURAL ANESTHESIA AND OTHER
ANESTHETIC TECHNIQUE
• The use of spinal or epidural anesthesia
to block afferent signals to the brain
during pelvic and lower-extremity
surgery dampen the pituitaryadrenal
response – improve nitrogen balance
and postoperatively morbidity reduced.
• When both spinal and epidural
blockade were combined with
laparoscopic colectomy, a dramatic
reduction in postoperative debility was
observed.