Surgery I Dineros, Karlo and Dizon, Charlotte


Case 1: Response to Injury

A 45 year old male, victim of a hit and run vehicular accident along commonwealth avenue that
happened 1 hour ago, was rushed to a big hospital nearby. You are on duty as an observer in
the emergency room. The patient has bleeding lacerations in the head. As he is shouting for
help, he is noted to have difficulty of breathing. There is a lagging right hemithorax with absence
of breath sounds. The abdomen appears to be enlarging. Vital signs: BP is 70 palpatory. PR is
110/m RR is 26/m. Your surgical resident on duty makes a quick assessment and says that your
patient is in severe case of hypovolemia secondary to blood loss. Corresponding treatment is
now being instituted.

1.Discuss in detail all the possible defense mechanisms (neuro-hormonal) that have worked to
keep him alive before resuscitative assistance was instituted.

The patient has severe case of hypovolemia secondary to blood loss which means that there is
a decrease of effective circulatory volume. Since there will be less stimulation in the stretch
receptors, it will stimulate the vasomotor center producing catecholamines. It will the cause
vasoconstriction and increase heart rate and blood pressure. It will also stimulate the release of
ADH that will cause reabsorption of water in the renal distal tubules and collecting ducts. This
will also stimulate splanchnic vasoconstriction and enhance glycogenolysis. RAAS system will
be activated wherein aldosterone will be produced which would retain Na+ and passively retain
water. So that there will be compensation from the decrease of effective circulatory volume.

2. Why is the process of INFLAMMATION important in the body? Objective?

Inflammation is the body's attempt at self-protection to remove harmful stimuli and begin the
healing process. The objectives of inflammation are:
1. To remove the invading organism, necrotic tissues
2. Repair damage tissues/ organs
3. To restore function

3.Local features of inflammation and the physiological reasons for them?

Local features of inflammation:

Rubor and Calor due to vasodilation or increased blood flow.Increased tissue perfusion in turn
causes redness (rubor), as more red blood cells pass through the tissue, and warmth (calor), as
blood carries body heat from the body's core to cooler peripheral tissues. Tumor or edema
because of increased vascular permeability which will cause fluid build up. Dolor or pain
because of edema and other substance like prostaglandins that caused by direct action on
nerve endings of the chemical agents released during inflammation.

4. Discuss thoroughly the MEDIATORS of inflammation?

Chemical Mediators by Event

1. Vasodilation: Histamine, Nitric Oxide, Prostaglandins
 2. Increased vascular permeability: Histamine, Complement Fragments (C3a and C5a),
Bradykinin, ROS, Leukotrienes
3. Chemotaxis: C5a, chemokines (TNF-alpha, IL-1, IL-8), Endotoxins
4. Fever: IL-1, TNF-alpha
5. Pain: kinins, Substance P, Prostaglandins
6. Tissue Damage: Lysosomal enzymes, ROS

Cytokines are glycoproteins secreted by macrophages and lymphocytes for the purpose of
altering the function of target cells in an endocrine, paracrine, or autocrine fashion. Most
importantly, they mediate and regulate immunity, inflammation and hematopoiesis by binding to
special cell membrane receptors which signal the cell through 2nd messengers (tyrosine
kinases) to alter its behavior.


Eicosanoids are signaling molecules that can both induce and inhibit inflammation, allergy,
fevers and other immune responses.


Nitric oxide was formerly known as endothelium derived relaxing factor. It activates guanylate
cyclase in smooth muscles to form cyclic guanosine monophosphate dependent vasodilation.

The complement system and its component fragments are an important part of the immune
system, enhancing the ability of antibodies and phagocytic cells to clear microbes during bouts
of inflammation.

Endotoxins that illicit a strong response from normal animal immune systems.monocytes,
dendritic cells, macrophages and B cells may bind to endotoxins promoting the secretion of pro-
inflammatory cytokines, nitric oxide, and eicosanoids.

Heat shock proteins share the function of chaperone, helping to direct proper protein
conformation and preventing protein aggregation.


Reactive can cause oxidative stress and apoptosis, but may also induce the host’s natural
defenses. Particularly, platelet aggregation causes a release of ROS that signals additional
platelets to come to the site of injury.

The Kallikrein-kinin system consists of the important inflammatory mediators bradykinin and
kallidin. These polypeptides are vasodilators that have action on many different cell types.

5. What is SIRS? Does the patient have it?

Systemic inflammatory response syndrome is clinical response to a nonspecific insult of either

infectious or noninfectious origin. At least two of the criteria needed to be met before declaring
the patient has it. These are:
· Fever of more than 38°C (100.4°F) or less than 36°C (96.8°F)
· Heart rate of more than 90 beats per minute
 · Respiratory rate of more than 20 breaths per minute or arterial carbon
dioxide tension (PaCO 2) of less than 32 mm Hg
· Abnormal white blood cell count (>12,000/µL or < 4,000/µL or >10%
immature [band] form
The patient has SIRS because two of the criteria were met by his conditions: heart rate of more
than 90 beats per minute (PR 110/m), and respiratory rate of more than 20 breaths per minute
(RR is 26/m).

6. What happens when the inflammatory process becomes uncontrollable and out of hand
(explain in detail)? Give 2 conditions that are examples of severe systemic inflammatory
process.

Many of the features of acute inflammation continue as the inflammation becomes chronic,
including increased blood flow and increased capillary permeability. Severe inflammation may
lead to acute multiple organ failure and early death after injury.
Neutrophils quickly enter the infected tissue, however, soon macrophages and lymphocytes
begin to be recruited. The sequence by which they bind to cell adhesion molecules and pass
through the endothelium is the same as for neutrophils. Thus, the primary cells of chronic
inflammation are macrophages and lymphocytes.
If homeostasis is not restored, a significant systemic reaction occurs. The cytokine release
leads to destruction rather than protection. A consequence of this is the activation of numerous
humoral cascades and the activation of the reticuloendothelial system and subsequent loss of
circulatory integrity. This leads to end organ dysfunction.
● Respiratory failure, ARDS Acute respiratory distress syndrome
● Cytokine-induced apoptosis of immune effector cells leading to a susceptibility to new
infections
● Loss of integrity of the gastrointestinal mucosal barrier, leading to bacterial and toxin
translocation from the intestines to the blood
● Massive induction of nitric oxide, leading to myocardial depression, peripheral
vasodilation, and shock
● Renal Failure

SIRS condition: two or more of following conditions are met:

Temp: >/ 38C (100.4F) or </ 36C (96.8F)
Heart rate >/ 90 beats per minute
RR >/ 20 breaths/ min
PaCO2 </ 32 mmhg or mechanical ventilation
White blood cell count >/ 12,000 microliter or </ 4000 microliter or >/ 10% band forms

7.How does the body regulate INFLAMMATION?

The body immune system has variety of endogenous factors such as IL-10, Il-13 and IL-4 that
has an anti-inflammatory response that may serve to modulate the proinflammatory phase and
direct a return to homeostasis accompanied by suppression of adaptive immunity. These ILs
suppress the inflammatory response by blocking activation of NF-κB. The data suggest that a
novel approach to inhibition of the inflammatory response would be to suppress the activation of
NF-κB in vivo. And also, cortisol contributes in regulation of inflammation by preventing
damaging effects of inflammatory response.

The patient is not responding very well despite of the resuscitative measures being given. The
Resident orders the patient to be wheeled to the operating room. The patient will undergo
explore lap. The patient has a tire mark in upper abdominal quadrants. You overheard your
resident saying it might be the liver, spleen or the intestines that is/are injured.

8. Thinking forward, what if the resident is correct and the surgery would need to cut part of the
intestines and put your patient on NPO for a long time, what will happen to the nutrition of the
patient.
a. Importance of nutrition?
The goal of nutritional support in the surgical patient is to prevent or reverse the catabolic
effects of disease or injury. Although several important biologic parameters have been used to
measure the efficacy of nutritional regimens, the ultimate validation for nutritional support in
surgical patients should be improvement in clinical outcome and restoration of function.

b. Discuss the difference of metabolic changes of one on simple starvation as against a

patient on NPO after a big surgical procedure?
Glycogenolysis occurs in simple starvation but it will be used up rapidly. Glucose production
occurs at the expense of protein stores ss lactate production from skeletal muscle is insufficient
to maintain systemic glucose needs, leading to increased proteolysis mainly within skeletal
muscles, producing muscle wasting. Proteolysis during starvation is due to decreased insulin
and increased cortisol release. Lipid stores provide 40% or more of caloric expenditure during
starvation, also due to decreased serum insulin and increased circulating glucagon and
catecholamines. In a patient on NPO after surgery, there is an increase in energy expenditure
mediated in part by sympathetic activation and catecholamine release. The primary source of
energy during injury are lipids (50-80%), mainly in response to catecholamine stimulus of the
hormone-sensitive triglyceride lipase.
c. Reason why sugar is elevated in injury? Why it is not utilized?
During injury, proinflammatory cytokines, Arginine, Angiotensin II will stimulate release of CRH
(Corticotrophin Releasing Hormone) which will stimulate release of ACTH (adrenocorticotrophic
hormone) which will increase cortisol. Cortisol will promote enzymatic activities leading to
gluconeogenesis in the liver.

It is not utilized because TNF alpha, IL1 and IL6 blocks the conversion of Acetyl Coa to pyruvate
during inflammatory response
d. If our patient is 80kg, how do you compute for his caloric needs? Distribute the
calories accordingly (CHO/Fats/Protein)
Estimation of the patient’s caloric needs may be determined with the use of the following
formula:
Resting Metabolic Rate = weight (kg) x 24kcal/day
= 80kg x 24kcal/day
=1920kcal/day
In this case, the condition of the patient would be classified as severe stress. Severe stress in a
patient would require the calculated caloric needs to be multiplied by a factor of 1.3.
= 1920kcal/day x 1.3 = 2496kcal/day
As the patient will have increased caloric needs due to injury, the CHO/Fat/Protein will be
(estimated):
CHO: 437g/day or 6g/kgBW/day
Fat: 69g/day or 0.86g/kgBW/day or 1g/kgBW/day
Protein: 94g/day or 1.2g/kgBW/day
e. Do this computation on a normal uninjured 80kg individual.
CHO: 336g/day or 4.2g/kgBW/day
Fat: 53g/day or 0.67g/kgBW/day
Protein: 72g/day or 0.9g/kgBW/day


f. How do you plan to deliver your calories to the patient? Explain.
As there is a possibility that parts of the patients GI tract are damaged, it would prefer to initially
deliver calories via total parenteral nutrition. This will give time for any injuries to the GI tract to
heal. While enteral feeding is preferred, the damage to the GI tract will not make this possible. It
will only be some time post op that enteral feeding will be started and nutrition will be gradually
moved from total parenteral nutrition to total enteral nutrition until the patient will be able to
tolerate a regular diet.