CONTENT

NO. CONTENT PAGE

1 Acknowledgement 2
2 Introduction 3
3 Signs and symptoms 6-7
4 Pathophysiology 8-18
5 Real cases 19-26
A- Patient History
B- Physical Examination
6 References A 27-29
7 References B 30-33
8 Discussion 34-36
9 Conclusion & Prognosis 36-38
10 References 39

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ACKNOWLEDGEMENT

In the name of Allah, The Most Gracious, Most Merciful. All praises to Him for allowing me to
complete this case study within the allocated time. Peace and blessings on His Prophet Muhammad
and companions.

Firstly, I would like to extend my gratitude towards Hospital Slim River and its personnel for
giving me the opportunity to obtain invaluable experience in a friendly and supporting
environment, not to mention all the facilities provided for us.

Next, I would like to thank the dean of UniKL Mestech, Dr Reezal Ishak for giving us, DMA
students the golden opportunity to attach to this wonderful hospital for our clinical postings for
preparing us for the real working environment.

Also, credit to all DMA clinical lecturers, namely Mr Muhammad Norzein Ab Rahim, Mr Zulaily
Yacob, Mr Rahimy Hj Abdul Rahim, Mr Abdul Razak Sulaiman and Madam Siti Murni Rosman
for all the knowledges that they have shared throughout my studies.

In preparation of my assignment, I had to take the help and guidance of some respected persons,
who deserve my deepest gratitude. They are our clinical instructors who never back down from
giving us the utmost guidance, Mr Mahidzir Hassan and Madam Maimunah Ahmad, thank you
and may Allah bless you with His love and care.

I would also like to take this opportunity to thank all the members and staffs of the Department of
Surgical, especially those of Ward 9 (surgical) for all their help and encouragements throughout
my posting there. Also, to my friends and classmates, the patients, and everyone who helped me
directly or indirectly, and making it possible for me to complete this study.

Last but definitely not least, a big thank you to Hafsah Binti Sagap, the patient of my real case for
the consent to be in this case study. May God grant you the health you are looking for.

Thank you.

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Overview
As common as it may sound, pneumonia (lung inflammation caused by infection) has

affected more than 450 million people annually. It has already become a major cause of death

among all age groups resulting in 4 million deaths (7% of the world’s annual total). Infections

from pneumonia can be acquired in many different places and is classified according to its places

of acquisition, namely: community-acquired pneumonia (acquired outside health care facilities),

hospital acquired pneumonia (acquired inside the hospital), and health care-associated

pneumonia (acquired inside other health care setting aside from the hospital. However, CAP

incidences are higher in intensive care unit admitted patients rising to 40% of incidences.

Older studies have shown that pneumonia, especially CAP, has been the major cause of

child mortality in every region of the world, which kills more children under five than AIDS,

malaria, and measles combined. But recent studies that have come into attention, stress out that

the impact of community-acquired pneumonia in the elderly population (people above 65 years

of age) is far greater than in other age groups. A study by Janssens and Krause (2004) explicates

that the yearly incidence of CAP in the elderly has risen to four-times than that of younger

populations. Furthermore, their study gives light to the increase in frequency and severity of

CAP in the elderly population. This is largely explained by the aging of body organs (the

respiratory tract, immune system, and digestive tract in particular) and the presence of

comorbidities due to age-associated diseases. As a result of aging body organs and the presence

of infection from CAP, the elderly people may be at the highest risk for sepsis (a systemic

inflammatory response syndrome), which can progress to severe sepsis (sepsis with organ

failure) and then to septic shock (severe sepsis with hypotension despite adequate fluid

resuscitation).

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 Sepsis is a disease most often caused by other diseases, such as CAP. Among a number

of infection complications that develop from pneumonia or other diseases that lead to death,

sepsis (along with its progressions) has maintained its position as the primary and most common

cause of infection-related death. It has a global incidence of more than 20 million case per year,

with mortality due to septic shock reaching up to 50 percent even in industrialized countries. In

the hospital setting, up to 70% of CAP patients initially have sepsis or may develop sepsis during

their hospital stay. In turn, 50% of sepsis cases develop from CAP. Though there is high

incidence of each diseases, there is only a number of studies relating to septic shock resulting

from CAP.

This study will focus on the case of a 95 year old female patient whom we called in the

code name Lola. She was diagnosed with septic shock secondary to CAP with high risk for

hypotension and hypoxia.

Definition

In humans, septic shock has a specific definition requiring several conditions to be met for
diagnosis:

Traditionally, SIRS (systemic inflammatory response syndrome) must first be diagnosed by

finding at least any two of the following:

Tachypnea (high respiratory rate) > 20 breaths per minute, or on blood gas, a PCO2 less than 32
mmHg signifying hyperventilation.

White blood cell count either significantly low, < 4000 cells/mm3 or elevated > 12000 cells/mm3.

Heart rate > 90 beats per minute

Temperature: Fever > 38.0 °C (100.4 °F) or hypothermia < 36.0 °C (96.8 °F)

However, according to current guidelines, all that is required are 'systemic manifestations of
infection,' broadening the definition beyond the above four.

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Second, there must be sepsis and not an alternative form cause of SIRS. Sepsis requires evidence
of infection, which may include positive blood culture, signs of pneumonia on chest x-ray, or other
radiologic or laboratory evidence of infection.

Third, signs of end-organ dysfunction are required such as renal failure, liver dysfunction, changes
in mental status, or elevated serum lactate.

Finally, septic shock is diagnosed if there is refractory hypotension (low blood pressure that does
not respond to treatment). This signifies that intravenous fluid administration alone is insufficient
to maintain a patient's blood pressure from becoming hypotensive.

Etiology
When bacteria or viruses are present in the bloodstream, the condition is known as bacteremia or
viremia. Sepsis is a constellation of symptoms secondary to infection that manifest as disruptions
in heart rate, respiratory rate, temperature and WBC. If sepsis worsens to the point of end-organ
dysfunction (renal failure, liver dysfunction, altered mental status, or heart damage), then the
condition is called severe sepsis. Once severe sepsis worsens to the point where blood pressure
can no longer be maintained with intravenous fluids alone, then the criteria have been met for
septic shock. The precipitating infections which may lead to septic shock if severe enough include,
but are not limited to, appendicitis, pneumonia, bacteremia, diverticulitis, pyelonephritis,
meningitis, pancreatitis, and necrotizing fasciitis.
Most patients who develop sepsis and septic shock have underlying circumstances that interfere
with local or systemic host defense mechanisms. Sepsis is seen most frequently in elderly persons
and in those with comorbid conditions that predispose to infection, such as diabetes or any
immunocompromising disease. Patients may also have genetic susceptibility, making them more
prone to developing septic shock from infections that are well tolerated in the general population.
[31, 32, 33, 34, 35]
The most common disease states predisposing to sepsis are malignancies, diabetes mellitus,
chronic liver disease, and chronic kidney disease. The use of immunosuppressive agents is also a
common predisposing factor. In addition, sepsis is a common complication after major surgery,
trauma, and extensive burns. Patients with indwelling catheters or devices are also at high risk.
In most patients with sepsis, a source of infection can be identified. The exceptions are patients
who are immunocompromised with neutropenia, in whom an obvious source often is not found.

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Sign And Symptom
Detrimental host responses to infection occupy a continuum that ranges from sepsis to severe
sepsis to septic shock and multiple organ dysfunction syndrome (MODS). The specific clinical
features depend on where the patient falls on that continuum.
Signs and symptoms of sepsis are often nonspecific and include the following:
 Fever, chills, or rigors
 Confusion
 Anxiety
 Difficulty breathing
 Fatigue, malaise
 Nausea and vomiting
Alternatively, typical symptoms of systemic inflammation may be absent in severe sepsis,
especially in elderly individuals.
It is important to identify any potential source of infection. Localizing signs and symptoms
referable to organ systems may provide useful clues to the etiology of sepsis and are as follows:
 Head and neck infections – Severe headache, neck stiffness, altered mental status, earache,
sore throat, sinus pain/tenderness, cervical/submandibular lymphadenopathy
 Chest and pulmonary infections – Cough (especially if productive), pleuritic chest pain,
dyspnea, dullness on percussion, bronchial breath sounds, localized rales, any evidence of
consolidation
 Cardiac infections – Any new murmur, especially in patients with a history of injection or
IV drug use
 Abdominal and gastrointestinal (GI) infections – Diarrhea, abdominal pain, abdominal
distention, guarding or rebound tenderness, rectal tenderness or swelling
 Pelvic and genitourinary (GU) infections – Pelvic or flank pain, adnexal tenderness or
masses, vaginal or urethral discharge, dysuria, frequency, urgency
 Bone and soft-tissue infections – Localized limb pain or tenderness, focal erythema, edema,
swollen joint, crepitus in necrotizing infections, joint effusions
Skin infections – Petechiae, purpura, erythema, ulceration, bullous formation, fluctuance

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Pathophysiology
The pathophysiology of septic shock is not precisely understood but is considered to involve a complex
interaction between the pathogen and the host’s immune system (see the image below). The normal
physiologic response to localized infection includes activation of host defense mechanisms that result in

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the influx of activated neutrophils and monocytes, release of inflammatory mediators, local vasodilation,
increased endothelial permeability, and activation of coagulation pathways.

Diagram depicting the pathogenesis of sepsis and multiorgan failure. DIC = disseminated intravascular
coagulation; IL = interleukin.

These response mechanisms occur during septic shock, but on a systemic scale, leading to diffuse
endothelial disruption, vascular permeability, vasodilation, and thrombosis of end-organ capillaries.
Endothelial damage itself can further activate inflammatory and coagulation cascades, creating, in effect, a
positive feedback loop and leading to further endothelial and end-organ damage.
Mediator-induced cellular injury
The evidence that sepsis results from an exaggerated systemic inflammatory response induced by infecting
organisms is compelling. Inflammatory mediators are the key players in the pathogenesis of sepsis
Immunologic abnormalities
The following 3 families of pattern recognition receptors are involved in the initiation of the sepsis response:
 Toll-like receptors (TLRs)
 Nucleotide-oligomerization domain leucine-rich repeat proteins
 Cytoplasmic caspase activation and recruiting domain helicases
These receptors trigger the innate immune response and modulate the adaptive immune response to
infection. [13]

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An initial step in the activation of innate immunity is the de novo synthesis of small polypeptides
(cytokines) that induce protean manifestations on most cell types, from immune effector cells to vascular
smooth muscle and parenchymal cells. Several cytokines are induced, including tumor necrosis factor
(TNF) and interleukins (ILs), especially IL-1. These factors help keep infections localized; however, once
the infection progresses, the effects can also be detrimental
Circulating levels of IL-6 correlate have a strong correlation with outcome. High levels of IL-6 are
associated with mortality, but the role of this cytokine in pathogenesis is not clear. IL-8 is an important
regulator of neutrophil function, synthesized and released in significant amounts during sepsis. IL-8
contributes to the lung injury and dysfunction of other organs.
Chemokines (eg, monocyte chemoattractant protein [MCP]-1) orchestrate the migration of leukocytes
during endotoxemia and sepsis. Other cytokines thought to play a role in sepsis include the following:
 IL-10
 Interferon gamma
 IL-12
 Macrophage migration inhibition factor (MIF or MMIF)
 Granulocyte colony-stimulating factor (G-CSF)
 Granulocyte macrophage colony-stimulating factor (GM-CSF)
In addition, cytokines activate the coagulation pathway, resulting in capillary microthrombi and end-organ
ischemia. [14, 15, 16] (See Abnormalities of coagulation and fibrinolysis, below.)
Gram-positive and gram-negative bacteria induce a variety of proinflammatory mediators, including the
cytokines mentioned above, which play a pivotal role in initiating sepsis and shock. Various bacterial cell-
wall components are known to release the cytokines, including lipopolysaccharide (LPS; gram-negative
bacteria), peptidoglycan (gram-positive and gram-negative bacteria), and lipoteichoic acid (gram-positive
bacteria).
Several of the harmful effects of bacteria are mediated by proinflammatory cytokines induced in host cells
(macrophages/monocytes and neutrophils) by the bacterial cell-wall component. The most toxic component
of gram-negative bacteria is the lipid A moiety of LPS, which leads to cytokine induction via lipoteichoic
acid. Additionally, gram-positive bacteria may secrete superantigen cytotoxins that bind directly to the
major histocompatibility complex (MHC) molecules and T-cell receptors, leading to massive cytokine
production.
The complement system is activated and contributes to the clearance of the infecting microorganisms but
probably also enhances the tissue damage. The contact systems become activated; consequently, bradykinin
is generated.

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Hypotension, the cardinal manifestation of sepsis, occurs via induction of nitric oxide (NO). NO plays a
major role in the hemodynamic alterations of septic shock, which is a hyperdynamic form of shock.
In a study that evaluated the role of active nitrogen molecules in the progression of septic shock,
investigators found not only that patients with sepsis and septic shock had elevated mean levels of nitrite
(NO2)/nitrate (NO3) (sepsis, 78.92 µmol/L; septic shock, 97.20 µmol/L) as well as TNF-α (sepsis, 213.50
pg/mL; septic shock, 227.38 pg/mL) but also that levels of these 3 mediators increased with the severity of
the sepsis. Another factor that contributes to the poor cellular oxygen utilization and tissue organ
dysfunction during sepsis is mitochondrial dysfunction. [18] This is associated with excessive generation
of peroxynitrates and reactive oxygen species (ROS) in combination with glutathione depletion.
A dual role exists for neutrophils: They are necessary for defense against microorganisms, but they may
also become toxic inflammatory mediators, thereby contributing to tissue damage and organ dysfunction.
Lipid mediators—eicosanoids, platelet-activating factor (PAF), and phospholipase A2—are generated
during sepsis, but their contributions to the sepsis syndrome remain to be established.
Neutrophils are constitutively proapoptotic, a capacity that is essential for the resolution of inflammation
and cell turnover. Poor apoptosis is associated with poor cell clearance and a proinflammatory state.
There is a growing body of evidence regarding sepsis-induced immunosuppression, which may culminate
in a worse prognosis and a greater predisposition to other nosocomial infections.] In addition, there is
evidence that patients with sepsis who have previously been infected with cytomegalovirus may have worse
outcomes than those who have not. That cytomegalovirus infection can also cause immunomodulation may
be another factor contributing to sepsis-induced immunosuppression.
Abnormalities of coagulation and fibrinolysis
An imbalance of homeostatic mechanisms leads to disseminated intravascular coagulopathy (DIC) and
microvascular thrombosis, causing organ dysfunction and death. Inflammatory mediators instigate direct
injury to the vascular endothelium; the endothelial cells release tissue factor (TF), triggering the extrinsic
coagulation cascade and accelerating thrombin production. Plasma levels of endothelial activation
biomarkers are higher in patients with sepsis-induced hypotension than in patients with hypotension from
other causes.
The coagulation factors are activated as a result of endothelial damage. The process is initiated through
binding of factor XII to the subendothelial surface, which activates factor XII. Subsequently, factor XI and,
eventually, factor X are activated by a complex of factor IX, factor VIII, calcium, and phospholipid. The
final product of the coagulation pathway is the production of thrombin, which converts soluble fibrinogen
to fibrin. The insoluble fibrin, along with aggregated platelets, forms intravascular clots.
Inflammatory cytokines, such as IL-1α, IL-1β, and TNF-α, initiate coagulation by activating TF. TF
interacts with factor VIIa to form factor VIIa-TF complex, which activates factors X and IX. Activation of

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coagulation in sepsis has been confirmed by marked increases in thrombin-antithrombin complexes and the
presence of D-dimer in plasma, indicating activation of the clotting system and fibrinolysis. [23, 24] Tissue
plasminogen activator (t-PA) facilitates conversion of plasminogen to plasmin, a natural fibrinolytic.
Endotoxins increase the activity of inhibitors of fibrinolysis—namely, plasminogen activator inhibitor
(PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI). levels of protein C and endogenous
activated protein C (APC) are also decreased in sepsis. Endogenous APC is an important inhibitor of
coagulation cofactors Va and VIIa. Thrombin, via thrombomodulin, activates protein C, which then acts as
an antithrombotic in the microvasculature. Endogenous APC also enhances fibrinolysis by neutralizing
PAI-1 and accelerating t-PA–dependent clot lysis.
The imbalance among inflammation, coagulation, and fibrinolysis results in widespread coagulopathy and
microvascular thrombosis and suppressed fibrinolysis, ultimately leading to multiple organ dysfunction and
death. The insidious nature of sepsis is such that microcirculatory dysfunction can occur while global
hemodynamic parameters such as blood pressure may remain normal.
Circulatory abnormalities
As noted (see Shock Classification, Terminology, and Staging), septic shock falls under the category of
distributive shock, which is characterized by pathologic vasodilation and shunting of blood from vital
organs to nonvital tissues (eg, skin, skeletal muscle, and fat). The endothelial dysfunction and vascular
maldistribution characteristic of distributive shock result in global tissue hypoxia or inadequate delivery of
oxygen to vital tissues. In addition, mitochondria can become dysfunctional, thus compromising oxygen
utilization at the cellular level.
The predominant hemodynamic feature of septic shock is arterial vasodilation. The mechanisms implicated
in this pathologic vasodilation are multifactorial, but the primary factors are thought to be (1) activation of
adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle cells and (2)
activation of NO synthase.
The potassium-ATP channels are directly activated by lactic acidosis. NO also activates potassium
channels. Potassium efflux from cells results in hyperpolarization, inhibition of calcium influx, and vascular
smooth muscle relaxation. The resulting vasodilation can be refractory to endogenous vasoactive hormones
(eg, norepinephrine and epinephrine) that are released during shock.
Diminished peripheral arterial vascular tone may cause blood pressure to be dependent on cardiac output,
so that vasodilation results in hypotension and shock if insufficiently compensated by a rise in cardiac
output. Early in septic shock, the rise in cardiac output is often limited by hypovolemia and a fall in preload
because of low cardiac filling pressures. When intravascular volume is augmented, the cardiac output
usually is elevated (hyperdynamic phase of sepsis and shock).

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Although cardiac output is elevated, the performance of the heart, reflected by stroke work as calculated
from stroke volume and blood pressure, is usually depressed. Factors responsible for myocardial depression
of sepsis include myocardial depressant substances, coronary blood flow abnormalities, pulmonary
hypertension, various cytokines, NO, and beta-receptor downregulation.
Although cardiac output is elevated, the arterial−mixed venous oxygen difference is usually narrow, and
the blood lactate level is elevated. This implies that low global tissue oxygen extraction is the mechanism
that may limit total body oxygen uptake in septic shock. The basic pathophysiologic problem seems to be
a disparity between oxygen uptake and oxygen demand in the tissues, which may be more pronounced in
some areas than in others.
This disparity is termed maldistribution of blood flow, either between or within organs, with a resultant
defect in the capacity for local extraction of oxygen. During a fall in the oxygen supply, cardiac output
becomes distributed so that the most vital organs, such as the heart and brain, remain relatively better
perfused than nonvital organs are. However, sepsis leads to regional changes in oxygen demand and
regional alteration in the blood flow of various organs.
The peripheral blood flow abnormalities result from the balance between local regulation of arterial tone
and the activity of central mechanisms (eg, the autonomic nervous system). Regional regulation and the
release of vasodilating substances (eg, NO and prostacyclin) and vasoconstricting substances (eg,
endothelin) affect regional blood flow. Increased systemic microvascular permeability also develops,
remote from the infectious focus, and contributes to edema of various organs (eg, the lung microcirculation)
and to the development of ARDS.
In patients experiencing septic shock, oxygen delivery is relatively high, but the global oxygen extraction
ratio is relatively low. Oxygen uptake increases with rising body temperature despite a fall in oxygen
extraction.
In patients with sepsis who have low oxygen extraction and elevated arterial lactate levels, oxygen uptake
depends on oxygen supply over a much wider range than normal. Therefore, oxygen extraction may be too
low for tissue needs at a given oxygen supply, and oxygen uptake may increase with a boost in oxygen
supply—a phenomenon termed oxygen uptake supply dependence or pathologic supply dependence. This
concept is controversial, however; some investigators argue that supply dependence is an artifact rather
than a real phenomenon.
Maldistribution of blood flow, disturbances in the microcirculation, and, consequently, peripheral shunting
of oxygen are responsible for diminished oxygen extraction and uptake, pathologic supply dependency of
oxygen, and lactate acidemia in patients experiencing septic shock.
Mechanisms of organ dysfunction

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Sepsis is described as an autodestructive process that permits the extension of the normal pathophysiologic
response to infection (involving otherwise normal tissues), resulting in MODS. Organ dysfunction or organ
failure may be the first clinical sign of sepsis, and no organ system is immune to the consequences of the
inflammatory excesses of sepsis.
The precise mechanisms of cell injury and resulting organ dysfunction in patients with sepsis are not fully
understood. MODS is associated with widespread endothelial and parenchymal cell injury occurring via
the following proposed mechanisms:
 Hypoxic hypoxia – The septic circulatory lesion disrupts tissue oxygenation, alters the metabolic
regulation of tissue oxygen delivery, and contributes to organ dysfunction; microvascular and
endothelial abnormalities contribute to the septic microcirculatory defect in sepsis; ROS, lytic
enzymes, vasoactive substances (eg, NO), and endothelial growth factors lead to microcirculatory
injury, which is compounded by the inability of the erythrocytes to navigate the septic
microcirculation
 Direct cytotoxicity – Endotoxin, TNF-α, and NO may cause damage to mitochondrial electron
transport, leading to disordered energy metabolism; this is called cytopathic or histotoxic anoxia
(ie, inability to use oxygen even when it is present)
 Apoptosis (programmed cell death) – This is the principal mechanism by which dysfunctional cells
are normally eliminated; the proinflammatory cytokines may delay apoptosis in activated
macrophages and neutrophils, but other tissues, such as the gut epithelium, may undergo
accelerated apoptosis; therefore, derangement of apoptosis plays a critical role in tissue injury in
patients with sepsis
 Immunosuppression – Interaction between proinflammatory and anti-inflammatory mediators may
lead to an imbalance and an inflammatory reaction, immunodeficiency may predominate, or both
may occur
 Coagulopathy – Subclinical coagulopathy signified by mild elevation of the thrombin time or
activated partial thromboplastin time (aPTT) or by a moderate reduction in platelet count is
extremely common, but overt DIC is rare; coagulopathy is caused by deficiencies of coagulation
system proteins, including protein C, antithrombin III, and TF inhibitors
Cardiovascular dysfunction
Significant derangement in the autoregulation of the circulatory system is typical in patients with sepsis.
Vasoactive mediators cause vasodilatation and increase the microvascular permeability at the site of
infection. NO plays a central role in the vasodilation of septic shock. Impaired secretion of vasopressin may
also occur, which may permit the persistence of vasodilatation.

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Changes in both systolic and diastolic ventricular performance occur in patients with sepsis. Through the
Frank-Starling mechanism, cardiac output is often increased to maintain blood pressure in the presence of
systemic vasodilatation. Patients with preexisting cardiac disease are unable to increase their cardiac output
appropriately.
Because sepsis interferes with the normal distribution of systemic blood flow to organ systems, core organs
may not receive appropriate oxygen delivery. The microcirculation is the key target organ for injury in
patients with sepsis. A decrease in the number of functional capillaries leads to an inability to extract oxygen
maximally; this inability is caused by intrinsic and extrinsic compression of capillaries and plugging of the
capillary lumen by blood cells. Increased endothelial permeability leads to widespread tissue edema
involving protein-rich fluid.
Hypotension is caused by the redistribution of intravascular fluid volume that results from reduced arterial
vascular tone, diminished venous return from venous dilation, and release of myocardial depressant
substances.
Pulmonary dysfunction
The pathogenesis of sepsis-induced ARDS is a pulmonary manifestation of SIRS. A complex interaction
between humoral and cellular mediators, inflammatory cytokines and chemokines, is involved in this
process. A direct or indirect injury to the endothelial and epithelial cells of the lung increases alveolar
capillary permeability, causing ensuing alveolar edema. The edema fluid is protein-rich; the ratio of alveolar
fluid edema to plasma is 0.75-1.0, whereas in patients with hydrostatic cardiogenic pulmonary edema, the
ratio is less than 0.65.
Injury to type II pneumocytes decreases surfactant production; furthermore, the plasma proteins in alveolar
fluid inactivate the surfactant previously manufactured. These enhance the surface tension at the air-fluid
interfaces, producing diffuse microatelectasis.
Neutrophil entrapment within the pulmonary microcirculation initiates and amplifies the injury to alveolar
capillary membrane. ARDS is a frequent manifestation of these effects.
ALI (mild ARDS in the Berlin Definition) is a type of pulmonary dysfunction secondary to parenchymal
cellular damage that is characterized by endothelial cell injury and destruction, deposition of platelet and
leukocyte aggregates, destruction of type I alveolar pneumocytes, an acute inflammatory response through
all injury phases, and repair and hyperplasia of type II pneumocytes. Migration of macrophages and
neutrophils into the interstitium and alveoli produces various mediators that contribute to the alveolar and
epithelial cell damage.
If addressed at an early stage, ALI may be reversible, but in many cases, the host response is uncontrolled,
and ALI progresses to more severe ARDS. Continued infiltration occurs with neutrophils and mononuclear
cells, lymphocytes, and fibroblasts. An alveolar inflammatory exudate persists, and type II pneumocyte

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proliferation is evident. If this process can be halted, complete resolution may occur. In other patients,
progressive respiratory failure and pulmonary fibrosis develop.
The central pathologic finding in ARDS is severe injury to the alveolocapillary unit. After initial
extravasation of intravascular fluid, inflammation and fibrosis of pulmonary parenchyma develop into a
morphologic picture termed diffuse alveolar damage (DAD). The clinical and pathologic evolution can be
categorized into the following 3 overlapping phases [27] :
 Exudative phase (edema and hemorrhage)
 Proliferative phase (organization and repair)
 Fibrotic phase (end-stage fibrosis)
The exudative phase of DAD occurs in the first week and is dominated by alveolar edema and hemorrhage
(see the images below). Other histologic features include dense eosinophilic hyaline membranes and
disruption of the capillary membranes. Necrosis of endothelial cells and type I pneumocytes occur, along
with leukoagglutination and deposition of platelet fibrin thrombi.

Acute respiratory distress syndrome

(ARDS), commonly observed in septic shock as a part of multiorgan failure syndrome, results in
pathologically diffuse alveolar damage (DAD). This photomicrograph shows early stage (exudative stage)
DAD.

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 Acute respiratory distress syndrome
(ARDS), commonly observed in septic shock as a part of multiorgan failure syndrome, results in
pathologically diffuse alveolar damage (DAD). This is a high-powered photomicrograph of early stage
(exudative stage) DAD.
View Media Gallery
The proliferative phase is prominent in the second and third week after the onset of ARDS, but it may begin
as early as day 3. Organization of the intra-alveolar and interstitial exudate, infiltration with chronic
inflammatory cells, parenchymal necrosis, and interstitial myofibroblast reaction occur. Proliferation of
type II cells and fibroblasts, which convert the exudate to cellular granulation tissue, is noted, as is excessive
collagen deposition, transforming into fibrous tissue (see the images below).

Photomicrograph showing delayed stage

(proliferative or organizing stage) of diffuse alveolar damage (DAD). Proliferation of type II pneumocytes
has occurred; hyaline membranes as well as collagen and fibroblasts are present.

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 Photomicrograph showing delayed stage
(proliferative or organizing stage) of diffuse alveolar damage (DAD). Fibrin stain depicts collagenous
tissue, which may develop into fibrotic stage of DAD.
View Media Gallery
The fibrotic phase occurs by the third or fourth week after the onset of ARDS, though it may begin as early
as the first week. The collagenous fibrosis completely remodels the lung, the air spaces are irregularly
enlarged, and alveolar duct fibrosis is apparent. Lung collagen deposition increases, and microcystic
honeycomb formation and traction bronchiectasis follow.
Gastrointestinal dysfunction
The gastrointestinal (GI) tract may help to propagate the injury of sepsis. Overgrowth of bacteria in the
upper GI tract may be aspirated into the lungs and produce nosocomial pneumonia. The gut’s normal barrier
function may be affected, thereby allowing translocation of bacteria and endotoxin into the systemic
circulation and extending the septic response.
Septic shock usually causes ileus, and the use of narcotics and sedatives delays the institution of enteral
feeding. This interferes with optimal nutritional intake, in the face of high protein and energy requirements.
Glutamine is necessary for normal enterocyte functioning. Its absence in commercial formulations of total
parenteral nutrition (TPN) leads to breakdown of the intestinal barrier and translocation of the gut flora into
the circulation. This may be one of the factors driving sepsis. In addition to inadequate glutamine levels,
this may lessen the immune response by decreasing leukocyte and natural killer (NK) cell counts, as well
as total B-cell and T-cell counts.
Hepatic and renal dysfunction
By virtue of the liver’s role in host defense, the abnormal synthetic functions caused by liver dysfunction
can contribute to both the initiation and the progression of sepsis. The hepatic reticuloendothelial system

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acts as a first line of defense in clearing bacteria and their products; liver dysfunction leads to a spillover of
these products into the systemic circulation.
Acute kidney injury (AKI)—previously termed acute renal failure (ARF)—with remarkably little overt
tubular necrosis but markedly impaired renal function often accompanies sepsis. The mechanism for sepsis-
induced AKI is poorly understood but is associated with systemic hypotension, cytokinemia (eg, TNF), and
activation of neutrophils by endotoxins and other peptides, which indirectly and directly contribute to renal
tubular injury.\

Treatment
Treatment primarily consists of the following.

 Volume resuscitation
 Early antibiotic administration
 Early goal directed therapy
 Rapid source identification and control.
 Support of major organ dysfunction.
 Sequestration of lipopolysaccharides.

Among the choices for vasopressors, norepinephrine is superior to dopamine in septic shock. Both
however are still listed as first line in guidelines.

Antimediator agents may be of some limited use in severe clinical situations however are
controversial:

Low dose steroids (hydrocortisone) for 5 – 7 days led to improved outcomes.

Recombinant activated protein C (drotrecogin alpha) in a 2011 Cochrane review was found not to
decrease mortality and thus was not recommended for use. Other reviews however comment that
it may be effective in those with very severe disease. The first and only activated protein C drug,
drotrecogin alfa (Xigris), was voluntarily withdrawn in October 2011 after it failed to show a
benefit in patients with septic shock, including the more severe disease subgroups.

CASES

REAL CASE

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Patient History Real case I studied is septic shock. Patient name, Hafsah Binti Sagap (RN 3954),
malay woman with 31 years old came to the Emergency department (ED), Hospital Slim River
on 21 may at 10.00 pm. He accompanied by his son. The chief complaint his mother made to
Medical Staff at Emergency department is he was feeling severe discomfort and pain since this
morning. The history of presenting complaint his mother made is this patient having low blood
count due to infection about 2 days with poor oral intake and fatigue due to not sleeping. The past
medical history face by this patient is nul. After gathering further information, the medical staff
knows that he was having septic shock since first month old and do regular follow up at Klinik
Hospital Slim River.

From patient’s family history, the patients daughter said 2 son and 2 daughters

Father 85 Years old (Patient) Mother 81 years old

1st son 52 years old 2nd son 45 years old 3rd daughter 40 years old 4th daughter 32 y/o

From the patient’s family information, we know that her husband is 81 years old man and clerk
at Tapah while she himself as a mother is 78 years old woman and work as housewive. Not only
that, after investigate about their past medical and surgical history, we found that they both do

19
not have any past medical and surgical history. Beside that, this patient have 2 son and 2
daughters where the first brother is 52 years old and second is 45years old. The social history of
this patient is she love to enjoy her lifestyle

. Physical examination

To identify the main causes, poor oral intake, fatigue, flu and infected about 2 days, doctor was
carry out some physical examinations. During general examination, this patient was look alert,
pink, good pulse volume conscious which achieve 15/15 Glasgow coma scale (GCS).At the same
time, this patient have fair hydration.

The initial vital signs of this patient is

Blood pressure (BP) 129/87 mmHg

Pulse rate (PR) 170 min
Respiration rate (RR) 20/min min
Body temperature (BT) 37. degree Celsius
Pain score 4

While the current vital sign of this patient is,

Blood pressure (BP) 104/54 mmHg

Pulse rate (PR) 157 min
Respiration rate (RR) 20/min
Body temperature (BT) 37.5 degree Celsius
Pain score 0

Cardiovascular system is shown dual rhythm no murmur (DRNM) and S1S2 heard clearly. When
auscultate the lungs, breath sound reduce bilaterally and bilateral rhonchi are found. While during
palpitation, stomach in soft, non-tender and no mass condition and at the same time, bowel sound
active were found on it.

20
C) Differential diagnosis

- Fluid overload secondary to non-compliance to restriction of fluid (ROF)

- Hypotension

- Congestive cardiac failure on restriction of fluid

- community- acquired pneumonia (CAP

Differential diagnosis and Investigation

The differential diagnosis that can made is gum pain,gum infected,root canal infection). After
undergo the patient’s history, physical examination and finding differential diagnosis, next doctor
carry out some laboratory and radiology investigation. For laboratory test, full blood count (FBC)
were taken. The result is as shown below:

Full blood count Result Normal range

Haemoglobin (Hb) 11.7 g/dl 11.1-14.1

White blood count (WBC) 19.78x10^3/UL 6.0-16.0

Platelet count 354x10^3/UL 150-450
Total red cell (TRC) 4.53x10^6/UL 39-51

While the result for renal profile (RP) is as shown below:

Renal profile Result Normal range

Blood urea nitrogen 2.5 mmol/L 1.7-6.4
Sodium 143.0 mmol/L 135-150
Potassium 3.7 mmol/L 3.6-5.4
Creatinine 22 umol/L 61-120

21
Pain at right side of abdominal(epigastric pain)

Investigation

After undergoing the history of patient, physical examination and finding differential diagnosis,
next doctor carries out some laboratory and radiology investigations to make a correct diagnosis.
For laboratory test, full blood count (FBC) were taken. The result is as shown below:

Full blood count Result Normal range

White blood count (WBC) 11.81 x10^3/UL 4.0-10.0

Total red cells 5.07 x10^6/UL 4.5-5.5

Haemoglobin 15.7 g/dl 13-18
Platelet count 193 x 10^3/UL 150-450
HCT 45.8 % 40-50
Next, result for renal profile (RP) is as shown below:

Renal profile Result Normal range

Blood urea nitrogen 3.6 mmol/L 1.7-8.3
Sodium 136.3 mmol/L 135-154
Potassium 3.8 mmol/L 3.6-5.4
Chloride 105.4 mmol/L 93-108
Creatinine 33 umol/L 48-95

22
Next laboratory test used by doctor in my case is INR which shows the result 1.05.

Arterial blood gas (ABG) also shows the result as shown below:

Arterial blood gas Result Normal range

pH 7.4 7.380-7.440
pCO2 38.4 mmol/L 35.0-40.0
pO2 68.1 mmol/L 75.0-100.0
Haematocrit 4.8% 36-50

Treatment and management

Initial Management

The initial management that done by the doctor in Emergency department is asking some
questions about his chief complaint and history of presenting complaint. After investigate, we
know that this patient is referred from Klinik Kesihatan Tanjung Malim. Then doctor asked
patient’s family, drug and social history. Then triage this patient at yellow zone. After triaging this
patients at yellow zone, Medical staff checked patient’s vital signs include blood pressure,
respiration rate, pulse rate, body temperature and pain score due to his age. After taking vital signs
and finding the differential diagnosis, patient admitted to Ward 9 (Surgical).

The routine ward management done to this patient is doing bed making in the morning, checking
patient’s vital sign 4 hourly, give medication to the patient in correct dosage based on doctor’s
order. Other routine ward management is observing the branula intact of this patient to avoid from
occurring bleeding and strict input and output I/O charting. Not only that, other routine ward
management is giving nursing care and always observe this patient rest on bed.

While the specific ward management is by giving analgesics or pain killer.Some other drug in
order to avoid severe complication which is by giving antibiotics

23
Pre-op Post-op
 Concern form must be done to proceed  Administer the medication that order
the operation by doctor
 Patient documentation for progress to  Monitor the input and output chart
patient  Monitor the IV drip of patient
 Ask patient to fasting before surgery  Maintain the patient personal hygiene
(fasting 6 hours)  Dressing the wound with normal saline
 Preparation for patient before started  Observed the abnormalities of the
the operation wound

Routine Management

- Doing bed making before patient arrive to red zone

- Checking for the patient’s vital sign every 15 minutes
- Insert branula and observe branula intact to avoid from occurring bleeding
- Take blood as doctor’s order
- Provide nursing care and patient rest in bed
- Give medication to patient based on doctor’s order
- Electrocardiogram is taken to see the rhythm of heart
- Strict input and output (I/O) chart

Specific Management

- Insert catheter bladder drainage (CBD) bag to patient after arriving to red zone
- Give 3 litre of nasal prong oxygen to maintain SPO2 above 97%
- Take blood glucose test (DXT) 4 hourly
- Patient refer to medical department for further management
- Doctor in medical department plan to admit this patient to ward 9

24
Treatment

Pharmacological treatment

Drugs Generic name Trade name Dose Indication

IV Augmentin Amoxicillin 1g AUGMENTIN ADULT: Infection caused by
1.2g stat &TDS &Clavulanate 1.2 g injection 1.2g by IV or susceptible organisms.
200mg injection intermittent Respiratory tract, skin
infusion 6-8 soft tissue, GUT
hourly infection, septicaemia
IM Pethidine Demerol 50-150 mg Moderate to severe
100 mg TDS every 4 hr if pain
needed
T.Paracetamol Paracetamol PANADOL ADULT: Mild to moderate pain
1g STAT 500mg stat Tablet 500-1000mg pyrexia
every 4-6
hours,
maximum of
4g daily
Iv Tracidol Cap Adult & Moderate to severe
metrodinazole adolescent pain.
500mg STAT >14 yr 50-
100 mg 6
hrly. Max:
400 mg

25
G) Advice

 Ask patient to have follow up at Klinik Kesihatan Tanjung Malim

 Eat medications followed by the dosage that had been prescribed by doctor
 Take plenty of rest
 Drink water according to doctors’ order, which is 1 litre per day
 Avoid stress
 Eat diabetic and vitamin rich diet
 Do simple exercise
 Avoid harmful environment factor such as smoke or dust and chemical
 Take care personal hygiene to avoid from infection
 Stop smoking

26
 Reference A
Definition
Sepsis is defined as life-threatening organ dysfunction due to dysregulated host response to
infection, and organ dysfunction is defined as an acute change in total Sequential Organ Failure Assessment
(SOFAS) score greater than 2 points secondary to the infection cause. Septic shock occurs in a subset of
patients with sepsis and comprises of an underlying circulatory and cellular/metabolic abnormality that is
associated with increased mortality. Septic shock is defined by persisting hypotension requiring
vasopressors to maintain a mean arterial pressure of 65 mm Hg or higher and a serum lactate level greater
than 2 mmol/L (18 mg/dL) despite adequate volume resuscitation. This new 2016 definition, also called
Sepsis-3, eliminates the requirement for the presence of systemic inflammatory response syndrome (SIRS)
to define sepsis, and it removed the severe sepsis definition. What was previously called severe sepsis is
now the new definition of sepsis.

Signs and symptoms

Detrimental host responses to infection occupy a continuum that ranges from sepsis to severe sepsis to
septic shock and multiple organ dysfunction syndrome (MODS). The specific clinical features depend on
where the patient falls on that continuum.
Signs and symptoms of sepsis are often nonspecific and include the following:
 Fever, chills, or rigors
 Confusion
 Anxiety
 Difficulty breathing
 Fatigue, malaise
 Nausea and vomiting
Alternatively, typical symptoms of systemic inflammation may be absent in severe sepsis, especially in
elderly individuals.
It is important to identify any potential source of infection. Localizing signs and symptoms referable to
organ systems may provide useful clues to the etiology of sepsis and are as follows:
 Head and neck infections – Severe headache, neck stiffness, altered mental status, earache, sore
throat, sinus pain/tenderness, cervical/submandibular lymphadenopathy
 Chest and pulmonary infections – Cough (especially if productive), pleuritic chest pain, dyspnea,
dullness on percussion, bronchial breath sounds, localized rales, any evidence of consolidation

27
  Cardiac infections – Any new murmur, especially in patients with a history of injection or IV drug
use
 Abdominal and gastrointestinal (GI) infections – Diarrhea, abdominal pain, abdominal distention,
guarding or rebound tenderness, rectal tenderness or swelling
 Pelvic and genitourinary (GU) infections – Pelvic or flank pain, adnexal tenderness or masses,
vaginal or urethral discharge, dysuria, frequency, urgency
 Bone and soft-tissue infections – Localized limb pain or tenderness, focal erythema, edema,
swollen joint, crepitus in necrotizing infections, joint effusions
Skin infections – Petechiae, purpura, erythema, ulceration, bullous formation, fluctuance

Etiology
When bacteria or viruses are present in the bloodstream, the condition is known as
bacteraemia or Viremia. Sepsis is a constellation of symptoms secondary to infection that
manifest as disruptions in heart rate, respiratory rate, temperature and WBC. Once severe
sepsis worsens to the point where blood pressure can no longer be maintained with
intravenous fluids alone, then the criteria have been met for septic shock. The precipitating
infections which may lead to septic shock if severe enough include appendicitis,
pneumonia, bacteraemia, diverticulitis, pyelonephritis, meningitis, pancreatitis, and
necrotizing fasciitis.

Risk factors
Risk factors for severe sepsis and septic shock include the following:
 Extremes of age (< 10 years and >70 years)
 Primary diseases (eg, liver cirrhosis, alcoholism, diabetes mellitus, cardiopulmonary diseases, solid
malignancy, and hematologic malignancy)
 Immunosuppression (eg, from neutropenia, immunosuppressive therapy [eg, in organ and bone
marrow transplant recipients], corticosteroid therapy, injection or IV drug use [see the image
below], complement deficiencies, asplenia)
 Major surgery, trauma, burns
 Invasive procedures (eg, placement of catheters, intravascular devices, prosthetic devices,
hemodialysis and peritoneal dialysis catheters, or endotracheal tubes)
 Previous antibiotic treatment

28
  Prolonged hospitalization
 Underlying genetic susceptibility
 Other factors (eg, childbirth, abortion, and malnutrition)

Diagnosis
Patients with sepsis may present in a myriad of ways, and a high index of clinical suspicion is necessary
to identify subtle presentations. The hallmarks of severe sepsis and septic shock are changes that occur at
the microvascular and cellular level and may not be clearly manifested in the vital signs or clinical
examination. This process includes diffuse activation of inflammatory and coagulation cascades,
vasodilation and vascular maldistribution, capillary endothelial leakage, and dysfunctional utilization of
oxygen and nutrients at the cellular level.
Cardiac monitoring, noninvasive blood pressure monitoring, and pulse oximetry are indicated in patients
with septic shock.

Treatment
Septic shock is a medical emergency. Patients are usually admitted to the intensive care unit of the
hospital.

Treatment may include:

 Breathing machine (mechanical ventilation)
 Drugs to treat low blood pressure, infection, or blood clotting
 Fluids given directly into a vein (intravenously)
 Oxygen
 Surgery
There are new drugs that act against the extreme inflammatory response seen in septic shock.
These may help limit organ damage.
Hemodynamic monitoring -- the evaluation of the pressures in the heart and lungs -- may be
required. This can only be done with special equipment and intensive care nursing

29
 Reference B
Definition
Septic shock is a life-threatening condition that happens when your blood pressure drops to a
dangerously low level.
The fall in blood pressure is a reaction to a serious infection that develops in the blood.
This causes a response from the body known as sepsis. If sepsis is not treated, it will lead to
septic shock.
Symptoms of septic Shock includes cold skin and an increased heartbeat.If you have septic
shock, you will usually be admitted to an intensive care unit (ICU) so that your body’s functions
and organs can be supported while the infection is treated.

Sign and Symptoms:

Septic shock can affect any part of the body, including the heart, brain, kidneys, liver, and
intestines. Symptoms may include:
 Cool, pale extremities
 High or very low temperature, chills
 Lightheadedness
 Low blood pressure, especially when standing
 Palpitations
 Rapid heart rate
 Restlessness, agitation, lethargy, or confusion
 Shortness of breath
 Skin rash or discoloration

 elderly people
 Anyone who is taking immunosuppressive medications (such as transplant recipients)
 People who are being treated with chemotherapy drugs or radiation
 People who have had their spleen surgically removed (the spleen helps fight certain
infections)
 People taking steroids (especially over the long term)
 People with longstanding diabetes, AIDS, or cirrhosis
 Someone who has very large burns or severe injuries
 People with infections such as
o pneumonia,
o meningitis,
o cellulitis,
o urinary tract infection

30
Risk factors for septic shock include:
 Diabetes
 Diseases of the genitourinary system, biliary system, or intestinal system
 Diseases that weaken the immune system such as AIDS
 Indwelling catheters (those that remain in place for extended periods, especially
intravenous lines and urinary catheters and plastic and metal stents used for drainage)
 Leukemia
 Long-term use of antibiotics
 Lymphoma
 Recent infection
 Recent surgery or medical procedure
 Recent use of steroid medications

Etiology
Causative microorganisms
Before the introduction of antibiotics, gram-positive bacteria were the principal organisms that caused
sepsis. Subsequently, gram-negative bacteria became the key pathogens causing severe sepsis and septic
shock. Currently, however, the rates of severe sepsis and septic shock due to gram-positive organisms are
rising again because of the more frequent use of invasive procedures and lines in critically ill patients. As
a result, gram-positive and gram-negative microorganisms are now about equally likely to be causative
pathogens in septic shock. [36, 37, 38, 39]
Respiratory tract and abdominal infections are the most frequent causes of sepsis, followed by urinary tract
and soft-tissue infections. [36, 37, 38, 39] Each organ system tends to be infected by a particular set of
pathogens (see below).
Lower respiratory tract infections cause septic shock in 35-50% of patients. [36, 37, 38, 39] The following
are the common pathogens:
 Streptococcus pneumoniae
 Klebsiella pneumoniae
 Escherichia coli
 Legionella spp
 Haemophilus spp
 Staphylococcus aureus

31
  Pseudomonas spp
 Anaerobes
 Gram-negative bacteria
 Fungi (see the image below)
Source of Infection
In septic shock, it is important to identify any potential source of infection. This is particularly
important in cases where a site of infection can be removed or drained, as in certain intra-
abdominal infections, soft-tissue abscesses and fasciitis, or perirectal abscesses. The following
physical signs help localize the source of an infection:
 Central nervous system (CNS) infection – Profound depression in mental status and signs
of meningismus (neck stiffness)
 Head and neck infections – Inflamed or swollen tympanic membranes, sinus tenderness,
nasal congestion or exudate, pharyngeal erythema and exudates, inspiratory stridor, and
cervical lymphadenopathy
 Chest and pulmonary infections – Dullness on percussion, bronchial breath sounds,
localized rales, or any evidence of consolidation
 Cardiac infections – Any new murmur, especially in patients with a history of injection or
IV drug use
 Abdominal and GI infections – Abdominal distention, localized tenderness, guarding or
rebound tenderness, and rectal tenderness or swelling
 Pelvic and GU infections – Costovertebral angle tenderness, pelvic tenderness, pain on
cervical motion, adnexal tenderness or masses, and cervical discharge
 Bone and soft-tissue infections – Focal erythema, edema, tenderness, crepitus in
necrotizing infections, fluctuance, pain with joint range of motion, and joint effusions and
associated warmth or erythema
 Skin infections – Petechiae, purpura, erythema, ulceration, bullous formation, and
fluctuance

32
Treatment
The first priority in any patient with severe sepsis or septic shock is stabilization of their airway
and breathing. Next, perfusion to the peripheral tissues should be restored.

Stabilize respiration

Supplemental oxygen should be supplied to all patients with sepsis and oxygenation should be
monitored continuously with pulse oximetry. Intubation and mechanical ventilation may be
required to support the increased work of breathing that typically accompanies sepsis, or for
airway protection since encephalopathy and a depressed level of consciousness frequently
complicate sepsis.

Sedative and induction agents (eg, etomidate) used to intubate patients with severe sepsis or
septic shock are discussed separately. Other aspects of intubation and mechanical ventilation are
similarly described elsewhere. (See "Sedation or induction agents for rapid sequence intubation
in adults" and"Advanced emergency airway management in adults" and "Rapid sequence
intubation in adults" and"The decision to intubate" and "The difficult airway in adults".)
Chest radiographs and arterial blood analysis should be obtained following initial stabilization.
These studies are used in combination with other clinical parameters to diagnose acute lung injury
(ALI) or acute respiratory distress syndrome (ARDS), which frequently complicate sepsis.
(See "Acute respiratory distress syndrome: Clinical features and diagnosis" and "Mechanical
ventilation in acute respiratory distress syndrome"

33
 DISCUSSION

SIMILARITY

There have a few similarity I found in real case (at Surgical ward 9), Reference A and
Reference B. First similarity I found in this three cases is its definition. Real case, Reference A
and B said that septic shock is rarely found in adults who were get infected and practicing low
hygiene and is characterized by stomach blockage that in which may cause food accumulated. At
the same time, bacteria infection, most often with Streptococcus and staphylococcus is
responsible for inflammation of the stomach muscle, particularly the stomach cell itself or
sometimes perforated cells. Both upper and lower respiratory tract symptoms are seen in this
illness which, for most previously healthy patients, is a self-limited and requires only supportive
care.

Second similarity I found is an aetiology of the bronchiolitis. The real case, Reference A
and B, said the causes of septic shock is Streptococcus, staphylococcus .But this three cases said
more frequent causes are streptococci pneumonia, Third similarity of septic shock is its sign and
symptoms. Real case, Reference A and Reference B said that the sign and symptom of the septic
shock is first start with rapid breathing, nause, vomiting, poor oral intake and fatigue.

Other similarity I found is an investigation of the septic shock. After investigate the real
case, Reference A and B, we can found that this three cases is made clinically on the basis of a
thorough history, physical examination to identify the correct diagnosis. Last but not least,
similarity I found in real case and references is the advices or prevention of septic shock. This
three cases said septic shock can be prevented by washing hands well and often. It may help to
keep patient away from airbone infection and other infection. Second advice is we can prevent
septic shock by protect the patient from smoke. This is because patient who are exposed to
cigarette smoke are more likely to develop severe oral-infection compared with those from
smoke-free homes. Third is advice the patient to eat healthy diet and drink plenty of water to
prevent from dehydration. At the same time, patient also have to take plenty of rest either in or
out of bed. Other than this, we can encourage daughter to take care of their mother, particularly
of longer duration, seems to have protective effective. Last but not least, we can advice patient to
eat medications followed by the dosage.

As a conclusion, we can understand that, real case, Reference A and B are used same
definition, sign and symptoms and aetiology of cellulitis.

34
 DIFFERENCE

There have a few difference found in this real case, Reference A and Reference B. First
difference I found from in real case and Reference A and B is even majority sign and symptoms
of cellulitis is same but have few symptoms are not same as in real case. Reference A said the
sign and symptoms of cellulitis is localized skin redness or inflammation that increases in size as
the infection spreads. But Reference B said sign and symptoms of septic shock is
lightheadedness, decreased energy, nausea and vomitting.

Second difference I found from in real case and Reference A and B is even majority
investigation is same but have few test that not same as in real case. For example according to
laboratory investigation, real case used blood test and renal profile test while Reference A and B
used rule duplex ultrasound and also vomiting sample may be done for microb testing to confirm
an infection and identify the specific infexted bacteria, but this test does not change clinical
decision making or outcomes.

In the term of pharmacology treatment, I found doctor prescribed drugs like IV

cefuroxime, IV Metrodinazole , Tramadol and paracetamol 1 gram. This drugs help to decrease
the sign and symptoms of septic shock. While author in Reference A and B suggest many
treatments for septic shock. First treatment which suggest by this two authors is providing were
treated with vancomycin or other antiMRSA therapy. In hospitalized pyloromyotomy is a
relatively simple procedure with excellent outcome, the operation is often performed by general
surgeons without subspecialty training in pediatric surgery. There has been controversy in the
literature about whether outcomes for this operation are the same when the operation is
performed by general surgeons as it is when the operation is performed by pediatric surgeons.
This controversy has become more heated in recent years, as evidence for volume-outcome and
training-outcome relationships accumulates for a variety of surgical procedures ,. In a view of
author in Reference A said intravenous fluids are necessary to correct dehydration and maintain
hydration in a patientwith poor oral intake secondary to the infection. For sicker adult, fluids
should be given intravenous (IV) initially, and the level of hydration should be monitored by
urine output and specific gravity and by serum electrolyte determinations. In other hand author in
Reference B said, empirical therapy for infection due streptococcus pneumonia and methicillin-
sensitive S. aureus is still recommended (A-II), whereas therapy for CA-MRSA is reserved for
patients who fail B-lactam therapy or who are severely ill. This statement shows that this authors
thought that if the first line treatment does not work then should use other type of treatment in
order to minimize the infection

As a conclusion, we can understand that the real case, Reference A and B is used
different pharmacology treatment as I wrote above. This shows there have a different
pharmacology treatment for septic shock cases. Other than that, even one investigation are same
but there also have a different laboratory test carry out by in real case, Reference A and B to

35
identify the correct diagnose. Not only that, there also have different sign and symptoms of
septic shock even majority is same as stated above.

Conclusion
Successful management of duodenal perforation is contingent on accurate intraoperative
recognition of the complication. The simplest surgical option is to repair the perforation with
several mucosal sutures, with or without the addition of an omental patch. Alternatively, some
surgeons completely close the myotomy, rotate the pylorus 180°, and perform a second myotomy
on the posterior side of the pylorus. Because this is a relatively rare complication, there are no
data in the literature that compare these approaches. Repeat operations after pyloromyotomy are
rarely performed, and usually due to an incomplete first operation or less commonly an
unrecognized perforation. Most authors recommend doing a second pyloromyotomy on the other
side of the pylorus in this situation. Recurrent HPS after few weeks of tolerating feeds and
weight gain has also been described, and probably represents a different process than incomplete
pyloromyotomy. Far more common causes for persistent vomiting postoperatively are
gastroesophageal reflux and gastritis; these should be considered if emesis persists, particularly if
the vomiting is not after every feed. Contrast radiography can demonstrate reflux or gastric outlet
obstruction, but is of little help postoperatively to determine whether there has been an
incomplete pyloromyotomy, since the radiological picture does not change perceptibly after
surgery.57 In rare cases, a child with HPS may also have a congenital cause of obstruction such
as duodenal web,which may cause persistent obstruction requiring additional surgery. Ultrasound
is also of limited value in the postoperative period, as the muscle thickness and length has been
shown to take up to 4 to 5 months to return to normal.58 Mortality after pyloromyotomy is less
than 0.4% in most major centers.1 Long-term sequelae are rare, but acquired HPS can result
from an unrecognized perforation and leak, and small bowel obstruction from adhesions has been
described.

Prognosis
Mortality figures for severe sepsis and septic shock have commonly been quoted as ranging from
20% to 50%. Clinical trials from the past decade have found the mortality associated with septic
shock to range from 24% to 41%. [36, 37, 38, 39] Although one report noted that crude hospital
mortality for severe sepsis was significantly lower in the United States (28%) than in Europe
(41%), the difference ceased to be significant when adjusted by disease severity. [38]
Important to note, in a 12-year (2000-2012) review of survival from severe sepsis from the
Australia and New Zealand ICU database, mortality has decreased from 35% to 18% with
decreasing occurrence in all age groups and across all types of hospital settings. These survival
improvements are especially important because in this same time span no new sepsis-specific

36
treatments were introduced, suggesting that improved overall quality of care was able to reduce
severe sepsis mortality by half. [47] Thus, studies using a before-and-after design to claim
improved sepsis survival are fundamentally flawed because of this nonspecific survival
improvement.
Mortality has been found to vary according to the degree of illness, which may range along a
spectrum extending from sepsis to severe sepsis to septic shock. The following clinical
characteristics are related to the severity of sepsis:
 Abnormal host response to infection
 Site and type of infection
 Timing and type of antimicrobial therapy
 Offending organism
 Development of shock
 Any underlying disease
 Patient’s long-term health condition
 Location of the patient at the time of septic shock onset
 Host immunogenetic variation
Factors consistently associated with increased mortality in sepsis include advanced age, comorbid
conditions, and clinical evidence of organ dysfunction. [40, 45] One study found that in the setting
of suspected infection, simply meeting SIRS criteria, without evidence of organ dysfunction, did
not predict increased mortality; this finding suggests that organ dysfunction is a better predictor
than SIRS criteria alone. [45] However, there is evidence that meeting greater numbers of SIRS
criteria is associated with increased mortality. [48]
Notably, tachypnea is the SIRS criterion that best predicts an adverse outcome. This is likely
because tachypnea is also an indicator of pulmonary organ dysfunction and a feature commonly
associated with pneumonia and ARDS, both of which are associated with increased mortality in
sepsis. Altered mental status is considered a sign of organ dysfunction and is also associated with
increased mortality.
In one epidemiologic study, reported mortality figures were 7% for SIRS, 16% for sepsis, 20% for
severe sepsis, and 46% for septic shock. [49] Poor prognostic factors included the following:
 Advanced age
 Infection with a resistant organism

37
  Impaired host immune status
 Poor prior functional status
 Continued need for vasopressors past 24 hours
 Development of sequential organ failure, despite adequate supportive measures and
antimicrobial therapy
A link between impaired adrenal function and higher septic shock mortality has been suggested.
The adrenal gland is enlarged in patients with septic shock as compared with control subjects. A
study by Jung et al found that the absence of this enlargement, indicated by total adrenal volume
of less than 10 cm3, was associated with increased 28-day mortality in patients with septic shock.
[50]
A multicenter prospective study published by Brun-Buisson et al reported a mortality of 56%
during ICU stays and 59% during hospital stays, [3] with 27% of all deaths occurring within 2
days of the onset of severe sepsis and 77% occurring within the first 14 days. The risk factors for
early mortality in this study were as follows:
 Higher severity of illness score
 Acute failure of 2 or more organ systems at the time of sepsis
 Shock
 Low blood pH (< 7.3)
Studies have shown that appropriate selection and early administration of antibiotics (ie, antibiotics
that are effective against the organism that is ultimately identified) lead to a significant reduction
in mortality. [51] For this reason, it is important to initiate broad-spectrum coverage until the
specific organism is cultured and antibiotic sensitivities are determined.
Although mortality is known to be high, the effect of sepsis on survivors’ quality of life of
survivors has not been well characterized until comparatively recently. It is increasingly evident
that septic shock is often a major sentinel event that has lasting effects on the patient’s
independence, reliance on family support, and need for long-term nursing home or institutionalized
care. [52]
Prolonged tissue hypoperfusion can lead to long-term neurologic and cognitive sequelae.
[14] Newer evidence shows that septic shock in elderly persons leads to significant long-term
cognitive and functional disability in comparison with hospitalized individuals who have
nonsepsis conditions

38
Reference;

file:///C:/Users/Dgreat/Downloads/74834425-pyloric-stenosis.pdf
 https://medlineplus.gov/ency/article/000668.htm
 https://www.healthline.com/health/septic-shock
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5538252/
 https://www.webmd.com/a-to-z-guides/sepsis-septicemia-blood-infection
 https://www.cancer.ca/en/cancer-information/diagnosis-and-treatment/managing-
side-effects/septic-shock/?region=on

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