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1
CASE REPORT
SEPSIS
Presenters : Shalini Shanmugalingam
M. Aripandi Wira
Day/Date :
Supervisor : dr. Wisman Dalimunthe, Sp.A(K)
CHAPTER 1
INTRODUCTION
1.1. Background
Tuberculosis is an ancient disease that is known to have existed in
prehistoric times, it remains one of the most important infectious disease in
the world. 1 Tuberculosis was recognized to be an infectious disease until
1882 when Koch identified Mycobacterium tuberculosis. 2
Tuberculosis still is one of the deadliest disease in the world killing nearly 2
million people every year. 1 More than nine per cent of all tuberculosis cases
occur in the developing countries, where limited resources are available for
optimal treatment.3 Tuberculosis continues to be an important cause of
morbidity and mortality for worldwide.4
According to statistics, one third of the world populations are infected with
Tuberculosis.4 In 2011, nearly 9 million people around the world become
sick with TB disease.5 From the total 9 million new cases of tuberculosis , 1
million are pediatrics age < 15 years old.5 A total of 10,528 TB cases (a
rate of 3.4 cases per 100,000 persons) were reported in the United States in
2011. Both the number of TB cases reported and the case rate decreased;
this represents a 5.8% and 6.4% decline, respectively, compared to 2010.5
2
Annually, 250.000 new cases of tuberculosis in Indonesia and
approximately 100.000 death because of tuberculosis.6 Tuberculosis is the
main cause of the death among the infection disease and the 3 rd cause of
death at all ages after cardiovascular and acute respiratory infection.6 Di
negara berkembang,TB pada anak berusia <15 tahun adalah 15% dari
seluruh kasus TB, sedangkan di negara maju, lebih rendah yaitu 5%-7%.
Pada survei nasional di Inggris dan Wales yang berlangsung selama setahun
pada tahun 1983, didapatkan bahwa 452 anak berusia <15 tahun menderita
TB.14 Laporan mengenai TB anak di Indonesia jarang didapatkan,
diperkirakan jumlah kasus TB anak adalah 5%-6% dari total kasus TB.
Berdasarkan laporan tahun 1985, dari 1261 kasus TB anak berusia <15
tahun, 63% di antaranya berusia <5 tahun. Hasil penelitian di dua
kecamatan di Kotamadya Bandung tahun 1999–2001, didapatkan 4,3%
(63/1482) anak usia 6–59 bulan, menderita TB.15 Data seluruh kasus TB
anak dari tujuh rumah sakit Pusat Pendidikan Indonesia selama 5 tahun
(1998-2002) dijumpai 1086 kasus TB dengan angka kematian bervariasi
dari 0%-14,1%. Kelompok usia terbanyak 12-60 bulan (42,9%), sedangkan
bayi <12 bulan didapatkan 16,5%.16 Laporan hasil Riset Kesehatan Dasar
(Riskesdas) tahun 2007, didapatkan
prevalensi 12 bulan TB paru klinis di Indonesia 1%
dengan kisaran 0,3% (Lampung) sampai 2,5% (Papua).
Berdasarkan kelompok umur dijumpai prevalensi TB,
kurang dari 1 tahun 0,47%, 1–4 tahun 0,76% dan
antara 5–14 tahun 0,53%.
16
Selama tahun 1985-1992, peningkatan TB
paling banyak terjadi pada usia 25-44 tahun
(54,5%), diikuti oleh usia 0-4 tahun (36,1%),
dan 5-12 tahun (38,1%). Pada tahun 2005,
diperkirakan kasus TB naik 58% dari tahun 1990,
90% di antaranya terjadi di negara berkembang. Di
3
Amerika Serikat dan Kanada, peningkatan TB pada
anak berusia 0-4 tahun 19%, sedangkan pada usia
5-15 tahun 40%. Di Asia Tenggara selama 10 tahun,
diperkirakan jumlah kasus baru 35,1 juta, 8% di
antaranya (2,8 juta) disertai infeksi HIV. M
1.2. Objective
The aim of this study is to explore more about the theoretical aspects on
sepsis, and to integrate the theory and apply it to the case that we found in clinical
settings.
CHAPTER 2
LITERATURE REVIEW
2.1. Definition
The systemic inflammatory response syndrome (SIRS) in pediatrics requires
the presence of abnormal temperature (hypothermia and hyperthermia) or
leukocytosis, in the presence of one other criterion (abnormal temperature,
leukocytosis, tachypnea, or tachycardia).4
Sepsis is defined as systemic inflammatory response syndrome (SIRS)
associated with infection triggered by a known or highly suspected pathogen.
Severe sepsis is defined as sepsis in the setting of acute respiratory distress
syndrome, cardiovascular organ dysfunction, or two or more other organ
dysfunctions (respiratory, renal, hematologic, neurologic, or hepatic).4,5
Septic shock is defined clinically as the presence of tachycardia and poor
perfusion with or without hypotension, the latter being marker of decompensated
shock and not required to make the diagnosis of septic shock as in adults.6
2.2. Epidemiology
4
In the developing world, sepsis accounts for 60-80% of lost lives per year in
childhood, killing more than 6 million neonates and children yearly and is
responsible for > 100.000 cases of maternal sepsis. Every hour, about 36 people
die from sepsis.2
Age is a major influence on the epidemiology of severe sepsis in the United
States. Differences are prevalent among children of different ages and between
children and adults. Most strikingly, adults and children differ in physiology,
predisposing diseases, and sepsis management strategies. For example, premature
birth is an obvious risk factor for pediatric sepsis that is not relevant in adults.
Similarly, national vaccination programs may have larger effects on sepsis in
pediatric vs. adult patients. Severe sepsis among infants is dominated by perinatal
events.7
After infancy, epidemiologic borders between populations are less distinct;
however, age-related differences continue to occur, especially regarding
underlying diseases, which occur in nearly half (49%) of children who develop
severe sepsis.7
Worldwide, 1.6 million neonates die every year from infection8 and 60% of
deaths in developing countries occur as a result of communicable disease.
Fortunately, sophisticated diagnostic tests and treatment strategies are not
requisite to improving sepsis outcomes.7
According to the site of infection and microbiologic etiology, the majority of
infections causing sepsis were respiratory (64%), followed by digestive and
urinary tract infections (18% and 12% respectively). Respiratory infections
predominated in toddlers (45% of the cases), whereas digestive sepsis was
particularly common in infants (36%). From the microbiologic aspect, gram-
negative bacteria caused the majority of infections that evolved with sepsis.
Enterobacteriaceae caused most of gram-negative infections (59%), with
Escherichia coli (56%) and Klebsiella pneumoniae (12%) being the most frequent
pathogens. Pseudomonas aeruginosa (10%) was the third most frequent agent of
Gram-negative sepsis. The most common Gram-positive infecting organism was
5
Staphylococcus aureus (75%). Atypical pathogens were identified in a minority of
patients (4%).9
2.3. Etiology and risk factor
Sepsis may develop as a complication of a localized infection or may follow
colonization and mucosal invasion by virulent pathogens (see Table 2-1).
Children 3 month to 3 year of age are at risk for occult bacteremia that will
occasionally progress to sepsis. Patients at risk for sepsis include infants, children
with serious injuries, children on chronic antibacterial therapy, malnourished
children, and children with chronic medical problems. Also, children who are
immune suppressed (transplant recipients on immunosuppressive regimens,
patients on chemotherapeutic agents or corticosteroids, patients with acquired or
congenital immune deficiencies) are at an increased risk for complications from
infection, including sepsis and septic shock.10
The infectious agents associated with sepsis in pediatric patients vary with
the patient's age and immune status. In the neonatal age group, group B
streptococcus, Escherichia coli, Listeria monocytogenes, enteroviruses, and herpes
simplex virus are the pathogens most commonly associated with sepsis. In older
children Streptococcus pneumoniae, Neisseria meningitidis, and Staphylococcus
aureus (methicillin-sensitive or resistant) are more common. Toxic shock
syndrome from group A streptococcus or S. azrreus can also be seen in older
children. Rickettsia rickettsi causing Rocky Mountain spotted fever occurs in
endemic areas and can lead to septic shock. Nosocomial (hospitalacquired)
infections pose a special risk to immunocompromised patients. Intravenous and
arterial catheters, urinary catheters, and endotracheal tubes are portals for the
development nosocomial infections. Invasive procedures can also lead to
nosocomial infections. Infections with gram-negative bacteria (e.g., Escherichia
coli, Pseudomonas, Acinetobacter, Klebsiella, Enterobacter, Serratia) and fungi
(e.g., Candida, Aspergilus) most often occur in immunocompromised and
hospitalized patients colonized with these organisms. Polymicrobial sepsis occurs
in high-risk patients and is associated with catheters, gastrointestinal disease,
6
neutropenia, and malignancy. Unusual pathogens should be suspected in patients
who have traveled or been exposed to products or people from distant lands or
who are immunocompromised secondary to malignancy, T- or B-cell defects, or
asplenia (acquired or congenital). Pseudobacteremia may be associated with
contaminated heparin flush solutions, intravenous solutions, albumin,
cryoprecipitate, and infusion equipment. Contaminants include water-borne
organisms such as Burkholderia cepacia, Pseudomonas aeruginosa, and Serratia.10
7
Table 2-1 Differential diagnosis of SIRS10
INFECTION CARDIO-PULMONARY
METABOLIC-ENDOCRINE
Bacteremia or meningitisViral illness EncephalitisRickettsiaeSyphilisVaccine reaction Toxin-mediated reaction
Pneumonia Pulmonary emboliCongestive heart failureArrhythmiaPericarditisMyocarditis
Adrenal insufficiencyElectrolyte disturbances Diabetes insipidusDiabetes mellitusInborn errors of metabolism HypoglycemiaReye's syndrome
GASTROINTESTINAL HEMATOLOGIC NEUROLOGIC and others
Gastroenteritis with dehydrationVolvulusIntussusceptionAppendicitisPeritonitis (spontaneous, associated with perforation or peritoneal dialysis)HepatitisHemorrhage
Anemia MethemoglobinemiaSplenic sequestration crisisLeukemia or lymphoma
Intoxication Intracranial hemorrhageInfant botulismTrauma Guillain-Barré syndromeMyasthenia gravisAnaphylaxis Hemolytic-uremic syndromeKawasaki diseaseErythema multiformeHemorrhagic shock–encephalopathy syndrome
Sepsis is more often occur in children with risk factor. The risk factor for
sepsis can be seen in the table below.11
Table 2-2 Risk Factor for Sepsis11
1. Prematurity2. Age3. Immune deficiency
MalnutritionA-gamma-globulinemiaSickle cell anemiaSevere combined immunodeficiency
AIDSAsplenismComplement DeficiencyNeutrophl chemotactic factor defect
4. History of Current illness
8
MalignancyGalactosemiaParaplegiaExtensive burn injury
Nephrotic syndromeUrinary tract infection from gonococcus Intravenous drug addiction
5. IatrogenicUrinary catheterization Surgery
Endotracheal intubationContinuous peritoneal dialysis
2.4. Pathogenesis10
Shock is a state of circulatory dysfunction that occurs from (1) decreased
cardiac output and or mal-distribution of regional blood flow and (2) increased
metabolic demands with or without impaired oxygen utilization at the cellular
level despite adequate oxygen delivery. Cardiac output may be high, low, or
normal. The body has compensatory mechanisms to maintain blood pressure
through increased heart rate and peripheral vasoconstriction. Hypotension, a late
finding in infants and children, occurs when the compensatory mechanisms are
failing and cardiorespiratory arrest is imminent. Septic shock is a combination of
the three classic types of shock: hypovolemic, cardiogenic, and distributive.
Hypovolemia from intravascular fluid losses occurs through capillary leak.
Cardiogenic shock results from the myocardial-depressant effects of sepsis.
Distributive shock is the result of decreased systemic vascular resistance. The
degree to which a patient will exhibit each of these responses is variable. Warm
shock occurs in some patients with increased cardiac output and decreased
systemic vascular resistance. Cold shock occurs in other patients with decreased
cardiac output and elevated systemic vascular resistance. In both cases, perfusion
to major organ systems may be compromised. Recent data suggest that, unlike
adults in septic shock who present with vasodilation and high cardiac output,
newborns and children may have fluid refractory shock and develop progressive
myocardial dysfunction. It is important to distinguish between the infection and
the host response to the infection, the inflammatory response. The host's immune
response, through the actions of the cellular and humoral immune systems, and
the reticular endothelium system, prevents the body from developing sepsis in
response to breaches in the host defense system. However, this host immune
9
response produces an inflammatory cascade of highly toxic mediators, including
hormones, cytokines, and enzymes. If this inflammatory cascade is uncontrolled,
SIRS occurs with subsequent organ and cellular dysfunction from derangement of
the microcirculatory system.
Microcirculatory dysfunction results in endothelial injury, release of
vasoactive substances, changes in cardiovascular tone, mechanical obstruction of
the capillary beds from aggregation of cellular elements, and activation of the
complement system. At the cellular level there is decreased oxidative
phosphorylation secondary to decreased oxygen delivery, anaerobic metabolism
secondary to decreased adenosine triphosphate (ATP), glycogen depletion, lactate
production, increased cytosolic calcium, activation of membrane phospholipases
(further depleting ATP), and release of fatty acids with prostaglandin formation.
The inflammatory cascade is initiated by toxins or superantigens.
Endotoxin (a lipopolysaccharide), mannose, and glycoprotein components of the
cell wall of gram-negative bacteria as well as fungi and yeast bind to macrophages
leading to activation and expression of inflammatory genes. Superantigens or
toxins associated with gram-positive bacteria, mycobacteria, and viruses activate
circulating lymphocytes and initiate an inflammatory mediator cascade.
Biochemical responses include the production of arachidonic acid
metabolites, release of myocardial depressant factors, release of endogenous
opiates, activation of the complement system, as well as the production and
release of many other mediators. Arachidonic acid metabolites include (1)
thromboxane A2, which causes vasoconstriction and platelet aggregation; (2)
prostaglandins, such as PGF2,, which causes vasoconstriction, and PGI,, which
causes vasodilation; and (3) leukotrienes that cause vasoconstriction,
bronchoconstriction, and increased capillary permeability. Myocardial depressant
factors, tumor necrosis factor-a (TNF), and some of the interleukins cause
myocardial depression not only via direct myocardial injury but also by an
intracardiac increase in inducible nitric oxide synthase. Endogenous opiates,
including P-endorphin, decrease sympathetic activitv, decrease mvocardial
contractilitv, and cause vasodilation. Activation of the complement system leads
10
to release of vasoactive mediators that increase capillary permeability, cause
vasodilation, and cause activation and aggregation of platelets and granulocytes.
Endogenous mediators of sepsis continue to be identified and currently
include TNF, interleukin 1 (IL-I), IL-2, IL-4, IL-6, IL- 8, platelet activating factor
(PAF), interferon-y, eicosanoids (leukotrienes B4, C4, D4, and E4; thromboxane A2;
prostaglandins EL and IL), granulocyte-macrophage colony-stimulating factor,
endothelium-derived relaxing factor, endothelin-1, complement fragments C3a
and C5a, toxic oxygen radicals, proteolytic enzymes from polymorphonuclear
neutrophils, platelets, transforming growth factor-p, vascular permeability factor,
macrophage-derived procoagulant and inflammatory cytokine, bradykinin,
thrombin, coagulation factors, fibrin, plasminogen activator inhibitor (PAI-I),
myocardial depressant substance, endorphin, heat shock proteins, and adhesion
molecules (endothelin-derived adhesion molecule [E-selectin]; intercellular
adhesion molecule-l [ICAM]; vascular adhesion molecule-1 [VCAM]).
The clinical manifestations of sepsis and shock are mediated through the
inflammatory cascade. Hypovolemia, cardiac and vascular failure, acute
respiratory distress syndrome, insulin resistance, decreased CYP450 activity
(decreased steroid synthesis), coagulopathy, and unresolved or secondary
infection are all results of the inflammatory cascade. TNF and other inflammatory
mediators increase vascular permeability, leading to diffuse capillary leak,
decreased vascular tone, and, at the microcirculatory level, an imbalance between
perfusion and metabolic demands of the tissue. TNF and IL-1 stimulate the
release of proinflammatory and anti-inflammatory mediators causing fever and
vasodilatation. Arachidonic acid metabolites lead to the development of fever,
tachypnea, ventilation-perfusion abnormalities, and lactic acidosis. Nitric oxide,
released from the endothelium or inflammatory cells, is a major contributor to
hypotension. Myocardial depression is caused by myocardial depressant factors,
TNF, and some interleukins through direct myocardial injury, depleted
catecholamines, increased P-endorphin, and production of myocardial nitric
oxide.
11
In addition to treating the underlying infection, therapies to augment the
host defense, block trigger events, prevent leukocyte endothelial interaction, and
inhibit vasoactive substances, cytokines or lipid mediators are being investigated.
To date, the results of clinical trials investigating drugs targeting the rnediators of
SIRS have been disappointing. Trials have been conducted with anti-endotoxin
antibodies, antioxidant compounds, an IL-1 receptor antagonist, IL-1 antibodies,
bradykinin-receptor antibodies, cyclo-oxygenase inhibitors, thromboxane
antagonists, PAF antagonists, inhibitors of leukocyte-adhesion molecules, nitric
oxide antagonists, anti-TNF antibody, bactericidal permeability increasing
protein, and recombinant human activated protein C. Recombinant human
activated protein C (drotrecogina) studies have shown improvement in the 28-day
survival in adults, but enrollment in a pediatric trial was closed early because of
an unfavorable risk-benefit ratio particularly in neonates. The best treatment is
early recognition, early antimicrobial therapy, and early goal-directed therapy.
2.5. Clinical Manifestation10
The initial signs and symptoms of sepsis include alterations in temperature
regulation (hyperthermia or hypothermia), tachycardia, and tachypnea. In the
early stages (hyperdynamic phase), the cardiac output increases in an attempt to
maintain adequate oxygen delivery to meet the increased metabolic demands of
tissues. As sepsis progresses, cardiac output falls in response to the effects of
numerous mediators. Although hypotension (systolic arterial pressure <2 standard
deviations below the mean for age) is a late finding in children with sepsis, it is
not a criteria for the diagnosis of shock in infants and young children. Other signs
of poor cardiac output include delayed capillary refill, diminished peripheral and
central pulses, cool extremities, and decreased urine output. Alterations in mental
status, including confusion, agitation, lethargy, anxiety, obtundation, or coma, can
also be signs of poor cardiac output. Capillary leak develops from altered vascular
permeability. Lactic acidosis occurs as shock progresses and is the consequence of
increased tissue production and decreased hepatic clearance.
12
Cutaneous lesions seen in septic patients include petechiae, diffuse
erythema, ecchymoses, ecthyma gangrenosum, and symmetric peripheral
gangrene. Jaundice can be seen either as a sign of infection or as a result of
MODS. The patient may also have evidence of focal infection such as meningitis,
pneumonia, arthritis, cellulitis, or pyelonephritis.
2.6. Diagnosis10
The diagnosis of sepsis requires SIRS in the presence of proven infection or
a clinical picture consistent with infection. An infectious etiology should be
sought by culturing clinically appropriate specimens taken from body fluids
(blood, urine, cerebrospinal fluid, abscesses, peritoneal fluid, etc.). Infectious
disease and intensive care consults are necessary. Cultures take time for
incubation and are not always positive. Additional evidence to identify an
infectious etiology as the cause of SIRS includes physical examination findings,
imaging (chest radiograph with evidence of pneumonia), presence of white cells
in normally sterile body fluids, and suggestive rashes such as petechiae and
purpura. Affected children should be admitted to an intensive care unit where
continuous, close invasive monitoring can be performed, including central venous
pressure and arterial blood pressure.
Laboratory findings often include evidence of hematologic abnormalities
and electrolyte disturbances. Hematologic abnormalities include
thrombocytopenia, prolonged prothrombin and partial thromboplastin times,
reduced serum fibrinogen levels and elevated fibrin split products, and anemia.
Also, elevated neutrophil and increased immature forms (bands, myelocytes,
promyelocytes), vacuolation of neutrophils, toxic granulations, and Dohle bodies
can be seen with infection. Neutropenia is an ominous sign of overwhelming
sepsis. Electrolyte abnormalities include hyperglycemia as a stress response or
hypoglycemia if glycogen reserves are exhausted. Other electrolyte abnormalities
include hypocalcemia, hypoalbuminemia, metabolic acidosis, and low serum
bicarbonate. Lactic acidosis can occur if there is significant anaerobic metabolism.
Renal and liver function may be abnormal if the patient develops MODS. Patients
13
with acute respiratory distress syndrome or pneumonia will have impaired
oxygenation (decreased PaO2) and ventilation (increased PaC02). Examination of
infected body fluids may reveal neutrophils and bacteria. Some biochemical
markers examination such as procalcitonin, CRP, etc, can be used to support the
diagnosis of sepsis.
Table 2-3 Laboratory indicators of sepsis12
Laboratory Test Findings CommentsWhite blood count
Leukocytosis /leucopenia
Endotoxemia may cause leucopenia
Platelet count Thrombocytosis or thrombocytopenia
High value early may be seen as acute phase response; low platelet counts seen in overt DIC
Coagulation cascade
Protein C deficiency; antithrombin deficiency; elevated D-dimer level; prolonged PT and PTT
Abnormalities can be observed onset of organ failure and without frank bleeding
Creatinine level Elevated from baseline Doubling-indicates acute renal injury
Lactic acid level Lactic acid > 4 mmol/L (36mg/dL)
Indicates tissue hypoxia
Liver enzyme level
Elevated alkaline phosphatase, AST, ALT, bilirubin levels
Indicates acute hepatocelular injury caused by hypoperfusion
Serum phosphate level
Hypophosphatemia Inversely correlated with proinflammatory cytokine levels
C-reactive protein (CRP) level
Elevated Acute phase response
Procalcitonin level
Elevated Differentiates infectious SIRS from noninfectious SIRS
2.7. Management
2.7.1 Initial Resuscitation5
The primary goals of therapy in the first hours following clinical
presentation are to maintain oxygenation and ventilation and achieve normal
perfusion. Important clinical parameters that are reflective of “normal perfusion”
14
include: capillary refill < 2 seconds, normal pulses with no differential between
the quality of peripheral and central pulses, warm extremities, normal mental
status, normal blood pressure for age and appropriate urine output for age.
2.7.2 Airway and oxygenation5
Early medical responders (e.g. EMS and transport personnel, ED staff)
should ensure a patent airway and appropriate protective airway reflexes are
present, especially if there is any alteration in mental status. When any degree of
distress or abnormal respiratory function is noted, the patient should be placed on
100% oxygen to ensure maximal oxygen saturation. While specific diagnosis of
sepsis is being evaluated, emergency support should include high flow
supplemental oxygen and evaluation for further respiratory support for acute
respiratory failure, which may be due to acute lung injury or shock. It includes
oxygen using non-rebreathing mask, nasal prong CPAP, tracheal tube with CPAP
or manual ventilation as per clinical situation. SpO2 of 94% is desirable.
Intubation and ventilation is indicated in-patients having hypoxemia not
responding to oxygen administration by non-invasive methods, hypotension
and/or clinical signs suggestive of myocardial dysfunction or pulmonary edema.12
In addition, myocardial dysfunction, which is often present in children with
sepsis, can be partially ameliorated by the application of positive pressure
ventilation by achieving a decrease in afterload (provided impairment of preload
is not too great). Therefore, early semi-elective intubation and positive pressure
mechanical ventilatory support should be strongly considered in this setting.
2.7.3 Fluid resuscitation
We recommend the protocolized resuscitation of a patient with sepsis
induced shock, defined as tissue hypoperfusion (hypotension persisting after
initial fluid challenge or blood lactate concentration 4 mmol/L). This protocol
should be initiated as soon as hypoperfusion is recognized and should not be
delayed pending ICU admission. During the first 6 hrs of resuscitation, the goals
15
of initial resuscitation of sepsis-induced hypoperfusion should include all of the
following as one part of a treatment protocol:
Central venous pressure 8–12 mmHg
Mean arterial pressure (MAP) ≥ 65mm Hg
Urine output 0.5 ml/kg/hr
Central venous (superior vena cava) or mixed venous oxygen saturation
70% or 65%, respectively.14
Early rapid fluid resuscitation is fundamental to septic shock survival. Pre-
load needs to be optimized to improve cardiac output and thus oxygen delivery.
Intravenous access may be difficult to achieve in children with poor
hemodynamics. In such a case, intraosseous line should be established if three
attempts have failed or 90 sec have lapsed.13
Fluid resuscitation is best initiated with rapid infusion of normal saline or
Ringer’s lactate. Recent evidence clearly support the use of crystalloid (normal
saline) in pediatric septic shock. There may be a role of colloids (albumin,
dextrans, starch and gelatin in saline) in patients with a pre-existing low plasma
oncotic pressure state such as protein energy malnutrition, nephrotic syndrome,
acute severe burns or liver disease, in patients with malaria and dengue shock
syndrome. In hypotensive patients, fluids should be given as rapidly as possible in
aliquots of 20 ml/kg using a syringe and a 3-way stopcock and rapid pullpush or
pressure bag system to achieve therapeutic goals. In patients with normal blood
pressure fluids should be given in aliquots of 20 ml/kg over 15–20 min. In a
randomized trial that compared slow and fast infusion rate, fast infusion did not
result in faster resolution of shock but incidence of pulmonary edema requiring
intubation doubled if fluids were given at rate of 40 ml in 15 min, compared to 20
ml over 15 min. Children with septic shock usually require 40–60 ml/kg,
sometimes up to 90–110 ml/kg in the first hour of resuscitation. It may go up to
200 ml in 6 hr or 240 ml in 8 hr in staphylococcal diseases presenting with septic
shock, vasodilatory shock or shock due to gastrointestinal sepsis.13
If signs of shock persist despite adequate volume replacement and
perfusion of vital organ is jeopardized, inotropic drugs may be used to improve
16
cardiac output. The effects of a particular drug in an individual patient are
unpredictable and must be closely monitored. Drugs commonly used in pediatric
ICU to increase myocardial contractility include the following:15
a. Dopamine
The primary indication for dopamine is the need to increase myocardial
contractility after preload restoration. The usual dose is 5-20 mcg/kg/min titrated
to desired effect. Dopamine (in doses of more than 5 mcg/kg/min) should
preferably be given via central line to prevent ischemic necrosis of the skin.
b. Dobutamine
It is a selective β-1 agonist. The reduction in afterload and improved
myocardial performance lowers ventricular filling pressures. The usual dose is 5-
20 mcg/kg/min. It should be not used alone in septic shock due to it could cause
further drop in blood pressure. Dopamine or adrenaline can be used to prevent
hypotension owing to vasoconstrictive effect.
c. Adrenaline (epinephrine)
It is used in which dominant hemodynamic feature is peripheral vascular
failure, as in septic shock. At higher doses severe vasoconstriction can lead to
lactic asidosis and renal splanchnic ischemia. The usual dose is 0.1-1 mcg/kg/min.
It should be titrared closely and the minimum dose should be used as required.
d. Noradrenaline
In severe septic shock with hypotension despite the use of adrenaline
secondary to intense vasodilatation, noradrenaline may be useful in increasing
peripheral vascular resistance to improve blood pressure. The dose is 0.05-1
mcg/kg/min.
2.7.4 Elimination of Pathogen10
Soon after diagnosed the patient should be administered by initial
antibiotics. The preferred antibiotics are those one’s that are broad spectrum and
are predicted to be able to eliminate the most often gram positive and negative
bacteria that cause sepsis. For the initial phase, Ampicilin (200mg/kg/day/iv in 4
dose) combined with aminoglycoside (garamicin 5-7mg/kg/day/iv or amikacin 15-
17
20mg/kg/day/iv or netilmicin 5-6 mg/kg/day/iv in 2 dose) are preferred. In a
septic shock setting, the use of aminoglycoside should be monitored cautiously
due to septic shock is prone to kidney injury, thus another combination is
preferred if monitoring aminoglycoside is difficult which is ampicilin with
cefotaksim (100 mg/kg/day/iv in 3 dose). If there is a suspicion of the presence of
an anaerobic bacteria (for instance a focus infection in the abdomen, pelvis, mouth
, rectum) then the patient should be administered metronidazole or clindamicin
with another antibiotic which is suitable for enteric gram-negative bacteria.
2.7.5 Glycemic control16
Hyperglycemia is a common occurrence in critically ill patients due to
peripheral insulin resistance, relative insulin deficiency and impaired glucose
metabolism. There have been many studies that have shown as association
between elevated glucose and mortality in critically ill children, however none
established a causal relationship between untreated hyperglycemia and mortality
nor did they show a decrease in mortality with strict glycemic control. Given the
ongoing concern regarding the detrimental effects of inducing hypoglycemia with
insulin therapy, and studies which have shown poorer outcomes withsignificant
glucose variability, we do not recommend the routine use of insulin in
hyperglycemic states. Attention should be paid to controlling the amount of
glucose administered in the setting of hyperglycemia and the treatment of
prolonged hyperglycemia should be reserved for those cases in which the
hyperglycemia is causing clinical compromise (in the form of osmotic diuresis or
ketoacidosis).
2.7.6 Corticosteroid10
The benefit of corticosteroid in septic shock is still controversial, there are
difference in experiment results. Corticosteroid is thought to have benefit if given
in the early stadium of sepsis, however has to be administered in the presence of
adrenal glandula bleeding. The corticosteroid that is given are metyl prednisolone
(30 mg/kg/dose/iv) or dexamethasone (3 mg/kg/dose/iv).
18
2.8 Prognosis9
Hospital mortality generally varied little with age, except for the
significantly higher rate among infants, who were incurred for 47% of all deaths.
Because hospital mortality varied little with age, the number of deaths per
population paralleled the incidence rate, with a high rate in infants that fell
dramatically in older children. There was no gender-related difference in hospital
mortality.
The mortality rate was significantly increased by the severity of the septic
process: among the severe sepsis cases the mortality rate was 5%, whereas among
the patents with septic shock it was much higher: 53%. The risk of death also
increased with increasing number of failing organs, from 3.8% for those with
single organ dysfunction to 53.2% for those with four organ systems or more
failing.
19
CHAPTER III
CASE REPORT
Name : MA
Age : 1 year 5months
Sex : Male
Address : Jl. Besar Klumpang Kec Hamparan
Date of Admission : October 7th 2012
Major Complaint : Loss of consciousness
History : Loss of consciousness was experienced by the patient
since twelve days ago. Loss of consciousness was preceded by seizure. The
seizure was experienced for 3 days and frequent, with a duration of ± 5-10
minutes, involving the whole body with the
eyes directed upwards and the upper and lower limbs rigid and the seizure was
preceded with fever. Fever was found and recurrent fever was for the last 3 weeks,
with a characteristic of high fever and gone with administration of antipyretic.
Diarrhea was not found but there is a history of diarrhea for the last 2 weeks, the
frequency is hard to determinate due to the presence of colostomy, with a volume
of ± 200cc/day, blood and mucus was not found. This patient was first admitted to
H. Adam Malik General Hospital with chief complaint of abdominal discomfort
and emesis on September 18th 2012 and was diagnosed invagination from the
Surgery Department and undergone a laparatomy emergency surgery with a result
of colostomy. Patient was then transferred to the pediatric ICU on September 27 th
2012 based on chief complaint of loss of consciousness.
History of Birth: spontaneous labor, first child, birth weight: 4100 gram, birth
length: 50cm, immediate crying (+), cyanosis (-)
Feeding History
From birth to 6 months : Breast milk only
From 6 month to 9 month : Milk Porridge + Breast milk
20
From 9 month to now : Baby rice + Breast Milk
History of Growth and Development:
- The patient was able to sit at age 7 month
- The patient could stand up by himself at age 9 month
- The patient could walk with guidance since age 11 month
History of Immunization : Complete for age
History of previous illness : ileosecum invagination, gastroenteritis
History of previous medications : unclear
Physical Examination :
Generalized status
Body weight: 8.6 kg, Body length: 81 cm
Body weight in 50th percentile according to age: 11.5 kg
Body length in 50th percentile according to age: 81 cm
Body weight in 50th percentile according to body length: 11.5 kg
BW/BL: 8.6/11.5 x 100% = 74.7 %
BW/age: 8.6/11.5 x 100% = 74.7 %
BL/ age : 81/81 x 100% = 100 %
Presence Status
Sensorium : Apathies, Temperature: 38.7C
Anemic (-),icteric (-), dyspnea (-), cyanotic (-), edema (-).
Body weight (BW): 8.6 kg. Body length (BL): 81 cm
CDC: BW/Age = %, BL/Age = %, BW/BL = %
Localized status:
Head : Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-). Nose : NGT (+), nasal canul (+).
Ear and mouth: within normal limit.
21
Neck : Lymph node enlargement (-)
Thorax : Symmetrical fusiformis. Chest retraction (+).RR: 62 tpm,
regular, crackles (+/+), HR: 146 bpm, regular, murmur (-).,
stridor (-)
Abdomen : Soepel, peristaltic (+), colostomy (+) LLQ. Liver and spleen
not palpable
Extremities : Pulse: 136 bpm, regular, adequate pressure/volume, warm
axilla, Capillary Refill Time (CRT) < 3” BP: 110/70 mmHg.
Urogenital : Male, within normal limit
Physiologic reflexes: KPR (+), APR(+)
Pathologic reflexes : Oppenheim (-), Hoffman (-), Babinsky (-), Chaddock (-),
Gordon(-), Nuchal rigidity (-)
Laboratory findings:
CBC25/09/2012 27/09/2012 6/10/2012
Hemoglobin (Hb)
13.00 g% 9.20 g% 10.20 g%
Erytrocyte (RBC)
5.14 x 106/mm3 3.73 x 106/mm3 4.50 x 106/mm3
Leukocyte (WBC)
19.91 x 103/mm3 20.53 x 103/mm3 7.62 x 103/mm3
Hematocrite 36.60 % 27.60 % 30.30 %Trombocyte (PLT)
425 x 103/mm3 216 x 103/mm3 162 x 103/mm3
MCV 71.20 fL 74.00 fL 67.30 fLMCH 25.30 pg 24.70 pg 22.70 pgMCHC 35.50 g% 33.30 g% 33.70 g%Neutrofil 68.20 % 82.90 % 60.10 %Lymphocyte 12.60 % 7.70 % 26.90 %Monocyte 19.10 % 9.40 % 12.70 %Eosinophil 0.00 % 0.00 % 0.00 %Basophil 0.10 % 0.00 % 0.30 %
Blood Gas25/09/2012 27/09/2012 6/10/2012
pH 7.588 7.563 7.455PCO2 20.7 mmHg 36.7 mmHg 30.3 mmHgpO2 177.4 mmHg 183.3 mmHg 165.9 mmHgBicarbonate 19.4 mmol/L 32.3 mmol/L 20.9 mmol/L
22
(HCO3)Total CO2 20.0 mmol/L 33.4 mmol/L 21.8 mmol/LBE -0.8 mmol/L 9.5 mmol/L 2.3 mmol/LOxygen saturation 99.4% 98.9% 99.3%
Electrolyte26/09/2012 27/09/2012 6/10/2012
Calcium (Ca) 6.6 mg/dL 7.1 mg/dL 6.6 mg/dLNatrium (Na) 124 mEq/L 132 mEq/L 125 mEq/LKalium (K) 1.7 mEq/L 2.1 mEq/L 3.9 mEq/LPhosphor 1.4 mEq/L 2.1 mEq/L 4.2 mEq/LChloride (Cl) 90 mEq/L 96 mEq/L 104 mEq/LMagnesium (Mg) 1.15 mEq/L 1.04 mEq/L 1.28 mEq/L
Other test26/09/2012 28/09/2012 2/10/2012
Procalcitonin 47.27 ng/mL 3.12 ng/mL 35.92 ng/mL27/09/2012 28/09/2012 2/10/2012
Lactic Acid 1.5 mmol/L 1.0 mmol/L 4.9 mmol/L
Result Normal valueHST
PT 1.12 xINR 1.14
APTT 1.14 xTT 1.21 x
Fibrinogen 329 mg/dL 150-400D-dimer 1031 ng/dL <500
LiverTotal Bilirubin 0.30 mg/dL <1
Direct Bilirubin 0.17 mg/dL 0-0.2ALP 105 U/L <281
AST/SGOT 124 U/L <38ALT/SGPT 30 U/L <41
RenalUreum 9.10 mg/dL <50
Creatinin 0.26 mg/dL 0.24-0.41Uric Acid 3.3 mg/dL <7.0
Result Normal valueCSF analysis
Colour transparant TransparentLDH 62 U/L <200
Total Protein 12.00 mg/dL 10-40Leucocyte 0.004 x 103/uL <32Eritrocyte 0.001 x 103/uL
23
Glucose 60 mg/dL 32-82pH 8.0 7-8
PMN 75%MN 25%
Radiologic Findings :
a. Thorax x-ray (AP) on September 28th 2012
b. d CT-Scan on October 3rd 2012
Intepretation:
Infratentorial : the 4th ventricle and the cerebellum seems normal.
Intepretation of x-ray :
No enlargement of the heart
Sinus and diaphragm
normal
Both hilus normal
No sign of infiltrate on both
lungs
Normal vascular and
bronchus pattern
Conclusion: no signs of
abnormality of the heart and lungs
24
Supratentorial : there seems to have a hypodense area on the right and left the fronto-temporo-parietal
There seems to be no mass or any midline shifting Ventricular system and cortical sulci normal There seems to be no pathologic enhancement
Conclusion: Encephalitis
Working Diagnosis:
Encephalitis + Post laparatomy a/i Ileosecal invagination + Bronchopneumonia +
Moderate malnutrition + Sepsis
Management:
Head elevation 30o P: - IVFD D5% NaCl 0.9% 20 gtt/i
E: Diet F100: 140cc/3hours/OGT + mineral mix 2,8cc Ampicillin inj. 450mg/6 hours/iv Cefotaxime 250mg/6 hours/iv Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’ Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’ Metronidazole inj. 75mg/8 hours/iv Farmadol inj. 100mg Morphine inj. 8.5mg in 50cc D5% (tapering off dose 0.5cc/hour) Zinc 1x20mg Folic acid 1x1mg Multivitamin without Fe 1 x Cth1/2
Diagnostic Planning:
Complete blood count
Anemia profile
Electrolyte profile
Random blood glucose
Blood Gas Analysis
Septic workout
Culture urine, blood, feces and CSF
25
Follow Up
8th October 2012
S Deterioration of consciousness(+), fever(+), diarrhea(-), seizure(-)
O CNS syst :
CV syst :
Resp syst :
Met. syst :
Infec. syst:MS syst :
Unstable, GCS 14 (E4V4M6)Head: Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-).Stable, HR: 138 bpm, reg, murmur (-), BP: 93/61mmHg, MAP: 71mmHg , UOP: 680cc/24 hours(3.27cc/kgBB/hour)Unstable, Thorax: SF, epigastrial retraction (+),RR: 50 tpm, reg
crackles (-/-) H: Nasal flare (-), Nasal canul: 1/2-1 L/i.
UnstableAbdomen: soepel, peristaltic(+)N, stoma(+), feses(+),
albumin: 2.7Ca/Na/K/Cl/Mg/Ph :7.8/132/4.2/106/6.6/1.50/4.5Stable, fever (-), T: 38.1oC, Procalcitonin: 1.18Stable, post surgery wound: dry
A Encephalitis + Post laparatomy (D-19) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Sepsis with unstable CNS and metabolic system
P - Head elevation 30o - Fluid requirements: 1100cc-1200cc/day
P: - IVFD D20% = D5% NaCl(364cc) + D40%(136cc) > 15gtt/i-Aminofusin 7cc/hour
E: Diet F100: 95cc/3hours/OGT- Ampicillin inj. 450mg/6 hours/iv (D-5)- Cefotaxime 250mg/6 hours/iv (D-5)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-12)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D1-2)- Metronidazole inj. 75mg/8 hours/iv (D-12)- Farmadol inj. 100mg - Morphine inj. 8.5mg in 50cc D5% (tapering off dose 0.5cc/hour)- Zinc 1x20mg (D-12)- Folic acid 1x1mg (D-12)- Multivitamin without Fe 1 x Cth1/2 (D-9)- Ca Gluconas 4.3cc in 3.3cc D5% within 20’
26
- Albumin 25% 9.6cc- Check Ca and albumin levels post correction
9th October 2012
S Deterioration of consciousness(+), fever(-), diarrhea(-), seizure(-), ruam kemerahan pada bekas colostomy
O CNS syst :
CV syst :
Resp syst :
Met. syst :
Infec. syst:MS syst :
Unstable, GCS 14 (E4V4M6)Head: Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-).Stable, HR: 150bpm, reg, murmur (-), pulse: 150 bpm, p/v adequate, BP: 100/70mmHg, MAP: 80mmHg, CVC placed (D-9), UOP: 920cc/24 hours (4.43cc/kgBB/hour)Stable, Thorax: SF, epigastrial retraction (+),RR: 44 tpm,
reg ,crackles (-/-) H: Nasal flare (-) Nasal canul: 1/2-1 L/i.
Unstable, Abdomen: soepel, peristaltic(+)N, stoma(+), feses(+), Ca: 8.9
Stable, fever (-), T: 36.8oCStable, post surgery wound: dry
A Encephalitis + Post laparatomy (D-20) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Irritant Contact Dermatitis + Sepsis with unstable CNS, and metabolic system
P - Head elevation 30o - Fluid requirements: HS+20%op besar: 1060cc/hr
P: - IVFD D20% = D5% NaCl(364cc) + D40%(136cc) > 15gtt/i-Aminofusin 7cc/hour
E: Diet F100: 95cc/3hours/OGT- Ampicill;in inj. 450mg/6 hours/iv (D-6)- Cefotaxime 250mg/6 hours/iv (D-6)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-13)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-13)- Metronidazole inj. 75mg/8 hours/iv (D-13)- Farmadol inj. 100mg - Morphine inj. 8.5mg in 50cc D5% (tapering off dose 0.5cc/hour) (D-
10)- Zinc 1x20mg (D-13)- Folic acid 1x1mg (D-13)- Multivitamin without Fe 1 x Cth1/2 (D-10)- Pediasure 95cc/3 hours/NGT
27
- Gentamicin zalf- Check Procalcitonin and lactic acid levels
10th October 2012
S Fever(+), deterioration of consciousness(+), diarrhea(-), seizure(-), ruam kemerahan pada bekas colostomy
O CNS syst :
CV syst :
Resp syst :
Met. syst :
Infec. syst:MS syst :
Unstable, GCS 14 (E4V4M6)Head: Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-).Stable, HR: 140bpm, reg, murmur (-), pulse: 140bpm, p/v adequate, BP: 100/50mmHg, MAP: 66mmHg, CVC placed (D-10), UOP: 1220cc/24 hours (5.7cc/kgBB/hour)Stable, Thorax: SF, epigastrial retraction (+),RR: 36 tpm,
reg ,crackles (-/-)H: Nasal flare (-), Nasal canul: 1/2-1 L/i.Unstable, Abdomen: soepel, peristaltic(+)N, stoma(+),
feces(+): vol.±50cc , Stable, fever(+), T: 38.9oC, Lactic acid: 2.4, Pro: 0.82Stable, post surgery wound: dry
A Encephalitis + Post laparatomy (D-21) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Irritant Contact Dermatitis + Sepsis ec Acinetobacter baumanii with unstable CNS, and metabolic system
P - Head elevation 30o - O2 ½-1 L/i- Fluid requirements: HS+20%op besar: 1060cc/hr
P: - IVFD D20% = D5% NaCl(364cc) + D40%(136cc) + KCl (10mEq) + Ca Gluconas (10cc) > 11gtt/i
-Aminofusin 11cc/hourE: Pediasure: 75cc/3hours/OGT
- Metronidazole inj. 75mg/8 hours/iv (D-14)- Ampicillin inj. 450mg/6 hours/iv (D-7)- Cefotaxime 250mg/6 hours/iv (D-7)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-14)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-14)- Farmadol inj. 100mg - Morphine inj. 0.5cc/hour (D-11)- Zinc 1x20mg (D-14)- Folic acid 1x1mg (D-14)
28
- Multivitamin without Fe 1 x Cth1/2 (D-11)- Gentamicin zalf- Pediasure 75cc/3 hours/NGT- Check urinalysis, feces analysis, and electrolyte
11th October 2012
S Fever(+), deterioration of consciousness(+), diarrhea(-), seizure(-), ruam kemerahan pada bekas colostomy
O CNS syst :
CV syst :
Resp syst :
Met. syst :
Infec. syst:MS syst :
Unstable, GCS 14 (E4V4M6)Head: Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-).Stable, HR: 160bpm, reg, murmur (-), pulse: 160bpm, t/v adequate, BP: 110/60mmHg, MAP: 90mmHg, CVC placed (D-11), UOP: 660cc/24 hours (3.27cc/kgBB/hour)Stable, Thorax: SF, epigastrial retraction (+),RR: 36 tpm,
reg ,crackles (-/-)H: Nasal flare (-), Nasal canul: 1/2-1 L/i.Unstable,Abdomen: soepel, peristaltic(+)N, stoma(+),
feces(+): vol.±150cc , Ca/Na/K/Cl/Mg/Ph : 8.1/128/3.7/104/1.9/4.0Urinalysis : within normal limitFecal analysis : within normal limitStable, fever(+), T: 38oC,Stable, post surgery wound: dry
A Encephalitis + Post laparatomy (D-21) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Irritant Contact Dermatitis + Sepsis ec Acinetobacter baumanii with unstable CNS, and metabolic system
P - Head elevation 30o - O2 ½-1 L/i- Fluid requirements: HS+20%op besar: 1060cc/hr
P: - IVFD D20% = D5% NaCl(364cc) + D40%(136cc) + KCl (10mEq) +
Ca Gluconas (10cc) > 11gtt/i-Aminofusin 11cc/hour
E: Pediasure: 80cc/3hours/OGT- Amikacin 220mg/hr in 50cc D5% within 30’- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-14)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-14)
29
- Farmadol inj. 100mg - Morphine inj. 0.5cc/hour (D-12)- Zinc 1x20mg (D-15)- Folic acid 1x1mg (D-15)- Multivitamin without Fe 1 x Cth1/2 (D-12)- Gentamicin zalf- Pediasure 80cc/3 hours/NGT- Citrizine 1x2.5mg
12th October 2012
S Deterioration of consciousness(+), fever(-), diarrhea(-), seizure(-), ruam kemerahan pada bekas colostomy
O CNS syst :
CV syst :
Resp syst :
Met. syst :
Infec. syst:MS syst :
Unstable, GCS 14 (E4V4M6)Head: Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-).Stable, HR: 130bpm, reg, murmur (-), pulse: 130bpm, p/v adequate, BP: 100/60mmHg, MAP: 73mmHg, CVC placed (D-12), UOP: 600cc/24 hours (2.9cc/kgBB/hour)Stable,Thorax: SF, epigastrial retraction (+),RR: 30 tpm,
reg ,crackles (-/-)H: nasal flare(-), Nasal canul: 1/2-1 L/i.Unstable,Abdomen: soepel, peristaltic(+)N, stoma(+),
feces(+): vol.±130cc , Stable, fever(+), T: 38oCStable, post surgery wound: dry
A Encephalitis + Post laparatomy (D-22) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Irritant Contact Dermatitis + Sepsis ec Acinetobacter baumanii with unstable CNS, and metabolic system
P - Head elevation 30o - O2 ½-1 L/i- Fluid requirements: HS±B
P: - IVFD D20%: 8gtt/-Aminofusin 5%: 3.5cc/hour
E: Pediasure: 100cc/3hours/OGT- Amikacin 160mg/hr in 50cc D5% within 30’(D-2)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-16)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-16)- Omeprazole 8mg/8 hour/iv
30
- Farmadol inj. 100mg - Morphine inj. 0.5cc/hour (D-13)- Citrizine 1x2.5mg- Zinc 1x20mg (D-16)- Folic acid 1x1mg (D-16)- Multivitamin without Fe 1 x Cth1/2 (D-13)- Gentamicin zalf- Pediasure 100cc/3 hours/NGT- Resomal 50-100cc/times diarrhea- Candistatin drop 3 x gttII- Check FBC, LFT, RFT, Electrolyte, procalcitonin, lactic acid
13th October 2012
S Fever(+), deterioration of consciousness(+), diarrhea(+), seizure(-), ruam kemerahan pada bekas colostomy
O CNS syst :
CV syst :
Resp syst :
Met. syst :
Infec. syst:MS syst :CBC :
Unstable, GCS 15 (E4V5M6)Head: Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-).Stable, HR: 146bpm, reg, murmur (-), pulse: 146bpm, p/v adequate, BP: 100/60mmHg, MAP: 73mmHg, CVC placed (D-13), UOP: 960cc/24 hours (4.76cc/kgBB/hour)Stable, Thorax: SF, epigastrial retraction (+),RR: 30 tpm,
reg ,crackles (-/-)H: Nasal flare(-), Nasal canul: 1/2-1 L/i.Unstable,Abdomen: soepel, peristaltic(+)N, stoma(+),feces(+):vol.±250cc,Albumin:3.4,Ca/Na/K/Cl/Mg/Ph :8.5/133/4/102/8.9/1.82/3.4Stable, fever(+), T: 39oC, lactic acid: 2.0, Pro: 0.81Unstable, post surgery wound: dry Hb/RBC/WBC/PLT/HT =
8.2/3.7x106/9.94x103/374x103/25.5MCV/MCH/MCHC/RDW = 68.9/22.2/32.2/29.1N/L/M/E/B = 57.7/29.7/11/1.3/0.3
A Encephalitis + Post laparatomy (D-23) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Irritant Contact Dermatitis + Sepsis ec Acinetobacter baumanii with unstable CNS, and metabolic system
P - Head elevation 30o - O2 ½-1 L/i- IVFD D5% = D5% NaCl(500cc)+ KCl (10mEq) + Ca Gluconas
(10cc) > 7gtt/I (micro)
31
- Amikacin 160mg/hr in 50cc D5% within 30’(D-3)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-17)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-17)- Omeprazole 8mg/8 hour/iv- Farmadol inj. 100mg - Citrizine 1x2.5mg- Folic acid 1x1mg - Multivitamin without Fe 1 x Cth1/2 (D-14)- Gentamicin zalf- Pediasure 110cc/3 hours/NGT- Resomal 50-100cc/times diarrhea- Candistatin drop 3 x gttII- PRC transfusion 50cc
14th October 2012
S Fever(+), deterioration of consciousness(+), diarrhea(+), seizure(-)
O Sens : CM T: 37oC W: 8.6kg
Head :
Thorax :
Abdomen:Extremity:
Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva palpebra (-/-).
Nose: NGT, nasal canule. Ear and mouth: within normal limit.
Symmetrical fusiformis, retraction(-), HR: 126bpm, reg, murmur (-), RR: 22 tpm, reg ,crackles (-/-)
Soepel, peristaltic(+)N, stoma(+), feces(+)Pulse: 126bpm, reg, CRT<3” BP: 100/60mmHg
A Encephalitis + Post laparatomy (D-24) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Sepsis ec Acinetobacter baumanii
P - Head elevation 30o - O2 ½-1 L/i- IVFD D5% = D5% NaCl(500cc)+ KCl (10mEq) + Ca Gluconas
(10cc) > 7gtt/I (micro)- Amikacin 160mg/hr in 50cc D5% within 30’(D-4)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-18)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-18)
32
- Omeprazole 8mg/8 hour/iv- Paracetamol 3x100mg- Citrizine 1x2.5mg- Folic acid 1x1mg - Multivitamin without Fe 1 x Cth1/2 (D-15)- Gentamicin zalf- Pediasure 110cc/3 hours/NGT- Resomal 50-100cc/times diarrhea- Candistatin drop 3 x gttII- Transfusi PRC Wash II (50cc)- Check FBC
15th October 2012
S Fever(+), deterioration of consciousness(+), diarrhea(+), seizure(+)
O Sens : CM T: 39.2oC W: 8.6kg
Head :
Thorax :
Abdomen:Extremity:
Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva palpebra (-/-).
Nose: NGT, nasal canule. Ear and mouth: within normal limit.
Symmetrical fusiformis, retraction(-), HR: 120bpm, reg, murmur (-), RR: 20 tpm, reg ,crackles (-/-)
Soepel, peristaltic(+)N, stoma(+), feces(+)Pulse: 120bpm, reg, CRT<3” BP: 100/60mmHg
A Encephalitis + Post laparatomy (D-24) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Sepsis ec Acinetobacter baumanii
P - Head elevation 30o - O2 ½-1 L/i- IVFD D5% NaCl 7gtt/I (micro)- Amikacin 160mg/hr in 50cc D5% within 30’(D-5)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-19)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-19)- Omeprazole 8mg/8 hour/iv- Paracetamol 3x100mg- Citrizine 1x2.5mg- Folic acid 1x1mg - Multivitamin without Fe 1 x Cth1/2 (D-16)
33
- Gentamicin zalf- Pediasure 110cc/3 hours/NGT- Resomal 50-100cc/times diarrhea- Candistatin drop 3 x gtt II
16th October 2012
S Fever(+), seizure(+)
O Sens : CM T: 38.2oC W: 8.6kg
Head :
Thorax :
Abdomen:
Extremity:
Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva palpebra (-/-).
Nose: NGT, nasal canule. Ear and mouth: within normal limit.
Symmetrical fusiformis, retraction(-), HR: 122bpm, reg, murmur (-), RR: 24 tpm, reg ,crackles (-/-)
Soepel, peristaltic(+)N, stoma(+), feces(+), Liver and Spleen: unpalpable
Pulse: 122bpm, reg, CRT<3” BP: 100/60mmHg A Encephalitis + Post laparatomy (D-25) a/i Ileosecal invagination +
Bronchopneumonia + Moderate malnutrition + Sepsis ec Acinetobacter baumanii
P - Head elevation 30o - O2 ½-1 L/i- IVFD D5% NaCl 7gtt/I (micro)- Amikacin 160mg/hr in 50cc D5% within 30’(D-6)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-20)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-20)s- Omeprazole 8mg/8 hour/iv- Paracetamol 3x100mg - Citrizine 1x2.5mg- Folic acid 1x1mg - Ferry syr 1x CthI- Gentamicin zalf- Pediasure 110cc/3 hours/NGT- Resomal 50-100cc/times diarrhea- Candistatin drop 3 x gtt II- Check FBC, electrolyte, blood gas, procalcitonin, lactic acid, CRP
17th October 2012
S Fever(+), seizure(+), diarrhea
34
O Sens : CM T: 37.8oC W: 8.85kg
Head :
Thorax :
Abdomen:
Extremity:CBC :
Electrolyte:Procalcitonin:Lactic acid :CRP :Blood gas :
Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva palpebra (-/-).
Nose: NGT, nasal canule. Ear and mouth: within normal limit.
Symmetrical fusiformis, retraction(-), intercostals space clearly seen, HR: 124bpm, reg, murmur (-), RR: 24 tpm, reg ,crackles (-/-)
Soepel, peristaltic(+)N, stoma(+), feces(+), Liver and Spleen: unpalpable
Pulse: 124bpm, reg, CRT<3” BP: 100/60mmHg Hb/RBC/WBC/PLT/HT =
12/4.63x106/14.15x103/74x103/34.1MCV/MCH/MCHC/RDW = 73.7/25.9/35.2/25.3N/L/M/E/B = 73.4/17.3/8.9/0.1/0.3 Ca/Na/K/Cl/Mg/Ph : 8.6/133/2.7/106/8.9/1.75/2.8 >100.003.8positive pH/pCO2/pO2/HCO3/TCO2/BE/SaO2= 7.403/29.9/104.1/18.2/19.1/-5.5/ 97.6
A Encephalitis + Post laparatomy (D-25) a/i Ileosecal invagination + Bronchopneumonia + Severe Malnutrition type marasmus + Sepsis ec Acinetobacter baumanii
P - Head elevation 30o - O2 ½-1 L/i- IVFD D5% NaCl 7gtt/I (micro)- Amikacin 160mg/hr in 50cc D5% within 30’(D-7)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-21)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-21)- Ketorolac inj. 2mg/6 hour/iv- Ranitidine 9mg/8 hour/iv- Paracetamol 3x100mg- Citrizine 1x2.5mg- Folic acid 1x1mg - Ferry syr 1x CthI- Gentamicin zalf- Pediasure 110cc/3 hours/NGT- Resomal 50-100cc/times diarrhoea- Candistatin drop 3 x gtt II- Diet F100 160cc/3 hours NGT + Mineral mix 3.2cc
18th October 2012
35
S Fever(-), seizure(-), diarrhea(+)
O Sens : CM T: 37.5oC W: 8.5kg
Head :
Thorax :
Abdomen:
Extremity:
Face: old man face (+)Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-).Nose: NGT, nasal canule. Ear and mouth: within normal
limit. Symmetrical fusiformis, retraction(-), intercostals space
clearly seen, HR: 122bpm, reg, murmur (-), RR: 22 tpm, reg ,crackles (-/-)
Soepel, peristaltic(+)N, stoma(+), feces(+), Liver and Spleen: unpalpable
Pulse: 124bpm, reg, CRT<3” BP: 110/80mmHg A Encephalitis + Post laparatomy (D-28) a/i Ileosecal invagination +
Severe Malnutrition type marasmus + Sepsis ec. Acinetobacter baumanii
P - Head elevation 30o - O2 ½-1 L/i- IVFD D5% NaCl 7gtt/I (micro)- Amikacin 160mg/hr in 50cc D5% within 30’(D-8)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-22)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-22)- Ketorolac inj. 2mg/6 hour/iv- Check blood gas
19th October 2012
S Fever(-), seizure(-), diarrhea(+)
O Sens : CM T: 37.5oC W: 8.5kg
Head :
Thorax :
Abdomen:
Face: old man face (+)Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-).Nose: NGT, nasal canule. Ear and mouth: within normal
limit. Symmetrical fusiformis, retraction(-), intercostals space
clearly seen, HR: 160bpm, reg, murmur (-), RR: 38 tpm, reg ,crackles (+/+)
Soepel, peristaltic(+)N, stoma(+), feces(+), Liver and Spleen: unpalpable
36
Extremity:Blood gas
Pulse: 160bpm, reg, CRT<3” BP: 150/120mmHgpH/pCO2/pO2/HCO3/TCO2/BE/SaO2= 7.376/30.1/190.7/17.3/18.2/-6.9/ 99.4
A Encephalitis + Post laparatomy (D-29) a/i Ileosecal invagination + Severe Malnutrition type marasmus + Sepsis ec. Acinetobacter baumanii
P - Head elevation 30o - O2 ½-1 L/i- IVFD D5% NaCl 7gtt/I (micro)- Amikacin 160mg/hr in 50cc D5% within 30’(D-9)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-23)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-23)- Ketorolac inj. 2mg/6 hour/iv- Carbamazepin 3x15mg (D-1)
20th October 2012
S Fever(+), seizure(-), diarrhea(-)
O Sens : CM T: 37.9oC W: 8.75kg
Head :
Thorax :
Abdomen:
Extremity:
Face: old man face (+)Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-).Nose: NGT, nasal canule. Ear and mouth: within normal
limit. Symmetrical fusiformis, retraction(-), nasal flare (+)
intercostals space clearly seen, HR: 120bpm, reg, murmur (-), RR: 40 tpm, reg ,crackles (+/+)
Soepel, peristaltic(+)N, stoma(+), feces(+), Liver and Spleen: unpalpable
Pulse: 160bpm, reg, CRT<3” BP: 130/100mmHg A Encephalitis + Post laparatomy (D-30) a/i Ileosecal invagination +
Severe Malnutrition type marasmus + Sepsis ec. Acinetobacter baumanii
P - Head elevation 30o - O2 ½-1 L/i- IVFD D5% NaCl 7gtt/I (micro)- Amikacin 160mg/hr in 50cc D5% within 30’(D-10)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-24)
37
- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’ (D-24)
- Ketorolac inj. 2mg/6 hour/iv- Carbamazepin 3x15mg (D-2)
21th October 2012
S Fever(-), seizure(-), diarrhea(+)
O Sens : CM T: 37oC W: 8.75kg
Head :
Thorax :
Abdomen:
Extremity:
Face: old man face (+)Eye: light reflex (+/+), isochoric pupil, pale inferior
conjunctiva palpebra (-/-).Nose: NGT, nasal canule. Ear and mouth: within normal
limit. Symmetrical fusiformis, retraction(-), nasal flare (-),
intercostals space, clearly seen,HR: 122bpm, reg, murmur (-), RR: 42 tpm, reg ,crackles (+/+)
Soepel, peristaltic(+)N, stoma(+), feces(+), Liver and Spleen: unpalpable
Pulse: 160bpm, reg, CRT<3” BP: 150/120mmHg A Encephalitis + Post laparatomy (D-31) a/i Ileosecal invagination +
Severe Malnutrition type marasmus + Sepsis ec. Acinetobacter baumanii
P - Head elevation 30o - O2 ½-1 L/i- IVFD D5% NaCl 7gtt/I (micro)- Amikacin 160mg/hr in 50cc D5% within 30’(D-11)- Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’
(D-25)- Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within
20’ (D-25)- Ketorolac inj. 2mg/6 hour/iv- Carbamazepin 3x15mg (D-3)
38
CHAPTER 4
DISCUSSION & SUMMARY
4.1 Discussion
MA, male, 1 year 5 months was admitted to Pediatrics Department of RSUP
HAM and was diagnosed with encephalitis with bronchopneumonia, moderate
malnutrition, and sepsis with unstable CNS, metabolic, and musculoskeletal
system and was a post laparatomy pasien due to ileoseptal invagination. The
diagnosis was established based on history taking, clinical manifestations,
radiology and laboratory findings. From history taking and clinical manifestations
patient experienced loss of consciousness, seizure, recurrent fever and diarrhoea.
The treatment given were IVFD D5% NaCl 0.9%, Diet F100: 140cc/3hours/OGT
+ mineral mix 2,8cc, Ampicillin inj. 450mg/6 hours/iv , Cefotaxime 250mg/6
hours/iv, Phenitoin inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’,
Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’,
Metronidazole inj. 75mg/8 hours/iv, Farmadol inj. 100mg, Morphine inj. 8.5mg in
50cc D5% (tapering off dose 0.5cc/hour), Zinc 1x20mg, Folic acid 1x1mg,
multivitamin without Fe 1 x Cth1/2
Sepsis may develop as a complication of a localized infection or may follow
colonization and mucosal invasion by virulent pathogens. Patients at risk for
sepsis include infants, children with serious injuries, children on chronic
antibacterial therapy, malnourished children, and children with chronic medical
problems.
In this case, MA is 1 year 5 month boy, with encephalitis,
bronchopneumonia, moderate malnutrition and is post laparatomy patient.
According to the site of infection and microbiologic etiology, the majority of
infections causing sepsis were respiratory (64%), followed by digestive and
39
urinary tract infections (18% and 12% respectively). From the microbiologic
aspect, gram-negative bacteria caused the majority of infections that evolved with
sepsis, with Escherichia coli and Klebsiella pneumoniae being the most frequent
pathogens. The most common Gram-positive infecting organism was
Staphylococcus aureus. Atypical pathogens were identified in a minority of
patients. Pseudobacteremia may be associated with contaminated heparin flush
solutions, intravenous solutions, albumin, cryoprecipitate, and infusion
equipment. Infections with gram-negative bacterla (e.g., Escherichia coli,
Pseudomonas, Acinetobacter, Klebsiella, Enterobacter, Serratia) and fungi (e.g.,
Candida, Aspergilus most often occur in immunocompromised and hospitalized
patients colonized with these organisms. Contaminants include water-borne
organisms such as Acinetobacter baumanii, Pseudomonas aeruginosa, and Serratia
The site of infection in this case is thought to be in the CNS with diagnose
of encephalitis. However, patient was also diagnosed with bronchopneumonia.
From the culture that was done there were a few microorganism that was found.
From the blood Acinetobacter baumanii was isolated. From the cerebrospinal
fluid Proteus mirabilis was isolated by BACTEC and Acinetobacter baumanii was
isolated from culture. And there was no growth of microorganism from the urine.
The initial signs and symptoms of sepsis include alterations in temperature
regulation (hyperthermia or hypothermia), tachycardia, and tachypnea. As sepsis
progresses, cardiac output falls in response to the effects of numerous mediators.
Signs of poor cardiac output include delayed capillary refill, diminished
peripheral and central pulses, cool extremities, and decreased urine output.
Alterations in mental status, including confusion, agitation, lethargy, anxiety,
obtundation, or coma, can also be signs of poor cardiac output.
In this case, the patient experienced frequent alternation of tempreture,
some days normal but somedays could have a tempreture reaching 38.90. This
phenomenom also occurred with the respiratory rate. The patient had CRT
40
<3”,warm extremities and no decrease in urine output. However, there was
alteration in mental status.
The diagnosis of sepsis requires SIRS in the presence of proven infection or
a clinical picture consistent with infection. An infectious etiology should be
sought by culturing clinically appropriate specimens taken from body fluids
(blood, urine, cerebrospinal fluid, abscesses, peritoneal fluid, etc.).
In this case the criteria of SIRS that was present is hyperthermia, tachypnea,
and also there was leucocytosis . And the infectious etiology was cultured from
CSF and blood. Giving rise to Acinetobacter baumanii from the blood and from
the CSF Proteus mirabilis and Burkholderia cepacia was isolated.
Laboratory findings often include evidence of hematologic abnormalities
and electrolyte disturbances. Hematologic abnormalities include
thrombocytopenia, prolonged prothrombin and partial thromboplastin times,
reduced serum fibrinogen levels and elevated fibrin split products, and anemia.
Electrolyte abnormalities include hyperglicemia, hypocalcemia,
hypoalbuminemia, metabolic acidosis, and low serum bicarbonate. Lactic acidosis
can occur if there is significant anaerobic metabolism. Some biochemical markers
examination such as procalcitonin, CRP, etc, can be used to support the diagnosis
of sepsis.
In this case, hematologic abnormalities that was seen were elevated D-
dimer and there was evidence once of thrombocytopenia. Electrolyte
abnormalities that was discovered were hypocalcemia, hyponatremia,
hypokalemia, hypoalbuniemia. There were no evidence of metabolic asidosis,
however low serum bicarbonate was seen. The levels of lactic acid, procalcitonin
and CRP was seen. And there was evidence of elevation of ALT and AST.
The mainstay of the treatment of sepsis include airway patency with
adequate oxygenation, fluid resuscitation, elimination of pathogen, treatment of
hyperglycemia, corticosteroid and other treatment according to organ dysfunction.
41
MA, was treated with oxygenation, fluid, and for the elimination of pathogen the
patient was given empiric antibiotic such as amphicilin, ceftriaxone , and
metronidazol. And from the result of sensitivity test amikasin was then the
antibiotic of choice.
4.2. Summary
MA, male, 1 year 5 months was admitted to Pediatrics Department of
RSUP HAM and was diagnosed with encephalitis with bronchopneumonia,
moderate malnutrition, and sepsis with unstable CNS, metabolic, and
musculoskeletal system and was a post laparatomy pasien due to ileoseptal
invagination. Patient is still hospitalized in Adam Malik General Hospital.
42
REFERENCES
1. Starke R.J., Tuberculosis. In: Gershon A.A., Hotez J.P., Katz L.S., Krugman’s
Infectious Disease of Children 11th edition. Philadelphia. 2004. P. 731-762.
2.
Angus DC, Linde-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR.
Epidemiology of severe sepsis in the United States: analysis of incidence,
outcome, and associates cost of care. Crit Care Med. 2001;29(7): 1303-10.
2. Kissson N, Carcillo JA, Espinosa V, Argent A, Devictor D, Madden M, et al.
World federation of pediatric intensive care and critical care societies: global
sepsis initiative. Pediatr Crit Care Med. 2011;12(5):494-503.
3. Kumar G, Kumar N, Taneja A, Kaleekal T, Tarima S, McGinley E, et al.
Nationwide trends of severe sepsis in the 21st century (2000-2007). Chest.
2011;140(5): 1223-31.
4. Goldstein B, Giroir B, Randolph A. International pediatrics sepsis consensus
conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit
Care Med. 2005:6; 413-40.
5. El-wiher N, Cornell, TT, Kissoon N, Shanley TP. Management and Treatment
Guidelines for Sepsis in Pediatrics Patients. The Open Inflammation Journal.
2011;4:101-9
6. Gebara BM. Values for systolic blood pressure. Pediatr Crit Care Med. 2005: 6;
500 (author reply-1).
7. Watson RS, Carcillo JA. Scope and epidemiology of pediatric sepsis. Pediatr
Crit Care Med. 2005;6:3-5.
8. The Global Burden of Disease: 2004 Update. Geneva, Switzerland, World
Health Organization, 2008.
9. Militaru M, Martinovici D. Our Experience in Pediatric Sepsis. Jurnalul
Pediatrului. 2005;8:26-31.
10. Enrione MA, Powell KR. Sepsis, Septic Shock, and Systemic Inflammatory
Response Syndrome. In: Behrman RE, Kliegman RM, Jenson HB, Stanton BF,
43
Ziteli BJ, Davis HW, editors. Nelson Textbook of Pediatrics. 18th ed.
Philadelphia: Saunders; 2007:1094-99
11. Soedarmo SS, Garna H, Hadinegoro SR, Satari HS. Buku Ajar Infeksi dan
Pediatri Tropis. 2nd ed. Jakarta: IDAI; 2012:358-363.
12. Somasetia DH. Tatalaksana Awal Sepsis Berat dan Syok Sepsis Anak. In: Ali
M, Dimyati Y, Adriansyah R, Trisnawati Y, editors. Tatalaksana Awal
Kegawatan pada Bayi dan Anak. Medan: IDAI-Sumut;38-61.
13. Singhi S, Argent AC, Baranwal AK, Santhanam I. Septic shock: Management
in emergency department with available resources. Journal of Pediatric Infectious
Diseases. 2009;4:85–98.
14. Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, et al.
Surviving Sepsis Campaign: International guidelines for management of severe
sepsis and septic shock: 2008. Crit Care Med. 2008;36:296-327.
15. Khilnani P. Clinical management guidelines of pediatric septic shock. Indian J
Crit Med. 2005;9(3): 164-172.
16. Singal M, Mizuno Y, Skippen P, Kissoon N. Sepsis in the pediatric intensive
care unit. Journal of Pediatric Infectious Diseases. 2009;4:99-106.