chapter 1-3 final.docx

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 :



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’


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 :



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’


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 :



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


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’


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 :



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


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’


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 :


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


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’


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’


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:




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’


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(+)


Head :

Thorax :

Abdomen:

Extremity:




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



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


Head :

Thorax :

Abdomen:

Extremity:CBC :

Electrolyte:Procalcitonin:Lactic acid :CRP :Blood gas :



Symmetrical fusiformis, retraction(-), intercostals space clearly seen, HR: 124bpm, reg, murmur (-), RR: 24 tpm, reg ,crackles (-/-)


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



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(+)


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 (-/-)



Severe Malnutrition type marasmus + Sepsis ec. Acinetobacter baumanii



20’ (D-22)- Ketorolac inj. 2mg/6 hour/iv- Check blood gas

19th October 2012



Head :

Thorax :

Abdomen:



limit. Symmetrical fusiformis, retraction(-), intercostals space

clearly seen, HR: 160bpm, reg, murmur (-), RR: 38 tpm, reg ,crackles (+/+)


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



20’ (D-23)- Ketorolac inj. 2mg/6 hour/iv- Carbamazepin 3x15mg (D-1)

20th October 2012

S Fever(+), seizure(-), diarrhea(-)


Head :

Thorax :

Abdomen:

Extremity:



limit. Symmetrical fusiformis, retraction(-), nasal flare (+)

intercostals space clearly seen, HR: 120bpm, reg, murmur (-), RR: 40 tpm, reg ,crackles (+/+)





(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


O Sens : CM T: 37oC W: 8.75kg

Head :

Thorax :

Abdomen:

Extremity:



limit. Symmetrical fusiformis, retraction(-), nasal flare (-),

intercostals space, clearly seen,HR: 122bpm, reg, murmur (-), RR: 42 tpm, reg ,crackles (+/+)






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.

chapter 1-3 final.docx

Documents