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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.
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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

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Annually, 250.000

new cases of tuberculosis in
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Indonesia and

approximately 100.000 death because of tuberculosis. Tuberculosis is the main cause of the death among the infection disease and the 3rd 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

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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

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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, gramnegative 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

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).g. In the neonatal age group. Toxic shock syndrome from group A streptococcus or S. enteroviruses.10 The infectious agents associated with sepsis in pediatric patients vary with the patient's age and immune status. children with serious injuries. Pseudomonas. azrreus can also be seen in older children. and endotracheal tubes are portals for the development nosocomial infections. children who are immune suppressed (transplant recipients on immunosuppressive regimens. Polymicrobial sepsis occurs in high-risk patients and is associated with catheters. 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. Infections with gram-negative bacteria (e. Invasive procedures can also lead to nosocomial infections.5 Staphylococcus aureus (75%). . gastrointestinal disease. Also. Intravenous and arterial catheters. group B streptococcus. Rickettsia rickettsi causing Rocky Mountain spotted fever occurs in endemic areas and can lead to septic shock. children on chronic antibacterial therapy. Aspergilus) most often occur in immunocompromised and hospitalized patients colonized with these organisms. Listeria monocytogenes. Neisseria meningitidis. In older children Streptococcus pneumoniae. Atypical pathogens were identified in a minority of patients (4%). urinary catheters. including sepsis and septic shock. Escherichia coli. and children with chronic medical problems. patients with acquired or congenital immune deficiencies) are at an increased risk for complications from infection.g. Enterobacter. and herpes simplex virus are the pathogens most commonly associated with sepsis. Serratia) and fungi (e. patients on chemotherapeutic agents or corticosteroids. Candida. Nosocomial (hospitalacquired) infections pose a special risk to immunocompromised patients. Acinetobacter. malnourished children. Klebsiella. and Staphylococcus aureus (methicillin-sensitive or resistant) are more common. Escherichia coli.3.9 2...

and malignancy. Pseudobacteremia may be associated with contaminated heparin flush solutions. Pseudomonas aeruginosa.10 . cryoprecipitate.or B-cell defects. or asplenia (acquired or congenital). and Serratia. Contaminants include water-borne organisms such as Burkholderia cepacia.6 neutropenia. intravenous solutions. T. 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. and infusion equipment. albumin.

The risk factor for sepsis can be seen in the table below. Age 3. associated with perforation or peritoneal dialysis) Hepatitis Hemorrhage CARDIOPULMONARY Pneumonia Pulmonary emboli Congestive heart failure Arrhythmia Pericarditis Myocarditis METABOLICENDOCRINE Adrenal insufficiency Electrolyte disturbances Diabetes insipidus Diabetes mellitus Inborn errors of metabolism Hypoglycemia Reye's syndrome NEUROLOGIC and others Intoxication Intracranial hemorrhage Infant botulism Trauma Guillain-Barré syndrome Myasthenia gravis Anaphylaxis Hemolytic-uremic syndrome Kawasaki disease Erythema multiforme Hemorrhagic shock– encephalopathy syndrome HEMATOLOGIC Anemia Methemoglobinemia Splenic sequestration crisis Leukemia or lymphoma Sepsis is more often occur in children with risk factor. Immune deficiency Malnutrition A-gamma-globulinemia Sickle cell anemia Severe combined immunodeficiency AIDS Asplenism Complement Deficiency Neutrophl chemotactic factor defect . Prematurity 2.7 Table 2-1 Differential diagnosis of SIRS10 INFECTION Bacteremia or meningitis Viral illness Encephalitis Rickettsiae Syphilis Vaccine reaction Toxin-mediated reaction GASTROINTESTINAL Gastroenteritis with dehydration Volvulus Intussusception Appendicitis Peritonitis (spontaneous.11 Table 2-2 Risk Factor for Sepsis11 1.

4. cardiogenic. Cold shock occurs in other patients with decreased cardiac output and elevated systemic vascular resistance. newborns and children may have fluid refractory shock and develop progressive myocardial dysfunction. Hypovolemia from intravascular fluid losses occurs through capillary leak. perfusion to major organ systems may be compromised. a late finding in infants and children. The degree to which a patient will exhibit each of these responses is variable. low. Warm shock occurs in some patients with increased cardiac output and decreased systemic vascular resistance. Hypotension. Iatrogenic Urinary catheterization Surgery 2. unlike adults in septic shock who present with vasodilation and high cardiac output. Cardiac output may be high. this host immune . In both cases. Distributive shock is the result of decreased systemic vascular resistance. and the reticular endothelium system. Septic shock is a combination of the three classic types of shock: hypovolemic. Pathogenesis10 Nephrotic syndrome Urinary tract infection gonococcus Intravenous drug addiction Endotracheal intubation Continuous peritoneal dialysis from 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. the inflammatory response.8 4. occurs when the compensatory mechanisms are failing and cardiorespiratory arrest is imminent. prevents the body from developing sepsis in response to breaches in the host defense system. However. The host's immune response. and distributive. or normal. The body has compensatory mechanisms to maintain blood pressure through increased heart rate and peripheral vasoconstriction. History of Current illness Malignancy Galactosemia Paraplegia Extensive burn injury 5. Cardiogenic shock results from the myocardial-depressant effects of sepsis. through the actions of the cellular and humoral immune systems. Recent data suggest that. It is important to distinguish between the infection and the host response to the infection.

increased cytosolic calcium. mannose. which causes vasoconstriction and platelet aggregation. Arachidonic acid metabolites include (1) thromboxane A2. mechanical obstruction of the capillary beds from aggregation of cellular elements. which causes vasodilation. 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. including hormones.. Myocardial depressant factors. and release of fatty acids with prostaglandin formation. At the cellular level there is decreased oxidative phosphorylation secondary to decreased oxygen delivery. Endogenous opiates. anaerobic metabolism secondary to decreased adenosine triphosphate (ATP). release of endogenous opiates. Biochemical responses include the production of arachidonic acid metabolites. and activation of the complement system. and PGI. which causes vasoconstriction.9 response produces an inflammatory cascade of highly toxic mediators. tumor necrosis factor-a (TNF). decrease mvocardial contractilitv. If this inflammatory cascade is uncontrolled. Activation of the complement system leads . activation of the complement system. activation of membrane phospholipases (further depleting ATP). lactate production. such as PGF2. and enzymes. release of vasoactive substances. Endotoxin (a lipopolysaccharide). 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. cytokines. bronchoconstriction. glycogen depletion. and cause vasodilation. and increased capillary permeability. SIRS occurs with subsequent organ and cellular dysfunction from derangement of the microcirculatory system. (2) prostaglandins. Microcirculatory dysfunction results in endothelial injury. decrease sympathetic activitv. release of myocardial depressant factors. and viruses activate circulating lymphocytes and initiate an inflammatory mediator cascade. and (3) leukotrienes that cause vasoconstriction.. mycobacteria. The inflammatory cascade is initiated by toxins or superantigens. as well as the production and release of many other mediators. including P-endorphin. changes in cardiovascular tone.

platelet activating factor (PAF). therapies to augment the host defense. Myocardial depression is caused by myocardial depressant factors. insulin resistance. and .10 to release of vasoactive mediators that increase capillary permeability. heat shock proteins. vascular permeability factor. and some interleukins through direct myocardial injury. interleukin 1 (IL-I). The clinical manifestations of sepsis and shock are mediated through the inflammatory cascade. tachypnea. at the microcirculatory level. C4. TNF and IL-1 stimulate the release of proinflammatory and anti-inflammatory mediators causing fever and vasodilatation. IL. acute respiratory distress syndrome. complement fragments C3a and C5a. and adhesion molecules (endothelin-derived adhesion molecule [E-selectin]. In addition to treating the underlying infection. and cause activation and aggregation of platelets and granulocytes. coagulopathy. IL-6. intercellular adhesion molecule-l [ICAM]. toxic oxygen radicals. Hypovolemia. fibrin. bradykinin. prostaglandins EL and IL). decreased vascular tone. and production of myocardial nitric oxide. TNF and other inflammatory mediators increase vascular permeability. proteolytic enzymes from polymorphonuclear neutrophils. granulocyte-macrophage colony-stimulating factor. cause vasodilation. thrombin. is a major contributor to hypotension. depleted catecholamines. Endogenous mediators of sepsis continue to be identified and currently include TNF. leading to diffuse capillary leak. IL-2. plasminogen activator inhibitor (PAI-I). IL-4. and E4. TNF. Arachidonic acid metabolites lead to the development of fever. and unresolved or secondary infection are all results of the inflammatory cascade. vascular adhesion molecule-1 [VCAM]). an imbalance between perfusion and metabolic demands of the tissue. eicosanoids (leukotrienes B4. endothelium-derived relaxing factor. released from the endothelium or inflammatory cells. endorphin. prevent leukocyte endothelial interaction. interferon-y. and lactic acidosis. endothelin-1. decreased CYP450 activity (decreased steroid synthesis). Nitric oxide. transforming growth factor-p. thromboxane A2. platelets. block trigger events. cardiac and vascular failure. macrophage-derived procoagulant and inflammatory cytokine. D4. and. coagulation factors.8. increased P-endorphin. myocardial depressant substance. ventilation-perfusion abnormalities.

As sepsis progresses. PAF antagonists. or coma. bactericidal permeability increasing protein. an IL-1 receptor antagonist. ecchymoses. Trials have been conducted with anti-endotoxin antibodies. 2. The best treatment is early recognition. Cutaneous lesions seen in septic patients include petechiae. tachycardia. ecthyma gangrenosum. Lactic acidosis occurs as shock progresses and is the consequence of increased tissue production and decreased hepatic clearance. Capillary leak develops from altered vascular permeability. agitation. the results of clinical trials investigating drugs targeting the rnediators of SIRS have been disappointing. diffuse erythema. To date. cardiac output falls in response to the effects of numerous mediators. anxiety. can also be signs of poor cardiac output. but enrollment in a pediatric trial was closed early because of an unfavorable risk-benefit ratio particularly in neonates. In the early stages (hyperdynamic phase). and symmetric peripheral gangrene. Recombinant human activated protein C (drotrecogina) studies have shown improvement in the 28-day survival in adults. cytokines or lipid mediators are being investigated. Other signs of poor cardiac output include delayed capillary refill. and decreased urine output. IL-1 antibodies. inhibitors of leukocyte-adhesion molecules. Although hypotension (systolic arterial pressure <2 standard deviations below the mean for age) is a late finding in children with sepsis. and early goal-directed therapy.11 inhibit vasoactive substances. bradykinin-receptor antibodies. cyclo-oxygenase inhibitors. and tachypnea. antioxidant compounds. the cardiac output increases in an attempt to maintain adequate oxygen delivery to meet the increased metabolic demands of tissues. Alterations in mental status. lethargy. diminished peripheral and central pulses. early antimicrobial therapy.5. anti-TNF antibody. cool extremities. obtundation. it is not a criteria for the diagnosis of shock in infants and young children. Clinical Manifestation10 The initial signs and symptoms of sepsis include alterations in temperature regulation (hyperthermia or hypothermia). nitric oxide antagonists. Jaundice can be seen either as a sign of infection or as a result of . including confusion. and recombinant human activated protein C. thromboxane antagonists.

reduced serum fibrinogen levels and elevated fibrin split products. Neutropenia is an ominous sign of overwhelming sepsis.12 MODS. hypoalbuminemia. peritoneal fluid. presence of white cells in normally sterile body fluids. arthritis. promyelocytes). metabolic acidosis. Electrolyte abnormalities include hyperglycemia as a stress response or hypoglycemia if glycogen reserves are exhausted. Examination of infected body fluids may reveal neutrophils and bacteria. An infectious etiology should be sought by culturing clinically appropriate specimens taken from body fluids (blood. and suggestive rashes such as petechiae and purpura. Laboratory findings often include evidence of hematologic abnormalities and electrolyte disturbances. vacuolation of neutrophils.6. Renal and liver function may be abnormal if the patient develops MODS. prolonged prothrombin and partial thromboplastin times. abscesses. pneumonia. Some biochemical . Other electrolyte abnormalities include hypocalcemia. Lactic acidosis can occur if there is significant anaerobic metabolism. imaging (chest radiograph with evidence of pneumonia). or pyelonephritis. Patients with acute respiratory distress syndrome or pneumonia will have impaired oxygenation (decreased PaO2) and ventilation (increased PaC02). elevated neutrophil and increased immature forms (bands. toxic granulations. and Dohle bodies can be seen with infection. including central venous pressure and arterial blood pressure. Additional evidence to identify an infectious etiology as the cause of SIRS includes physical examination findings. Cultures take time for incubation and are not always positive. etc. Infectious disease and intensive care consults are necessary.). Diagnosis10 The diagnosis of sepsis requires SIRS in the presence of proven infection or a clinical picture consistent with infection. 2. urine. cerebrospinal fluid. myelocytes. and low serum bicarbonate. Affected children should be admitted to an intensive care unit where continuous. cellulitis. Hematologic abnormalities include thrombocytopenia. The patient may also have evidence of focal infection such as meningitis. Also. and anemia. close invasive monitoring can be performed.

Management Protein C deficiency.7. elevated Ddimer level. can be used to support the diagnosis of sepsis. warm extremities. ALT. low platelet counts seen in overt DIC Abnormalities can be observed onset of organ failure and without frank bleeding Doubling-indicates acute renal injury Indicates tissue hypoxia Indicates acute hepatocelular injury caused by hypoperfusion Inversely correlated with proinflammatory cytokine levels Acute phase response Differentiates infectious SIRS from noninfectious SIRS Coagulation cascade Creatinine level Lactic acid level Liver enzyme level Serum phosphate level C-reactive protein (CRP) level Procalcitonin level 2. normal pulses with no differential between the quality of peripheral and central pulses.13 markers examination such as procalcitonin. prolonged PT and PTT Elevated from baseline Lactic acid > 4 mmol/L (36mg/dL) Elevated alkaline phosphatase. normal mental status. . AST. bilirubin levels Hypophosphatemia Elevated Elevated 2. CRP.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. etc. Important clinical parameters that are reflective of “normal perfusion” include: capillary refill < 2 seconds. normal blood pressure for age and appropriate urine output for age.7. antithrombin deficiency. Table 2-3 Laboratory indicators of sepsis12 Laboratory Test White blood count Platelet count Findings Leukocytosis /leucopenia Thrombocytosis or thrombocytopenia Comments Endotoxemia may cause leucopenia High value early may be seen as acute phase response.

14 2. nasal prong CPAP.12 In addition. which may be due to acute lung injury or shock. defined as tissue hypoperfusion (hypotension persisting after initial fluid challenge or blood lactate concentration 4 mmol/L). 2.2 Airway and oxygenation5 Early medical responders (e. ED staff) should ensure a patent airway and appropriate protective airway reflexes are present. This protocol should be initiated as soon as hypoperfusion is recognized and should not be delayed pending ICU admission. hypotension and/or clinical signs suggestive of myocardial dysfunction or pulmonary edema. myocardial dysfunction. early semi-elective intubation and positive pressure mechanical ventilatory support should be strongly considered in this setting. While specific diagnosis of sepsis is being evaluated. 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). tracheal tube with CPAP or manual ventilation as per clinical situation. emergency support should include high flow supplemental oxygen and evaluation for further respiratory support for acute respiratory failure.7. the goals 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 . EMS and transport personnel. the patient should be placed on 100% oxygen to ensure maximal oxygen saturation. It includes oxygen using non-rebreathing mask.g. SpO2 of 94% is desirable. Therefore.7. When any degree of distress or abnormal respiratory function is noted.3 Fluid resuscitation We recommend the protocolized resuscitation of a patient with sepsis induced shock. which is often present in children with sepsis. Intubation and ventilation is indicated in-patients having hypoxemia not responding to oxygen administration by non-invasive methods. During the first 6 hrs of resuscitation. especially if there is any alteration in mental status.

Intravenous access may be difficult to achieve in children with poor hemodynamics. inotropic drugs may be used to improve cardiac output. In a randomized trial that compared slow and fast infusion rate. In patients with normal blood pressure fluids should be given in aliquots of 20 ml/kg over 15–20 min. acute severe burns or liver disease. 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. nephrotic syndrome. Pre- load needs to be optimized to improve cardiac output and thus oxygen delivery. dextrans.13 If signs of shock persist despite adequate volume replacement and perfusion of vital organ is jeopardized.14 Early rapid fluid resuscitation is fundamental to septic shock survival. in patients with malaria and dengue shock syndrome. It may go up to 200 ml in 6 hr or 240 ml in 8 hr in staphylococcal diseases presenting with septic shock. Drugs commonly used in pediatric ICU to increase myocardial contractility include the following:15 a. There may be a role of colloids (albumin. 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.5 ml/kg/hr Central venous (superior vena cava) or mixed venous oxygen saturation 70% or 65%. In such a case. Dopamine . vasodilatory shock or shock due to gastrointestinal sepsis. In hypotensive patients. Recent evidence clearly support the use of crystalloid (normal saline) in pediatric septic shock. intraosseous line should be established if three attempts have failed or 90 sec have lapsed. The effects of a particular drug in an individual patient are unpredictable and must be closely monitored. starch and gelatin in saline) in patients with a pre-existing low plasma oncotic pressure state such as protein energy malnutrition. respectively. Children with septic shock usually require 40–60 ml/kg. compared to 20 ml over 15 min.15   Urine output 0.13 Fluid resuscitation is best initiated with rapid infusion of normal saline or Ringer’s lactate. sometimes up to 90–110 ml/kg in the first hour of resuscitation.

At higher doses severe vasoconstriction can lead to lactic asidosis and renal splanchnic ischemia. the use of aminoglycoside should be monitored cautiously due to septic shock is prone to kidney injury.16 The primary indication for dopamine is the need to increase myocardial contractility after preload restoration. It should be not used alone in septic shock due to it could cause further drop in blood pressure. The usual dose is 520 mcg/kg/min. c. Dobutamine It is a selective β-1 agonist.05-1 mcg/kg/min. Noradrenaline In severe septic shock with hypotension despite the use of adrenaline secondary to intense vasodilatation. as in septic shock.7. 2. The usual dose is 0. b. It should be titrared closely and the minimum dose should be used as required. The usual dose is 5-20 mcg/kg/min titrated to desired effect. In a septic shock setting. Dopamine or adrenaline can be used to prevent hypotension owing to vasoconstrictive effect. Ampicilin (200mg/kg/day/iv in 4 dose) combined with aminoglycoside (garamicin 5-7mg/kg/day/iv or amikacin 1520mg/kg/day/iv or netilmicin 5-6 mg/kg/day/iv in 2 dose) are preferred. d. thus another combination is preferred if monitoring aminoglycoside is difficult which is ampicilin with cefotaksim (100 . Dopamine (in doses of more than 5 mcg/kg/min) should preferably be given via central line to prevent ischemic necrosis of the skin. The dose is 0. The reduction in afterload and improved myocardial performance lowers ventricular filling pressures. For the initial phase.4 Elimination of Pathogen10 Soon after diagnosed the patient should be administered by initial antibiotics. Adrenaline (epinephrine) It is used in which dominant hemodynamic feature is peripheral vascular failure. noradrenaline may be useful in increasing peripheral vascular resistance to improve blood pressure.1-1 mcg/kg/min. 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.

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). The corticosteroid that is given are metyl prednisolone (30 mg/kg/dose/iv) or dexamethasone (3 mg/kg/dose/iv). There have been many studies that have shown as association between elevated glucose and mortality in critically ill children. Corticosteroid is thought to have benefit if given in the early stadium of sepsis. If there is a suspicion of the presence of an anaerobic bacteria (for instance a focus infection in the abdomen. relative insulin deficiency and impaired glucose metabolism. mouth .17 mg/kg/day/iv in 3 dose).5 Glycemic control16 Hyperglycemia is a common occurrence in critically ill patients due to peripheral insulin resistance.7. who were incurred for 47% of all deaths. pelvis. and studies which have shown poorer outcomes withsignificant glucose variability. 2.7. however none established a causal relationship between untreated hyperglycemia and mortality nor did they show a decrease in mortality with strict glycemic control. Prognosis9 Hospital mortality generally varied little with age. 2. except for the significantly higher rate among infants.8 .6 Corticosteroid10 The benefit of corticosteroid in septic shock is still controversial. however has to be administered in the presence of adrenal glandula bleeding. there are difference in experiment results. rectum) then the patient should be administered metronidazole or clindamicin with another antibiotic which is suitable for enteric gram-negative bacteria. Given the ongoing concern regarding the detrimental effects of inducing hypoglycemia with insulin therapy. we do not recommend the routine use of insulin in hyperglycemic states. 2.

18 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. The mortality rate was significantly increased by the severity of the septic process: among the severe sepsis cases the mortality rate was 5%.2% for those with four organ systems or more failing. whereas among the patents with septic shock it was much higher: 53%. from 3.8% for those with single organ dysfunction to 53. There was no gender-related difference in hospital mortality. The risk of death also increased with increasing number of failing organs.

blood and mucus was not found. Diarrhea was not found but there is a history of diarrhea for the last 2 weeks. Patient was then transferred to the pediatric ICU on September 27th 2012 based on chief complaint of loss of consciousness. birth weight: 4100 gram. immediate crying (+). birth length: 50cm. cyanosis (-) Feeding History From birth to 6 months From 6 month to 9 month : Breast milk only : Milk Porridge + Breast milk .19 CHAPTER III CASE REPORT Name Age Sex Address Date of Admission : MA : 1 year 5months : Male : Jl. with a duration of ± 5-10 minutes. Loss of consciousness was preceded by seizure. the frequency is hard to determinate due to the presence of colostomy. first child. Besar Klumpang Kec Hamparan : October 7th 2012 Major Complaint History : Loss of consciousness : Loss of consciousness was experienced by the patient since twelve days ago. involving the whole body with the eyes directed upwards and the upper and lower limbs rigid and the seizure was preceded with fever. 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. This patient was first admitted to H. with a characteristic of high fever and gone with administration of antipyretic. The seizure was experienced for 3 days and frequent. with a volume of ± 200cc/day. History of Birth: spontaneous labor. Fever was found and recurrent fever was for the last 3 weeks.

gastroenteritis : unclear Physical Examination : Generalized status Body weight: 8. dyspnea (-).5 x 100% = 74. Ear and mouth: within normal limit.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 History of previous illness History of previous medications : Complete for age : ileosecum invagination.6/11. nasal canul (+).6 kg.5 kg BW/BL: 8.6 kg. pale inferior conjunctiva palpebra (-/-). cyanotic (-). edema (-).7 % BW/age: 8. Nose : NGT (+). Body length: 81 cm Body weight in 50th percentile according to age: 11.6/11. Temperature: 38.7 % BL/ age : 81/81 x 100% = 100 % Presence Status Sensorium : Apathies. BW/BL = % Localized status: Head : Eye: light reflex (+/+). Body length (BL): 81 cm CDC: BW/Age = %. Body weight (BW): 8. isochoric pupil.icteric (-).7C Anemic (-). .5 x 100% = 74. BL/Age = %.5 kg Body length in 50th percentile according to age: 81 cm Body weight in 50th percentile according to body length: 11.

00 % 0.70 % 0.9 mmHg 20. Chest retraction (+). Gordon(-).20 % 82.563 20. HR: 146 bpm. Hoffman (-).10 % 0.70 pg 33.70 g% 60. colostomy (+) LLQ. Liver and spleen not palpable Extremities : Pulse: 136 bpm. APR(+) Pathologic reflexes : Oppenheim (-).20 g% 3.20 fL 74. adequate pressure/volume.21 Neck Thorax : Lymph node enlargement (-) : Symmetrical fusiformis.30 % 162 x 103/mm3 67. peristaltic (+). Nuchal rigidity (-) Laboratory findings: CBC Hemoglobin (Hb) Erytrocyte (RBC) Leukocyte (WBC) Hematocrite Trombocyte (PLT) MCV MCH MCHC Neutrofil Lymphocyte Monocyte Eosinophil Basophil 25/09/2012 13.00 % 0.30 pg 24. Capillary Refill Time (CRT) < 3” BP: 110/70 mmHg.3 mmHg 165.30 g% 68.10 % 9.53 x 103/mm3 27.00 % Blood Gas 25/09/2012 27/09/2012 7..60 % 7.70 % 19. within normal limit Physiologic reflexes: KPR (+). warm axilla. Babinsky (-). regular.RR: 62 tpm. regular.00 g% 5.7 mmHg 36.60 % 216 x 103/mm3 6/10/2012 10. crackles (+/+).9 mmol/L pH PCO2 pO2 Bicarbonate 71.10 % 26.30 % 6/10/2012 7.588 7. stridor (-) Abdomen : Soepel.14 x 106/mm3 19. murmur (-).50 g% 33.70 pg 35.7 mmHg 177.4 mmHg 183. Urogenital : Male.00 fL 25.60 % 425 x 103/mm3 27/09/2012 9.50 x 106/mm3 7.455 30.90 % 12.20 g% 4.73 x 106/mm3 20.00 % 0.90 % 12.40 % 0.3 mmHg 19.4 mmol/L 32.30 fL 22.91 x 103/mm3 36. regular.3 mmol/L . Chaddock (-).62 x 103/mm3 30.

4 mEq/L 2.1 mEq/L 90 mEq/L 96 mEq/L 1.12 ng/mL 27/09/2012 28/09/2012 1.0 mmol/L -0.2 mEq/L 104 mEq/L 1.3 mmol/L 99.0 mmol/L Result HST PT INR APTT TT Fibrinogen D-dimer Liver Total Bilirubin Direct Bilirubin ALP AST/SGOT ALT/SGPT Renal Ureum Creatinin Uric Acid 1.21 x 329 mg/dL 1031 ng/dL 0.8 mmol/L 99.12 x 1.14 1.6 mg/dL 125 mEq/L 3.00 mg/dL 0.5 mmol/L 98.1 mEq/L 1.9 mEq/L 4.001 x 103/uL .28 mEq/L 2/10/2012 35.8 mmol/L 2.5 mmol/L 1.1 mg/dL 124 mEq/L 132 mEq/L 1.10 mg/dL 0.41 <7.26 mg/dL 3.004 x 103/uL 0.3% 6/10/2012 6.27 ng/mL 3.9 mmol/L Normal value Calcium (Ca) Natrium (Na) Kalium (K) Phosphor Chloride (Cl) Magnesium (Mg) Procalcitonin Lactic Acid Electrolyte 26/09/2012 27/09/2012 6.7 mEq/L 2.17 mg/dL 105 U/L 124 U/L 30 U/L 9.4% 33.6 mg/dL 7.24-0.2 <281 <38 <41 <50 0.22 (HCO3) Total CO2 BE Oxygen saturation 20.0 Normal value Transparent <200 10-40 <32 CSF analysis Colour LDH Total Protein Leucocyte Eritrocyte transparant 62 U/L 12.9% 21.4 mmol/L 9.15 mEq/L 1.30 mg/dL 0.14 x 1.92 ng/mL 2/10/2012 4.3 mg/dL Result 150-400 <500 <1 0-0.04 mEq/L Other test 26/09/2012 28/09/2012 47.

Thorax x-ray (AP) on September 28th 2012 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 b. d CT-Scan on October 3rd 2012 Intepretation:  Infratentorial : the 4th ventricle and the cerebellum seems normal. .0 75% 25% 32-82 7-8 a.23 Glucose pH PMN MN Radiologic Findings : 60 mg/dL 8.

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: .9% within 20’  Metronidazole inj. feces and CSF . 75mg/8 hours/iv  Farmadol inj. 100mg  Morphine inj. blood.IVFD D5% NaCl 0.9%  20 gtt/i E: Diet F100: 140cc/3hours/OGT + mineral mix 2.5mg in 50cc D5% (tapering off dose 0. 8. MD 25mg/12 hours/iv in 10cc NaCl 0.9% within 20’  Phenobarbital inj. 450mg/6 hours/iv  Cefotaxime 250mg/6 hours/iv  Phenitoin inj.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. MD 25mg/12 hours/iv in 10cc NaCl 0.8cc  Ampicillin inj.

2/106/6. stoma(+). 450mg/6 hours/iv (D-5) .7 Ca/Na/K/Cl/Mg/Ph :7.5 Infec.Cefotaxime 250mg/6 hours/iv (D-5) .5mg in 50cc D5% (tapering off dose 0. GCS 14 (E4V4M6) Head: Eye: light reflex (+/+). 75mg/8 hours/iv (D-12) .Ca Gluconas 4.Farmadol inj.8/132/4.Metronidazole inj. HR: 138 bpm.Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0. MAP: 71mmHg .9% within 20’ (D-12) .Head elevation 30o . peristaltic(+)N.5cc/hour) . murmur (-). 8.6/1.RR: 50 tpm. fever (-). T: 38. reg crackles (-/-) H: Nasal flare (-). syst: Stable. Procalcitonin: 1.3cc D5% within 20’ A P .Phenitoin inj. syst : Unstable Abdomen: soepel. Thorax: SF.Multivitamin without Fe 1 x Cth1/2 (D-9) .Ampicillin inj.Zinc 1x20mg (D-12) . seizure(-) CNS syst : Unstable. Met. CV syst : Stable. BP: 93/61mmHg. epigastrial retraction (+).Fluid requirements: 1100cc-1200cc/day P: .3cc in 3. diarrhea(-).27cc/kgBB/hour) Resp syst : Unstable.9% within 20’ (D1-2) . feses(+).Morphine inj.18 MS syst : Stable. reg.50/4. fever(+). pale inferior conjunctiva palpebra (-/-). UOP: 680cc/24 hours(3.IVFD D20% = D5% NaCl(364cc) + D40%(136cc) > 15gtt/i .1oC. 100mg .Aminofusin 7cc/hour E: Diet F100: 95cc/3hours/OGT . MD 25mg/12 hours/iv in 10cc NaCl 0.25 Follow Up 8th October 2012 S O Deterioration of consciousness(+).Folic acid 1x1mg (D-12) . Nasal canul: 1/2-1 L/i. albumin: 2. isochoric pupil. post surgery wound: dry Encephalitis + Post laparatomy (D-19) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Sepsis with unstable CNS and metabolic system .

Met.Pediasure 95cc/3 hours/NGT A P . UOP: 920cc/24 hours (4.6cc . MD 25mg/12 hours/iv in 10cc NaCl 0.Fluid requirements: HS+20%op besar: 1060cc/hr P: . pale inferior conjunctiva palpebra (-/-).Phenobarbital inj. Abdomen: soepel.5cc/hour) (D10) .crackles (-/-) H: Nasal flare (-) Nasal canul: 1/21 L/i.Metronidazole inj.9 Infec. MAP: 80mmHg. diarrhea(-). HR: 150bpm. feses(+). murmur (-). pulse: 150 bpm.RR: 44 tpm. p/v adequate.Ampicill. CVC placed (D-9). reg . fever(-).IVFD D20% = D5% NaCl(364cc) + D40%(136cc) > 15gtt/i . syst: Stable.Albumin 25% 9. syst : Unstable.9% within 20’ (D-13) . epigastrial retraction (+).in inj. stoma(+).43cc/kgBB/hour) Resp syst : Stable. ruam kemerahan pada bekas colostomy CNS syst : Unstable.Cefotaxime 250mg/6 hours/iv (D-6) . BP: 100/70mmHg. Ca: 8. post surgery wound: dry Encephalitis + Post laparatomy (D-20) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Irritant Contact Dermatitis + Sepsis with unstable CNS. 8. GCS 14 (E4V4M6) Head: Eye: light reflex (+/+).Phenitoin inj.5mg in 50cc D5% (tapering off dose 0.26 . fever (-).Zinc 1x20mg (D-13) .Morphine inj. CV syst : Stable. MD 25mg/12 hours/iv in 10cc NaCl 0. Thorax: SF. peristaltic(+)N. T: 36.Aminofusin 7cc/hour E: Diet F100: 95cc/3hours/OGT . seizure(-). and metabolic system . 75mg/8 hours/iv (D-13) .Head elevation 30o . reg. 450mg/6 hours/iv (D-6) .Check Ca and albumin levels post correction 9th October 2012 S O Deterioration of consciousness(+).Farmadol inj.Multivitamin without Fe 1 x Cth1/2 (D-10) . isochoric pupil.Folic acid 1x1mg (D-13) .8oC MS syst : Stable. 100mg .9% within 20’ (D-13) .

syst : Unstable. murmur (-).5cc/hour (D-11) .9oC.RR: 36 tpm.Check Procalcitonin and lactic acid levels 10th October 2012 S O Fever(+). and metabolic system . pale inferior conjunctiva palpebra (-/-). T: 38. deterioration of consciousness(+). p/v adequate. seizure(-). MD 25mg/12 hours/iv in 10cc NaCl 0. feces(+): vol. reg.82 MS syst : Stable.9% within 20’ (D-14) . isochoric pupil.Phenobarbital inj. Lactic acid: 2. Abdomen: soepel. HR: 140bpm. 100mg . 0.Folic acid 1x1mg (D-14) A P . Infec. MAP: 66mmHg.±50cc . Thorax: SF. stoma(+). Met. UOP: 1220cc/24 hours (5. GCS 14 (E4V4M6) Head: Eye: light reflex (+/+).IVFD D20% = D5% NaCl(364cc) + D40%(136cc) + KCl (10mEq) + Ca Gluconas (10cc) > 11gtt/i .Phenitoin inj.Metronidazole inj.Cefotaxime 250mg/6 hours/iv (D-7) . syst: Stable.Ampicillin inj.27 .Farmadol inj. BP: 100/50mmHg. Nasal canul: 1/2-1 L/i. peristaltic(+)N.Morphine inj. reg . ruam kemerahan pada bekas colostomy CNS syst : Unstable.Zinc 1x20mg (D-14) . fever(+). 75mg/8 hours/iv (D-14) .Head elevation 30o . epigastrial retraction (+).9% within 20’ (D-14) . MD 25mg/12 hours/iv in 10cc NaCl 0.4.Aminofusin 11cc/hour E: Pediasure: 75cc/3hours/OGT . CV syst : Stable.O2 ½-1 L/i . pulse: 140bpm. post surgery wound: dry Encephalitis + Post laparatomy (D-21) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Irritant Contact Dermatitis + Sepsis ec Acinetobacter baumanii with unstable CNS. diarrhea(-).crackles (-/-) H: Nasal flare (-).Gentamicin zalf .7cc/kgBB/hour) Resp syst : Stable.Fluid requirements: HS+20%op besar: 1060cc/hr P: . 450mg/6 hours/iv (D-7) . CVC placed (D-10). Pro: 0.

27cc/kgBB/hour) Resp syst : Stable.±150cc . MS syst : Stable.Amikacin 220mg/hr in 50cc D5% within 30’ . epigastrial retraction (+). reg .IVFD D20% = D5% NaCl(364cc) + D40%(136cc) + KCl (10mEq) + Ca Gluconas (10cc) > 11gtt/i . isochoric pupil. and metabolic system . CVC placed (D-11). GCS 14 (E4V4M6) Head: Eye: light reflex (+/+). and electrolyte 11th October 2012 A P Fever(+). HR: 160bpm.crackles (-/-) H: Nasal flare (-).0 Urinalysis : within normal limit Fecal analysis : within normal limit Infec.9/4. diarrhea(-). T: 38oC. Thorax: SF. syst : Unstable.28 S O Multivitamin without Fe 1 x Cth1/2 (D-11) Gentamicin zalf Pediasure 75cc/3 hours/NGT Check urinalysis.O2 ½-1 L/i .RR: 36 tpm.1/128/3.Head elevation 30o . murmur (-). ruam kemerahan pada bekas colostomy CNS syst : Unstable. CV syst : Stable. MD 25mg/12 hours/iv in 10cc NaCl 0. stoma(+). t/v adequate. reg. MAP: 90mmHg.Abdomen: soepel.Aminofusin 11cc/hour E: Pediasure: 80cc/3hours/OGT . UOP: 660cc/24 hours (3.Fluid requirements: HS+20%op besar: 1060cc/hr P: . pale inferior conjunctiva palpebra (-/-).Phenitoin inj. feces(+): vol. Nasal canul: 1/2-1 L/i.Phenobarbital inj. Ca/Na/K/Cl/Mg/Ph : 8. deterioration of consciousness(+).9% within 20’ (D-14) . fever(+). seizure(-). pulse: 160bpm. feces analysis. MD 25mg/12 hours/iv in 10cc NaCl 0. peristaltic(+)N. Met.7/104/1. post surgery wound: dry Encephalitis + Post laparatomy (D-21) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Irritant Contact Dermatitis + Sepsis ec Acinetobacter baumanii with unstable CNS. BP: 110/60mmHg.9% within 20’ (D-14) . syst: Stable.

0.IVFD D20%: 8gtt/ . HR: 130bpm. reg. UOP: 600cc/24 hours (2. MAP: 73mmHg.9% within 20’ (D-16) .O2 ½-1 L/i . post surgery wound: dry Encephalitis + Post laparatomy (D-22) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Irritant Contact Dermatitis + Sepsis ec Acinetobacter baumanii with unstable CNS. diarrhea(-). feces(+): vol. BP: 100/60mmHg.Phenitoin inj.9cc/kgBB/hour) Resp syst : Stable. Nasal canul: 1/2-1 L/i. p/v adequate.Omeprazole 8mg/8 hour/iv . ruam kemerahan pada bekas colostomy CNS syst : Unstable. CVC placed (D-12).Head elevation 30o . 100mg Morphine inj.29 S O Farmadol inj. T: 38oC MS syst : Stable. isochoric pupil. syst : Unstable. Met.±130cc . fever(-). GCS 14 (E4V4M6) Head: Eye: light reflex (+/+).RR: 30 tpm. Infec. pulse: 130bpm.5cc/hour E: Pediasure: 100cc/3hours/OGT .Abdomen: soepel.9% within 20’ (D-16) .Aminofusin 5%: 3. reg . stoma(+). pale inferior conjunctiva palpebra (-/-).Thorax: SF. epigastrial retraction (+). fever(+).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. and metabolic system . peristaltic(+)N.Fluid requirements: HS±B P: .Phenobarbital inj. MD 25mg/12 hours/iv in 10cc NaCl 0.5mg 12th October 2012 A P Deterioration of consciousness(+). CV syst : Stable.crackles (-/-) H: nasal flare(-). syst: Stable. seizure(-). murmur (-). MD 25mg/12 hours/iv in 10cc NaCl 0.Amikacin 160mg/hr in 50cc D5% within 30’(D-2) .

82/3. diarrhea(+).Head elevation 30o .9/22. Ca/Na/K/Cl/Mg/Ph :8.94x10 /374x10 /25. deterioration of consciousness(+). BP: 100/60mmHg.RR: 30 tpm. HR: 146bpm.30 S O Farmadol inj.2/3. Electrolyte. lactic acid 13th October 2012 A P Fever(+). reg. pale inferior conjunctiva palpebra (-/-).3 Encephalitis + Post laparatomy (D-23) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Irritant Contact Dermatitis + Sepsis ec Acinetobacter baumanii with unstable CNS. reg . 100mg Morphine inj. Nasal canul: 1/2-1 L/i. T: 39oC. p/v adequate.7/29.7/11/1. CVC placed (D-13). isochoric pupil. Pro: 0. CV syst : Stable. murmur (-). peristaltic(+)N.±250cc. procalcitonin. syst: Stable.4. Met.76cc/kgBB/hour) Resp syst : Stable.5cc/hour (D-13) Citrizine 1x2. seizure(-).7x10 /9. lactic acid: 2.9/1.O2 ½-1 L/i .crackles (-/-) H: Nasal flare(-).5 MCV/MCH/MCHC/RDW = 68.1 N/L/M/E/B = 57. GCS 15 (E4V5M6) Head: Eye: light reflex (+/+).IVFD D5% = D5% NaCl(500cc)+ KCl (10mEq) + Ca Gluconas (10cc) > 7gtt/I (micro) . Thorax: SF.feces(+):vol. post surgery wound: dry CBC : Hb/RBC/WBC/PLT/HT = 6 3 3 8. UOP: 960cc/24 hours (4.4 Infec.81 MS syst : Unstable.Abdomen: soepel. stoma(+).2/32. epigastrial retraction (+). fever(+). LFT. RFT.3/0.5/133/4/102/8. and metabolic system . MAP: 73mmHg. 0.Albumin:3. pulse: 146bpm. syst : Unstable.0.5mg 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. ruam kemerahan pada bekas colostomy CNS syst : Unstable.2/29.

9% within 20’ (D-18) .Multivitamin without Fe 1 x Cth1/2 (D-14) . MD 25mg/12 hours/iv in 10cc NaCl 0. peristaltic(+)N. stoma(+).Amikacin 160mg/hr in 50cc D5% within 30’(D-4) . 100mg . isochoric pupil. seizure(-) Sens : CM Head : T: 37oC W: 8.9% within 20’ (D-18) P . Nose: NGT. HR: 126bpm.PRC transfusion 50cc 14th October 2012 S O Fever(+). feces(+) Extremity: Pulse: 126bpm.Pediasure 110cc/3 hours/NGT .Farmadol inj. retraction(-).6kg Eye: light reflex (+/+). MD 25mg/12 hours/iv in 10cc NaCl 0.Folic acid 1x1mg . reg.Phenitoin inj. deterioration of consciousness(+).Amikacin 160mg/hr in 50cc D5% within 30’(D-3) .Gentamicin zalf .O2 ½-1 L/i .Phenobarbital inj.crackles (-/-) Abdomen: Soepel. murmur (-). diarrhea(+).Omeprazole 8mg/8 hour/iv . MD 25mg/12 hours/iv in 10cc NaCl 0. reg .Citrizine 1x2. Thorax : Symmetrical fusiformis.31 . CRT<3” BP: 100/60mmHg A Encephalitis + Post laparatomy (D-24) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Sepsis ec Acinetobacter baumanii . MD 25mg/12 hours/iv in 10cc NaCl 0. Ear and mouth: within normal limit.Phenitoin inj.Candistatin drop 3 x gttII . reg.Head elevation 30o .9% within 20’ (D-17) . nasal canule.5mg .9% within 20’ (D-17) .Resomal 50-100cc/times diarrhea . RR: 22 tpm.IVFD D5% = D5% NaCl(500cc)+ KCl (10mEq) + Ca Gluconas (10cc) > 7gtt/I (micro) .Phenobarbital inj. pale inferior conjunctiva palpebra (-/-).

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 T: 39. retraction(-).6kg Eye: light reflex (+/+). deterioration of consciousness(+).Head elevation 30o .Citrizine 1x2.Omeprazole 8mg/8 hour/iv .9% within 20’ (D-19) . seizure(+) Sens : CM Head : W: 8. murmur (-). Ear and mouth: within normal limit. reg. RR: 20 tpm.Multivitamin without Fe 1 x Cth1/2 (D-16) P .Folic acid 1x1mg . reg .IVFD D5% NaCl 7gtt/I (micro) .Phenobarbital inj.2oC Fever(+). isochoric pupil. nasal canule. MD 25mg/12 hours/iv in 10cc NaCl 0. peristaltic(+)N.Amikacin 160mg/hr in 50cc D5% within 30’(D-5) .O2 ½-1 L/i . HR: 120bpm. stoma(+). CRT<3” BP: 100/60mmHg A Encephalitis + Post laparatomy (D-24) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Sepsis ec Acinetobacter baumanii . feces(+) Extremity: Pulse: 120bpm. Nose: NGT.32 S O Omeprazole 8mg/8 hour/iv Paracetamol 3x100mg Citrizine 1x2. Thorax : Symmetrical fusiformis. MD 25mg/12 hours/iv in 10cc NaCl 0. pale inferior conjunctiva palpebra (-/-).Paracetamol 3x100mg .9% within 20’ (D-19) .5mg .crackles (-/-) Abdomen: Soepel. reg. diarrhea(+).Phenitoin inj.

feces(+).Folic acid 1x1mg .Citrizine 1x2.33 S O Gentamicin zalf Pediasure 110cc/3 hours/NGT Resomal 50-100cc/times diarrhea Candistatin drop 3 x gtt II 16th October 2012 T: 38.Phenobarbital inj. Ear and mouth: within normal limit.O2 ½-1 L/i .IVFD D5% NaCl 7gtt/I (micro) . procalcitonin.Omeprazole 8mg/8 hour/iv . blood gas.2oC Fever(+). pale inferior conjunctiva palpebra (-/-).crackles (-/-) Abdomen: Soepel.Head elevation 30o .5mg .Check FBC.Resomal 50-100cc/times diarrhea . RR: 24 tpm. peristaltic(+)N.6kg A P Eye: light reflex (+/+).Candistatin drop 3 x gtt II .Paracetamol 3x100mg . CRT<3” BP: 100/60mmHg Encephalitis + Post laparatomy (D-25) a/i Ileosecal invagination + Bronchopneumonia + Moderate malnutrition + Sepsis ec Acinetobacter baumanii . reg. retraction(-). seizure(+) Sens : CM Head : W: 8. nasal canule.Ferry syr 1x CthI . MD 25mg/12 hours/iv in 10cc NaCl 0. reg . isochoric pupil. MD 25mg/12 hours/iv in 10cc NaCl 0.Phenitoin inj. CRP 17th October 2012 . Nose: NGT. Thorax : Symmetrical fusiformis. reg. HR: 122bpm. murmur (-).Amikacin 160mg/hr in 50cc D5% within 30’(D-6) .9% within 20’ (D-20) .Gentamicin zalf .Pediasure 110cc/3 hours/NGT .9% within 20’ (D-20)s . Liver and Spleen: unpalpable Extremity: Pulse: 122bpm. electrolyte. stoma(+). lactic acid.

diarrhea Sens : CM Head : T: 37. Nose: NGT. retraction(-).8 Lactic acid : positive CRP : pH/pCO2/pO2/HCO3/TCO2/BE/SaO2= Blood gas : 7.85kg A P Eye: light reflex (+/+).9/0.crackles (-/-) Abdomen: Soepel.5/ 97.9% within 20’ (D-21) . reg. seizure(+).1 MCV/MCH/MCHC/RDW = 73. CRT<3” BP: 100/60mmHg CBC : Hb/RBC/WBC/PLT/HT = 12/4.8 Procalcitonin: >100.Phenobarbital inj.Paracetamol 3x100mg .5mg . intercostals space clearly seen. Thorax : Symmetrical fusiformis. Ear and mouth: within normal limit.2cc .Gentamicin zalf .IVFD D5% NaCl 7gtt/I (micro) .2/25. RR: 24 tpm.1/0. 2mg/6 hour/iv .6/133/2. MD 25mg/12 hours/iv in 10cc NaCl 0.Amikacin 160mg/hr in 50cc D5% within 30’(D-7) .7/25.Pediasure 110cc/3 hours/NGT .6 Encephalitis + Post laparatomy (D-25) a/i Ileosecal invagination + Bronchopneumonia + Severe Malnutrition type marasmus + Sepsis ec Acinetobacter baumanii .63x106/14.3 Electrolyte: Ca/Na/K/Cl/Mg/Ph : 8. murmur (-).34 S O Fever(+).1/-5.Ketorolac inj.O2 ½-1 L/i .9% within 20’ (D-21) .15x103/74x103/34. stoma(+).4/17.2/19.Ranitidine 9mg/8 hour/iv . peristaltic(+)N.403/29.9/104.3 N/L/M/E/B = 73.7/106/8.8oC W: 8.9/35.9/1.1/18.Diet F100 160cc/3 hours NGT + Mineral mix 3.75/2.00 3.Citrizine 1x2. MD 25mg/12 hours/iv in 10cc NaCl 0.Head elevation 30o .Folic acid 1x1mg .3/8. nasal canule.Ferry syr 1x CthI .Resomal 50-100cc/times diarrhoea .Phenitoin inj. Liver and Spleen: unpalpable Extremity: Pulse: 124bpm. reg. feces(+). reg . HR: 124bpm. isochoric pupil. pale inferior conjunctiva palpebra (-/-).Candistatin drop 3 x gtt II .

Thorax : Symmetrical fusiformis. murmur (-).IVFD D5% NaCl 7gtt/I (micro) . Acinetobacter baumanii .Ketorolac inj. nasal canule.Check blood gas 19th October 2012 Fever(-).Phenitoin inj. isochoric pupil. intercostals space clearly seen.5kg A P Face: old man face (+) Eye: light reflex (+/+).9% within 20’ (D-22) .9% within 20’ (D-22) .5oC W: 8. seizure(-). peristaltic(+)N. diarrhea(+) Sens : CM T: 37. retraction(-).35 18th October 2012 S O Fever(-). reg . Ear and mouth: within normal limit. HR: 122bpm.5oC W: 8. CRT<3” BP: 110/80mmHg Encephalitis + Post laparatomy (D-28) a/i Ileosecal invagination + Severe Malnutrition type marasmus + Sepsis ec. seizure(-). diarrhea(+) Sens : CM Head : T: 37.5kg S O . reg. feces(+). RR: 22 tpm. MD 25mg/12 hours/iv in 10cc NaCl 0.Amikacin 160mg/hr in 50cc D5% within 30’(D-8) . MD 25mg/12 hours/iv in 10cc NaCl 0.Head elevation 30o . pale inferior conjunctiva palpebra (-/-).Phenobarbital inj.crackles (-/-) Abdomen: Soepel. Nose: NGT.O2 ½-1 L/i . 2mg/6 hour/iv . Liver and Spleen: unpalpable Extremity: Pulse: 124bpm. stoma(+). reg.

nasal canule. reg . reg . Liver and Spleen: unpalpable Extremity: Pulse: 160bpm. Nose: NGT. intercostals space clearly seen.1/190. Nose: NGT.9% within 20’ (D-23) .O2 ½-1 L/i .9/ 99. isochoric pupil.crackles (+/+) Abdomen: Soepel. reg. murmur (-). diarrhea(-) Sens : CM Head : T: 37. Liver and Spleen: unpalpable .Amikacin 160mg/hr in 50cc D5% within 30’(D-9) . murmur (-). HR: 120bpm. stoma(+). pale inferior conjunctiva palpebra (-/-).Phenobarbital inj. stoma(+). RR: 40 tpm. reg. Ear and mouth: within normal limit. seizure(-). Thorax : Symmetrical fusiformis.4 Encephalitis + Post laparatomy (D-29) a/i Ileosecal invagination + Severe Malnutrition type marasmus + Sepsis ec.3/18.75kg : S O Face: old man face (+) Eye: light reflex (+/+).Ketorolac inj. Acinetobacter baumanii . RR: 38 tpm. isochoric pupil.Head elevation 30o .36 Head A P Face: old man face (+) Eye: light reflex (+/+). Thorax : Symmetrical fusiformis.7/17. feces(+). nasal flare (+) intercostals space clearly seen.9% within 20’ (D-23) .IVFD D5% NaCl 7gtt/I (micro) . peristaltic(+)N. reg. HR: 160bpm.Carbamazepin 3x15mg (D-1) 20th October 2012 Fever(+). retraction(-). CRT<3” BP: 150/120mmHg Blood gas pH/pCO2/pO2/HCO3/TCO2/BE/SaO2= 7. MD 25mg/12 hours/iv in 10cc NaCl 0.9oC W: 8. feces(+).crackles (+/+) Abdomen: Soepel.Phenitoin inj. retraction(-). nasal canule. pale inferior conjunctiva palpebra (-/-).376/30. 2mg/6 hour/iv . Ear and mouth: within normal limit.2/-6. MD 25mg/12 hours/iv in 10cc NaCl 0. peristaltic(+)N.

pale inferior conjunctiva palpebra (-/-). peristaltic(+)N. Acinetobacter baumanii . CRT<3” BP: 130/100mmHg A P Encephalitis + Post laparatomy (D-30) a/i Ileosecal invagination + Severe Malnutrition type marasmus + Sepsis ec. isochoric pupil. Acinetobacter baumanii . RR: 42 tpm.O2 ½-1 L/i .9% within 20’ (D-24) . MD 25mg/12 hours/iv in 10cc NaCl 0.HR: 122bpm. retraction(-).37 Extremity: Pulse: 160bpm.crackles (+/+) Abdomen: Soepel. MD 25mg/12 hours/iv in 10cc NaCl 0. Thorax : Symmetrical fusiformis. 2mg/6 hour/iv . reg.Phenitoin inj. feces(+). seizure(-).Ketorolac inj. Ear and mouth: within normal limit. Liver and Spleen: unpalpable Extremity: Pulse: 160bpm.9% within 20’ (D-24) .Carbamazepin 3x15mg (D-2) 21th October 2012 Fever(-). Nose: NGT.Amikacin 160mg/hr in 50cc D5% within 30’(D-10) .Phenobarbital inj. reg. intercostals space. nasal flare (-). CRT<3” BP: 150/120mmHg Encephalitis + Post laparatomy (D-31) a/i Ileosecal invagination + Severe Malnutrition type marasmus + Sepsis ec. reg. reg .75kg S O A Face: old man face (+) Eye: light reflex (+/+). diarrhea(+) Sens : CM Head : T: 37oC W: 8. clearly seen. nasal canule.Head elevation 30o .IVFD D5% NaCl 7gtt/I (micro) . stoma(+). murmur (-).

Carbamazepin 3x15mg (D-3) - . 2mg/6 hour/iv .9% within 20’ (D-25) .9% within 20’ (D-25) .Phenobarbital inj.Ketorolac inj.38 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. MD 25mg/12 hours/iv in 10cc NaCl 0.

and children with chronic medical problems.5mg in 50cc D5% (tapering off dose 0. radiology and laboratory findings. MA is 1 year 5 month boy. with encephalitis. malnourished children. children on chronic antibacterial therapy. According to the site of infection and microbiologic etiology. Phenitoin inj. bronchopneumonia. the majority of infections causing sepsis were respiratory (64%).8cc. The diagnosis was established based on history taking.9%.9% within 20’. seizure. and musculoskeletal system and was a post laparatomy pasien due to ileoseptal invagination. 100mg.5cc/hour). MD 25mg/12 hours/iv in 10cc NaCl 0. 8. Cefotaxime 250mg/6 hours/iv.9% within 20’. 75mg/8 hours/iv. male. 1 year 5 months was admitted to Pediatrics Department of RSUP HAM and was diagnosed with encephalitis with bronchopneumonia. moderate malnutrition. Zinc 1x20mg. Diet F100: 140cc/3hours/OGT + mineral mix 2. Phenobarbital inj. Folic acid 1x1mg.1 Discussion MA. followed by digestive and . Ampicillin inj. From history taking and clinical manifestations patient experienced loss of consciousness. children with serious injuries. 450mg/6 hours/iv . Farmadol inj. Patients at risk for sepsis include infants. The treatment given were IVFD D5% NaCl 0. Morphine inj. 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. metabolic. Metronidazole inj. In this case.39 CHAPTER 4 DISCUSSION & SUMMARY 4. clinical manifestations. and sepsis with unstable CNS. moderate malnutrition and is post laparatomy patient. MD 25mg/12 hours/iv in 10cc NaCl 0. recurrent fever and diarrhoea.

From the culture that was done there were a few microorganism that was found. agitation. and tachypnea. lethargy. Candida. Pseudobacteremia may be associated with contaminated heparin flush solutions. Infections with gram-negative bacterla (e. obtundation. can also be signs of poor cardiac output. or coma. Aspergilus most often occur in immunocompromised and hospitalized patients colonized with these organisms. gram-negative bacteria caused the majority of infections that evolved with sepsis. However. The patient had CRT . including confusion. patient was also diagnosed with bronchopneumonia. albumin. Escherichia coli.g. This phenomenom also occurred with the respiratory rate.90. Pseudomonas. and decreased urine output. In this case. cardiac output falls in response to the effects of numerous mediators. with Escherichia coli and Klebsiella pneumoniae being the most frequent pathogens. As sepsis progresses. Klebsiella. the patient experienced frequent alternation of tempreture. From the blood Acinetobacter baumanii was isolated. Acinetobacter. cool extremities. The most common Gram-positive infecting organism was Staphylococcus aureus. From the cerebrospinal fluid Proteus mirabilis was isolated by BACTEC and Acinetobacter baumanii was isolated from culture. From the microbiologic aspect.. and infusion equipment. tachycardia. intravenous solutions. some days normal but somedays could have a tempreture reaching 38. and Serratia The site of infection in this case is thought to be in the CNS with diagnose of encephalitis. The initial signs and symptoms of sepsis include alterations in temperature regulation (hyperthermia or hypothermia). Atypical pathogens were identified in a minority of patients. Signs of poor cardiac output include delayed capillary refill. anxiety.g. And there was no growth of microorganism from the urine. cryoprecipitate. diminished peripheral and central pulses. Enterobacter.40 urinary tract infections (18% and 12% respectively).. Serratia) and fungi (e. Pseudomonas aeruginosa. Alterations in mental status. Contaminants include water-borne organisms such as Acinetobacter baumanii.

reduced serum fibrinogen levels and elevated fibrin split products. can be used to support the diagnosis of sepsis. . In this case. hematologic abnormalities that was seen were elevated Ddimer and there was evidence once of thrombocytopenia. corticosteroid and other treatment according to organ dysfunction. CRP. Some biochemical markers examination such as procalcitonin. hypocalcemia. etc. In this case the criteria of SIRS that was present is hyperthermia. elimination of pathogen. The levels of lactic acid. peritoneal fluid. prolonged prothrombin and partial thromboplastin times.). And the infectious etiology was cultured from CSF and blood. etc. treatment of hyperglycemia. fluid resuscitation. Hematologic abnormalities include thrombocytopenia. tachypnea. metabolic acidosis. Electrolyte abnormalities that was discovered were hypocalcemia. and anemia. however low serum bicarbonate was seen. An infectious etiology should be sought by culturing clinically appropriate specimens taken from body fluids (blood. There were no evidence of metabolic asidosis. However. Laboratory findings often include evidence of hematologic abnormalities and electrolyte disturbances.warm extremities and no decrease in urine output. there was alteration in mental status. hypokalemia. procalcitonin and CRP was seen. cerebrospinal fluid. And there was evidence of elevation of ALT and AST. The diagnosis of sepsis requires SIRS in the presence of proven infection or a clinical picture consistent with infection. Electrolyte abnormalities include hyperglicemia. Giving rise to Acinetobacter baumanii from the blood and from the CSF Proteus mirabilis and Burkholderia cepacia was isolated. hypoalbuminemia. and also there was leucocytosis . hypoalbuniemia. Lactic acidosis can occur if there is significant anaerobic metabolism. and low serum bicarbonate. The mainstay of the treatment of sepsis include airway patency with adequate oxygenation. abscesses. hyponatremia. urine.41 <3”.

And from the result of sensitivity test amikasin was then the antibiotic of choice.42 MA. . moderate malnutrition. Patient is still hospitalized in Adam Malik General Hospital. fluid. and metronidazol. and musculoskeletal system and was a post laparatomy pasien due to ileoseptal invagination. male. ceftriaxone . 1 year 5 months was admitted to Pediatrics Department of RSUP HAM and was diagnosed with encephalitis with bronchopneumonia. and for the elimination of pathogen the patient was given empiric antibiotic such as amphicilin. metabolic. 4. and sepsis with unstable CNS.2. Summary MA. was treated with oxygenation.

Management and Treatment Guidelines for Sepsis in Pediatrics Patients. World federation of pediatric intensive care and critical care societies: global sepsis initiative. P. Powell KR.S. Values for systolic blood pressure. 2005: 6. Chest. International pediatrics sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. 2011. Starke R. Devictor D. et al. and associates cost of care. Cornell. Taneja A.6:3-5. 2011. Espinosa V. Argent A. Angus DC. Pediatr Crit Care Med. Kumar G.. The Global Burden of Disease: 2004 Update. Carcillo JA. Tarima S. Nationwide trends of severe sepsis in the 21st century (2000-2007). Kliegman RM. Geneva. 5. Enrione MA. Lidicker J.. Crit Care Med. Pediatr Crit Care Med. 7. Carcillo JA. 2005. Randolph A. 2005. Martinovici D. 413-40. Pinsky MR. Kissson N. 2005:6. 2001.. TT.4:101-9 6. Pediatr Crit Care Med.J. Jurnalul Pediatrului. World Health Organization. Hotez J. Pediatr Crit Care Med. Militaru M. outcome. Carcillo J. Linde-Zwirble WT. Epidemiology of severe sepsis in the United States: analysis of incidence. .29(7): 1303-10. Giroir B. In: Behrman RE. Tuberculosis. 2. Stanton BF. Krugman’s Infectious Disease of Children 11th edition. 9. El-wiher N. Kumar N.P. 2004. Gebara BM.43 REFERENCES 1. Switzerland. Madden M.12(5):494-503. Kissoon N. Philadelphia.140(5): 1223-31. Jenson HB.8:26-31. Our Experience in Pediatric Sepsis. Clermont G. Katz L. 731-762. The Open Inflammation Journal. 4. et al. and Systemic Inflammatory Response Syndrome. 2011. 10. 2. 3. 8. Septic Shock.A. In: Gershon A. Shanley TP.. McGinley E. Watson RS. Scope and epidemiology of pediatric sepsis. 500 (author reply-1). Sepsis. Goldstein B. Kaleekal T. 2008.

4:99-106. 2008. Argent AC. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Tatalaksana Awal Sepsis Berat dan Syok Sepsis Anak. Adriansyah R. 2009. Journal of Pediatric Infectious Diseases.38-61. 2nd ed. Philadelphia: Saunders. 18th ed. Indian J Crit Med. Jaeschke R.9(3): 164-172. Septic shock: Management in emergency department with available resources. Santhanam I. 2007:1094-99 11. Nelson Textbook of Pediatrics. Jakarta: IDAI. Satari HS. Clinical management guidelines of pediatric septic shock. 13. Buku Ajar Infeksi dan Pediatri Tropis. Medan: IDAI-Sumut. 16. et al. In: Ali M. Skippen P. editors. . Khilnani P. 2009. Trisnawati Y. Somasetia DH. Parker MM. 14. 2012:358-363. Tatalaksana Awal Kegawatan pada Bayi dan Anak. Baranwal AK. Dimyati Y.44 Ziteli BJ. 2005. Davis HW. Journal of Pediatric Infectious Diseases. Soedarmo SS. Hadinegoro SR. Sepsis in the pediatric intensive care unit. 15. Dellinger RP. Kissoon N. editors. Mizuno Y. Crit Care Med. Levy MM. Carlet JM.4:85–98. Singhi S.36:296-327. Singal M. Garna H. Bion J. 12.

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