CASE PRESENTATIONSHOCK SEPSIS ON COMMUNITY-ACQUIRED PNEUMONIA

Arranged by:Florence Low (0906550751)

Resource Person:dr. Dita Aditianingsih, Sp,An-KIC

Intensive Care Elective Practice Module Faculty of Medicine, Universitas IndonesiaMay 2015

Case IllustrationPatients IdentityNama: Mr. RNo. Rekam Medis: 404-01-92Tanggal Lahir: 12 September 1962 (52 tahunJenis Kelamin: Laki-lakiPekerjaan: Ketua RTPendidikan: SDStatus Perkawinan: MenikahAgama: IslamAlamat: Kramat JatiTanggal masuk: 14 Mei 2015

AnanmnesisData didapat dari anamnesis dan rekam medis pada tanggal 18 Mei 2015.

Keluhan UtamaPenurunan kesadaran sejak 7 jam sebelum masuk rumah sakit.

Riwayat Penyakit SekarangPasien dirujuk ke RSCM dari RS daerah karena pneurunan kesadaran yang membutuhkan perawatn ICU. 3 hari SMRS, pasien mengeluhkan sesak yang memburuk. Sesak tidak dipengaruhi posisi ataupun aktivitas. Mengi disangkal. Terdapat demam namun suhu tidak diukur. Pasien sebelumnya hanya minum obat warung untuk mengurangi demam. Satu hari SMRS, pasien tampak mengantuk dan lemas. Pasien masih dapat diajak berbicara namun lebih memilih untuk tidur terus. Nafsu makan pasien juga menurun. 7 jam SMRS, sesak bertambah parah, nafas bertambah cepat dan pasien tidak dapat berbicara. Kesadaran pasien juga menurun dan pasien tidak menjawab bila dipanggil. Sakit kepala disangkal, mulut mencong dan kelemahan satu sisi juga disangkal, kejang disangkal. Pasien lalu dibawa ke RS daerah.2 minggu SMRS, pasien mulai batuk berdahak, batuk darah disangkal. Pada waktu itu, demam belum muncul. Pasien tidak berobat dan hanya mengkonsumsi obat warung. Riwayat batuk lama, keringat pada malam hari, dan penurunan berat badan disangkal. Psien menyangkal riwayat sakit paru ataupun asma. Pasien didiagnosis diabetes mellitus type II sejak 2,5 tahun yang lalu. Pasien tidak rutin berobat. Pasien mengaku bahwa gula darah rata-rata 300 mg/dL..

Riwayat Penyakit DahuluTerdapat riwayat darah tinggi, stroke dan penyakit jantung sebelumnya. Pasien tidak memiliki pengobatan apapun.

Riwayat Penyakit dalam KeluargaRiwayat DM, hypertensi, asma dan penyakit jantung dalam keluarga disangkal.

Riwayat SosioekonomicPasien sudah menikah, memiliki 4 anak. Pasien bekerja sebagai ketua RT. Untuk pembiayaan, pasien menggunakan KJS.

Pemeriksaan Fisik(Dilakukan tanggal 18 Mei 2015)Status Generalis: tampak sakit beratKesadaran: coma (dalam pengaruh obat)Tanda Vital Tekanan darah: 182/41 mmHg Nadi: 104x/minute, Pernapasan: 20x/minute, on ventilator Suhu: 36.7C Berat badan: 60 kgPemeriksaan Kepala: normocephal, tidak ada tanda deformitas Mata: konjuntiva pucat +/+, sklera ikterik -/-, pupil isokor 3mm, RCL +/+, RCTL +/+ Hidung: on NGT Mulut: on ETT Leher: tidak teraba pembesaran KGB, terpasang CVC Dada: simetris statis dinamis Jantung: S1 S2 normal, murmur -/-, gallop -/- Paru: simetris, perkusi kiri sama dengan perkusis kanan, vesikuler +/+, terdengar rhonki basah halus pada kedua lapang paru Abdomen: buncit, kenyal, tidak teraba massa, bising usus normal Ekstremitas: akral hangat, CRT< 2, edema pada kedua lengan Kulit: pada region inguinal bilateral hingga skrotim, tampak lasi plakat multiple diskret ireguler, batas tegas denga lesi satelit

Pemeriksaan PenunjangPemeriksaan Laboratorium14/4/1518/5/1518/5/15 (post HD)19/5/1520/5/1521/5/1522/5/15

Hb (g/dL)7.7510,59,2728,79,928,4811,19.74

Ht (%)25,232,728,730,72433,430.4

Leukosit (/L)9970175002010021300124001220025200

Trombosit (L)4270001980001310001180001020005480071.900

MCV (fL)73,170,070,07273,674,4

MCH (Pg)23,722,622,625,424,423,8

PT12,4 (12,6)11,2 (11,8)11,9 (11,8)13,8 (11,2)13,0 (12,7)14,0 (10,8)

APTT69,9 (35,5)53,2 (32,5)65,2 (34,5)55,7 (36,3)>180 (35,1)

Na (mmol/dL)132135125135130127127

K (mmol/dL)4.55,04,24,33,84,84,4

Cl (mmol/dL)1061061031021009697

Ca7,98,48,389

Mg2,262,042,83,39

Ur (mg/dL)25,281,466,774,992,9117,294

Cr (mg/dL)1,3923,53,13,3473,8634,1043,316

AGD

pH7,2727,0767,2137,1906,864

pCO226,434,928,447,154,493,1

pO2206,5158,4149,5189,3188,4117,6

HCO312,310,311,517,215,917,7

BE-17,5-14,2-9,3-13,5-15,6

SaO295,996,198,997,997,492,5

Albumin (g/dL)2,052,272,16

Keton4

GDS

Prokalsitonin17,93

Laktat0,70,51,51,1

UrinalisisPada urinalisis ditemukan protein +2, keton +1, darah +1 dan leukosit 1-2

Pemeriksaan Radiologis Chest X-ray (18/5/15) 18/5/15: Tampak inflitrat di parakardial kanan dan suprhiler kiri, sugestif gambaran tanda awal bendungan paru 20/5/15: dibandingkan dengan foto sebelunya, infiltrate di parakardial kanan berkurang

Daftar Masalah1. Penurunan Kesadaran ec sepsis dd metabolik2. Shock sepsis ec CAP3. Ketoacidosis diabetikum pada DM type II tidak terkontrol4. AKI dd Acute on CKD

Rencana Diagnosis1. Kultur sputum dan darah2. Tes resistensi and sensitivitas antibiotic

Rencana Terapi1. Rawat ICU dengan ventilator pemantauan hemodinamik2. IVFD RF 50cc/jam3. Diet per NGT nutriflex4. Atasi sepsis dan CAPa. Stabilisasi hemodinamik: norepinephrine 0,1 mcg/kg/min IV, dobutamin 20mcg/kg IVb. Antibiotik: meropenem 3 x 1gr IV dikombinasikan dengan levofloxacin 1 x 750mg IVc. Anti-fungal fluconazole 1 x 400mg IOd. Pengeluaran mucus: fluimucyl 3 x 1 sach, suction aktif / 4jam dan inhalasi B:V:N / 6jame. Atasi demam: paracetamol 3 x 500mg5. Anti stress-ulcera. omeprazole 2 x 40mgb. Sucralfat 4 x 1 Corigc. Metoclopramid 3 x 1amp6. Atasi hiperglikemia: Ringer Insulin 1Unit/jam, GDS per 6 jam7. Sedasi midazolam 15 mg8. Anuria dengan fluid overload furosemide 20 mg IV, balans diuresis negatif9. Jaga higienis mulut dan kulit

Follow up 16/5/2015S: perawatan hari ke-1; pasien masuk ICUO: BP 100-120/60-80; MAP 50-89 CVP +17,5 cmH2ORR 12-16x; Pola ventilator PC 12, PEEP +5, RR 12, FiO2 40%, GDS 109, 85, 162, 325Input: 2221,2 ccOutput 420 cc Rate diuresis 0,29/kgBB/jamBalans/24 jam +1801,2 ccA: Shock sepsis ec CAP, KAD, AKI dd acute on CKDP: RDx: cek PCT, kultur sputum dan darah, sputum BTA 3xRTh1. Lanjutkan terapi2. Sedasi morfin 1mg/jam dan midazolam 1mg/jam3. IVFD NS 500cc/24jam4. MC 30cc/jam5. Nutriflex 1 /24jam6. RI 1 unit/jam7. NE 0,05mcg/kgBB/min

Follow up 17/5/2015S: perawatan hari ke-2; pasien arrest dan di-RJP, re-intubasi karena mucus plugO: BP 120-140/60-80; MAP 66-103 CVP +15 cmH2ORR 12-16x; Pola ventilator SIMV 14, PC 12, PEEP +7, RR 16, FiO2 40%, GDS 324, 304, 311, 219, 150, 118Input: 3183,3 ccOutput 781 cc Rate diuresis 0,54cc/kgBB/jamBalans/24 jam +2402,3 ccA: Shock sepsis ec CAP, KAD, AKI dd acute on CKDP: RDx: DPL, Ur/Cr, P/APTT, AGD, elektrolit, GDSRTh1. MC 50cc/jam2. Nutriflex 1/24jam3. RF 50cc/jam4. RI 1 unit/jam titrasi5. Midazolam 2mg/jam6. MAP 50 NE dinaikkan darri 0,15mcg ke 0.75mcg7. Arrest bradicardi 36x; BP 36/29 Dilakukan RJP 2 siklus, mendapat SA 6 ampul, Adrenalin 1 amp NE 1,1 mcg, dobutamin start dosis 5-10mcg Reintubasi ETT ditemukan sekret kental putih (mucus plug)

Follow up 18/5/2015S: perawatan hari ke-3, pasien HD, ditarik cairan sebanyak 1500ccO: BP 182/82; MAP 90-124; CVP +22cmH2ORR 16-20x; Pola ventilator PC 14, PEEP +7, RR 16 FiO2 50%, GDS 188, 207, 306, 203Input: 3984,4 ccOutput 2520cc Rate diuresis 0,63/kgBB/jamBalans/24 jam +1464,4ccA: Shock sepsis ec CAP, KAD, AKI dd acute on CKD, riwayat cardiac arrestP: RDx: cek ulang PT/APTT, konsul nefrologiRTh:1. lanjutkan terapi2. Peptamen 30cc/jam per NGT3. Nutriflex 1/24jam4. RF 50cc/jam5. RI 1 unit/jam titrasi6. NE 0,3mcg/kgBB7. Lasix 2mg/jam8. MAP >100 Titrasi Norepinephrine 0,1mcg

Follow up 19/5/2015S: perawatan hari ke-4, residu makanan keluar dari NGTO: BP 140-120/80-90; MAP 92-100; CVP +12cmH2ORR 16-20x; Pola ventilator PC 12, PEEP +7, RR 12, FiO2 50%, GDS 146, 104, 157, 38, 75Input: 2358,6 ccOutput 550cc Rate diuresis 0,38/kgBB/jamBalans/24 jam +1808,6 ccA: Shock sepsis ec CAP, KAD, AKI dd acute on CKD, riwayat cardiac arrestP: RDx: GDS berkala, rencana echocardiographyRTh: RI 1U/jam titrasi NE 0,4mcg/kgBB RF 20cc/jam Lasix drip 2mg/jam miloz 1mg/jam GDS menurun, stop RI pasien dipuasakan GDS menurun, stop RI; pasien dipuasakan

Follow up 20/5/15S: perawatan hari ke-5; GDS menurun, residu makanan keluar dari NGTO: BP 140-110/80-90; MAP 50-89 CVP +17,5 cmH2ORR 12-16x; Pola ventilator PC 12, PEEP +7, RR 12, FiO2 60%, GDS 75, 68, 121, 112,Input: 2412 ccOutput 830 cc Rate diuresis 0,26/kgBB/jamBalans/24 jam +1582,2 ccBalans kumulatif +9058,7A: Shock sepsis ec CAP, KAD, AKI dd acute on CKD, riwayat cardiac arrestP: RDx: cek PCT, konsul radiologi untuk USG abdomenRTh: GDS menurun stop RI, bolus D40%, cek GDS berkala Peptamen stop, ganti CF 30cc/jam, konsul IPD Rencana HD Koreksi albumin untuk persiapan HD Hb 8,48 Transfusi PRC 1 bag Ganti ETT MAP 50 dosis NE 0,8mcg, dobutamin 15mcg Rencana HD menjadi CVVH karena hemodinamik tidak stabil start epinephrine 0,1 mcg

Follow up 21/5/15S: Perawatan hari ke-6, pasien mulai CVVHO: BP 96-105/58-66; MAP 50-70; CVP +12cmH2ORR 16-20x; Pola ventilator PC 12, PEEP +7, RR 15, FiO2 60%, Input: 2579,4 ccOutput 400cc Rate diuresis 0,27/kgBB/jamBalans/24 jam +2179,4 ccA: Shock sepsis ec CAP, KAD, AKI dd acute on CKD, riwayat cardiac arrestP: RDx: rencana USG abdomenRTh: MAP 70 titrasi epinephrine hingga 0,5mcg, bila tercapai mulai titrasi NE

Literature ReviewCommunity-Acquired PneumoniaPneumonia is defined as infection of lung parenchyma. Clasically, pneumonia can be classified to 3 type: community-acquired (CAP), hospital-acquired (HAP), and ventilator-associated (VAP). Each types have different pathogens causing the infection. Streptococcus pneumonia, Mycoplasma pneumonia, Haemophilus pneumonia are the most common typical bacteria associated with CAP. Less common typical bacteria include Staphylococcus aureus and Pseudomonas aeruginosa. Pneumonia results from combination of pathogens activity at alveoli and hosts response to these activities. Normally, when pathogens are inhaled, mechanical factors of respiratory system will act to capture the particles. Then mucociliary clearance and local antibacterial factor will response to either clear or kill the pathogens. If the pathogens managed to reach the alveolar level, local alveolar macrophages then act to eliminate it. However, if macrophages are overwhelmed by thse pathogens, colonization of pathogens occurs. Inflammation response are triggered causing release of inflammatory mediators causing the clinical manifestation of pneumonia. Interleukin (IL)-1 and tumour necrosis factors (TNF) wresults in fever while chemokines stimulates the release of neutrophils, resulting in increase of leukocytes and production of purulent and mucus. These mediators also caused capillary leakage which can be seen in radiographic examination as infiltrate and rales which are detectable on auscultation. The leakage will cause alveolar filling which in turn caused hypoxemia. All this contributes to dyspnoea. Clinical manifestations of CAP are fever with tachycardia, productive or non-productive cough, and shortness of breath. Pleuritic chest pain and haemoptysis may also occurs. In cases of atypical pneumonia, low-grade fever and non-productive cough may be seen. American Thoracic Society (ATS) recommend laboratory testing such as sputum and blood culture to identify the aetiology accompanied by chest radiographic to appropriately diagnose pneumonia. Initial assessment of severity is important in determining whether patient can be managed as outpatients or in the hospital. British Thoracic Society (BTS) recommends the CURB-65 score for this assessment while ATS used Pneumonia Severity Index (PSI) to assess the severity of CAP. Below are the scoring system of CURB-65 and PSI.

The decision of ICU treatment for CAP patients is performed on second-level admission. Based on ATS guidelines, patients with septic shock requiring vasopressor or those with acute respiratory failure requiring intubation and mechanical ventilation fulfilled the criteria for ICU. Patients with severe CAP are also recommended for ICU admission.

Determining the severity of CAP is also important for the antibiotic selection. Empirical antibiotic therapies are given before responsible pathogens are identified by culture. For inpatient in non-ICU settings, respiratory fluroquinolone are -lactam plus macrolide can be used for hospitalized patients without complication. In ICU settings, antibiotic of choice are -lactam (cefotaxime, ceftriazone, ampicillin-sulbactam) plus either azithromycin or fluoroquinolone. In the suspicion of pseudomonas infection, anti-pseudomonas -lactam such as carbapenem plus fluoroquinolones can be given. As soon as specific pathogen responsible for CAP are identified, therapy should be switch to antimicrobial therapy directly targeted for the specific pathogens.

Sepsis and Septic ShockSepsis is defined as systemic inflammation in response to infection. The diagnosis of sepsis can be established when systemic inflammation response syndrome (SIRS) are documented along with the presence of infection. Severe sepsis occurs when one or more signs of organ dysfunction is found. Organ dysfunction occurs due to lack of tissue perfusion induced by sepsis. When sepsis-indeuced hypotension cannot be manage despite adequate fluid resuscitation, septic shock occurs.Inflammation ConditionCriteria

Systemic Inflammation Response Syndrome (SIRS)1. Fever more than 38.3oC or hyperthermia 90x/min)3. Tachypnoea (RR> 24x/min)4. Leukocytosis >12000/L, leukopenia 1mmol/L)2. Oliguria (output < 0.5ml/kgBW/h)3. ALI with hypoxemia (PaO2< 300)4. Creatinine> 2mg/dL5. Bilirubin >2mg/dL6. Thrombocytopenia 1.5)

In patient with severe sepsis, initial resuscitation is important in preventing further organ dysfunction. The target for resuscitation includes CVP 8-12mmHg, MAP >65mmHg, urine output >0.5mL/kgBW/h, central venous or mixed vein oxygen saturation 70% or 65% respectively and normalized lactate. Further management should be identification of microbes by culture along with initial empirical anti-infective therapy. Anti-microbes recommended in cases of respiratory failure and septic shock is combination of broad-spectrum beta-lactam and aminoglycoside or fluoroquinolone.

Diabetic KetoacidosisDiabetic ketoacidosis (DKA) is an acute complication of diabetes mellitus (DM). Although it is usually found in DM type I patients, it can also be seen several DM type II patients. Clinical manifestation of DKA includes nausea-vomiting, thirst, decrease of consciousness, Kussmaul breathing, abdominal tenderness, lethargy, tachycardia and signs of dehydration. DKA is usually precipitated by certain condition in the patient such acute myocardial infarction, stroke or acute infection. Laboratory findings of DKA includes hyperglycemia with blood glucose of >250mg/dL, metabolic acidosis and ketosis in the form of ketonemia or ketonuria. Pathophysiology of DKA can be seen from hormonal onbalance betwenn regulatory hormones of blood glucose. Deficit in insulin hormone, coupled with excess in its counterregulatory hormones such as glucagon cause increase in gluconeogenesis, glycogenolysis causing increase in glucose synthesis. Reduced insulin level and elevation of catecholamine promoted release of free fatty acids from adypocutes, which is metabolized in the liver, forming ketone body due to hyperglucagonemia, causing ketosis.In the management of DKA, monitoring of electrolytes, acid-base status and renal functions are important. Fluid therapy at the first 6 hours of hospital admission is important along with management of hyperglycemia with insulin. Based on guidelines by Indonesian Society of Endocrinology (PERKENI), 2-3 L of NaCl 0.9% must be given in the first 3 hours, then on the second hour, insulin must be administered with dosage of 280mU/kgBW bolus, continued with drip of dosage 90mU/kgBW/hours in NaCl0.9%. Dosage can be lowered based on the level of blood glucose. Correction of potassium and bicarbonate can be given of necessary. Since potassium stores are depleted in DKA, hypokalemia commonly occurred. 50 mEq/6 hours can be given then after administration, addition of potassium can be added if hypokalemia still occurring. Vital signs and blood glucose level must be monitored every hour while blood gas analysis and electrolyte level can be measured every 6 hours until patient is stable. Acute Kidney InjuryBased on Kidney Disease Inmproving Global Outcome (KDIGO) guidelines, acute kidney injury (AKI) is defined as increase in serum creatinine of more than 0.3 mg/dL within 48 hours or increase of more than 1.5x baseline or decrease urine output of less than 0.5 ml/kg/hour for 6 hours. Based on serum creatinine level and urine output, AKI can be divided to 3 stages. Other criteria which can be used is the RIFLE, stages includes risk, injury, failure, loss, and end-stage renal disease (ESRD). These stages determined types of treatment AKI patients should receive. Determination of cause of AKI is important to prevent worsening of condition, decrease kidney perfusion, glomerulonephritis, urinary tract obstruction are among the common cause of AKI. Among the cause, persistent hypotension in patient with shock who are not responsive towards fluid resuscitation increase the risk of development of AKI. Vassopressor are recommended in septic shock patients for prevention and even treatment of patient with AKI.. Noreponephrine, dopamine and vasopressin are the drugs of choice used. Vasopressin are quite effective increasing blood pressure and enhance diuresis. Diuretics are not recommended in the management of AKI except volume overload is present in the patient. DiscussionSince patient was admitted to ICU, the antibiotics of choices are -lactam plus fluoroquinolone or azithromycin. However, patient has history of hospitalization for 2 days prior to this admission. P. aeruginosa infection should be considered in this patient. Hence, anti-pseudomonas is considered in this patient. Therapy given in this patient, which is levofloxacin and meropenem is appropriate for the settings. Anti-fungal such as fluconazole can be considered in patient suspected with Candida sp. infection. Length of treatment should be 3-5 days and can be extended to 7-10 days in patient with slow clinical response. Procalcitonin can be use as biomarkers for the effectivity of empiric antibiotics.In case of life-threatening hypotension, vasopressor therapy should be initialized with target MAP of 65mmHg. The drug of choice used is norepinephrine. Norepinephrine was used to increase atrial blood pressure, increase myocardial contractility and cardiac output. It was given in continuous infusion in the range of 1-20 g/min. Vasopressin can be added to norepinephrine to increase the target MAP while epinephrine can be used as potential substitute for norepinephrine or as addition to increase cardiac output rather than to increase MAP.Managemeent of AKI in patient with fluid overload and increasing creatinine level is according to the RIFLE criteria. In this patient, the creatinine level is already above 4mg/dL with decrease urine output less than 0.3cc/kgBW/hour. Based on this criteria, patient is already classified in AKI stage 3 or RIFLE criteria of failure. Moreover, patient also had acid-base imbalance from the DKA condition with unstable haemodynamic condition. hence patient is indicated for hemodialysis therapy. On the day-7, patient has low pH with a high PCO2 and near normal HCO3. This shown that patient develop respiratory acidosis due to poor oxygenation despite breathing on ventilator. The ventilator mode in this patient was pressure control with PEEP. Patient was shown to be struggling a bit with the ventilator and still have several spontaneous breathing. Pressure-control is still appropriate in this patient since he showed a poor lung compliance, hence PC mode can reduce the risk of barotrauma on this patient. SIMV can also be applied since patient sometimes still has spontaneous breathing and SIMV mode can make sure that ventilation given does not collide with patients own breathing. It can be given with lower tidal volume might be more appropriate since in ensures patient to have minimum ventilation but still protect the lung from further injury due to mechanical ventilation.

References1. Dellinger RP et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock 2012. Crit Care Med 2013;41:580-637. 2. Mandell LA, Wunderink RG, Anzueto A, et al. Infectious diseases society of America/ American thoracic society consensus guidelines on the management of community-acquired pneumonia in adults. Clinical Infectious Diseases. 2007; 44:S2772.3. KDIGO. KDIGO Clinical practice guidelines for acute kidney injury. KDIGO Kidney International Supplements. 2012;2:1; doi:10.1038/kisup.2012.24. Miller RD, Pardo MC. Basics of anesthesia. 6th edition. Philadelphia (PA): Elsevier Saunders; 2011.5. Longo DL, Kasper DL, Fauci AS, et al. Harrisons principle of internal medicine. 18th edition. New York (NY): McGraw-Hill; 2012. 6. PERKENI. Petunkuk praktis pengelolaan diabetes mellitus tipe II. Jakarta: PB PERKENI; 2002.