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Case Presentation:-

بسم الله الرحمن الرحيم وزارة الدفاع رئاسة الأركان المشتركة الادارة العامة للخدمات الطبية قسم العناية المكثفة. Case Presentation:-. Prepared by : Dr.Altayeb M.Altayeb Abdalaziz ICU – Resident Supervised by : Dr.Kamal Osman Mergani Consultant Intensivist.

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Case Presentation:-

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  1. بسم الله الرحمن الرحيموزارة الدفاعرئاسة الأركان المشتركةالادارة العامة للخدمات الطبيةقسم العناية المكثفة

  2. Case Presentation:- Prepared by : Dr.AltayebM.AltayebAbdalaziz ICU – Resident Supervised by : Dr.KamalOsmanMergani Consultant Intensivist

  3. Case Presentation :- • Mss. S.A.A.M is a 75 yrs old female who is known to be Hypertensive for 5 yrs on regular treatment, not known to be diabetic, referred to our department as a case of severe sepsis due to hospital acquired pneumonia. • She was admitted on 10th.0ct.2012 & her examination on admission was as follow:

  4. Vital Signs • GCS: 15/15, B.P: 110/60 , PR: 120/min , RR:22/min, Temp.:38C • CNS: Unremarkable. • CVS: Unremarkable • Respiratory System :Fine crepes bilaterally • Abdominal & Renal system : Unremarkable • What To Do NEXT ?

  5. 1. Patient Received (1)L of Normal Saline. 2. Blood sent for Investigations(CBC,RFTS). 3. Patient started antibiotics(Meropenem1gTDS) 4. Observation of Vital signs & urine output hourly.

  6. Patient Follow up: (11th.Oct.2012) • General: Unwell , BP:130/80 , PR: 100/min , RR:20/min, Temp. 37.6 C , U.O.P : Adequate at (0.5-1)ml/kg/hr • Chest: Fine Crepes bilaterally • CNS, CVS, Abdomen —> Unremarkable

  7. Event Clock UOP NIL 12 UOP:50ml/hr BP110/60 11 1 Another Liter of N.S UOP Still  NIL B.P:100/50(55) 10 MazenK 2 1L N.S Septic Shock UOP:20ml/hr B.P100/50 9 3 AT : 16:15 Confused.Tachypnic + type II Resp.Failure on ABG Quartz 8 4 • Investigations: • CBC:TWBCS(12.2) ,Hb(9) ,Plt(400) • RFT&elect: Urea(40), Creat(2), Na+KNormal N.E 0.25MCG/KG/MIN 7 5 6 Dopamine 20mcg/kg/min Hydrocortisone 50mgQ6hrs B.P:100/50 UOP:NIL ABG: Met. acidosis • Connected To MV • BP:110/60 • Continue Antibiotic • F/U via ABG & Vital signs

  8. What to Do Next ?

  9. Pt supported by Fluids & Inotropes (N.E+Dopamine Max.Dose) 2.Add Vancomycine (Renal dose). 3.Septic Screening Sent( Blood, Urine, Sputum) 4.Continue f/u of vital signs, UOP, DVT & Stress ulcer Prophylaxis.

  10. P.t condition continues to deteriorate in the next days despite maximum Inotropic & fluid support, Deterioration is Summarized as follows : • Hypotensive on max. inotropes. • Decrease LOC . • Anuria + Impaired Renal profile. • Progressive rising in TWBC. • Chest crepes became worse. • ABG: Metabolic Acidosis &Requiring more ventilator Support.

  11. ANY Suggestions? A few observation and much reasoning leads to error, many observations and little reasoning to truth Alexis Carrel (1873-1944)

  12. Ketoconazole is added at 15th.10.012 • Patient condition continues to deteriorate clinically and investigation wise as follows:

  13. P.t ABGs As follow:-

  14. Other Investigations:- • CT Abd.  unremarkable. • Echo : E.F=64%, PASP:32mmhg, No LV dysfunction or Valvular abnormality. • CXR: Reticulonodular infiltration of both upper lobes, free costo/cardiophrenic angles with normal cardiac configuration.

  15. Culture Result:- (16th.10.012) • Blood & urine: • No Growth. • Sputum culture: • Acenitobacterbaumanii[Aerobic Gm –vecoccobacilli] . • Multidrug resistance to: • MeropenemGentamicine • Vancomycine. Piperacilline • AmikacineCiprofloxacine • Cephalosporine.

  16. What NEXT ?

  17. Stop All antibiotics. • Put patient in a contact isolation • Continue with the other supportive therapy. • Search for : (Colistine OR Tigicycline). =Unfortunately BOTH are not available in Sudan =

  18. 0n 18th.Oct.O12 patient arrested at 7:00PM , didn’t respond to CPR and death declared at 7:30pm

  19. Faculty of medicine U of G in Autumn ( wadmadani )SUDAN

  20. AcenitobacterBaumannii:- “We are born to see, but have to train ourselves to observe”

  21. Background: Acinetobacterbaumannii • Gram negative Coccobacillus . • Strictly Aerobic, Non motile. • Water and soil. • Associated with antibiotic resistance. • Not part of normal human flora • Infections and outbreaks • Intensive care unit and healthcare settings • Compromised immune systems and risk • Colonized and infected patients as point sources

  22. Acinetobacterbaumannii Infections in Iraq war • Since Operation Iraqi Freedom began in 2003, more than 700 US soldiers have been infected or colonized with Acinetobacterbaumannii. A significant number of additional cases have been found in the Canadian and British armed forces, and among wounded Iraqi civilians.

  23. Global pockets of Acinetobacterbaumanii infections

  24. Risk factors include: • hospitalization • significant co-morbidity • mechanical ventilation • cardio respiratory failure • previous infection • antimicrobial therapy • CVP lines • urinary catheters

  25. Hospitalized patients are highly venerable to Acinetobacter Infections • Acinetobacter infections are uncommon and occur almost exclusively in hospitalized patients

  26. “A doctor is a person • who kills your ills • with pills, & then • kills you with his • bills” • Anonymous

  27. "It is nice to have money and the things that money can buy, but it's important to make sure you haven't lost the things money can't buy." George Lorimer1867-1937, Editor of "Saturday Evening Post"

  28. Diagnosis of Acinetobacter Infections • Infection or colonization with Acinetobacter is usually diagnosed by clinical culture of blood, sputum, urine, wound, sterile body fluid, etc. Microbiologic cultures can be processed by standard methods on routine media.

  29. Biochemical Reactions • Oxidase negative (opposite to Neisseria spp. or Moraxella spp.) • Haemolytic • Indole negative. • Catalase positive. • Nonmotile • Strictly aerobic • Gram negative coccobacillus • Highly antibiotic resistant

  30. Figure 1. Gram’s Staining of Sputum Specimen from a Patient with Suspected Ventilator-Associated Pneumonia. Acinetobacter baumannii was recovered from this specimen, which shows gram-negative coccobacilli1; the diplococcal features help explain one of the early designations of acinetobacter as neisseria.

  31. Acinetobacter outbreaks 1977-2000 Extensive Literature review and summary of 51 Acinetobacter outbreaks Villegas M, Hartstein A. Infect Control Hosp Epidemiol. 2003;24:284-295

  32. Source of A. baumaniiNosocomial Bloodstream Infection Abdominal infection 19% respiratory tract is an important reservoir for Acinetobacter bloodstream infections Central venous line 8% Respiratory tract 71% N=37 Garcia-Garmendia J-L et al. Clin Infect Dis 2001;33:939-946.

  33. Inflammatory Response to A. baumaniiNosocomial Bloodstream Infection Severe sepsis 21% Septic shock 24% Sepsis 55% N=42 Garcia-Garmendia J-L et al. Clin Infect Dis 2001;33:939-946.

  34. Complex mechanisms of Drug Resitance makes treatment options difficult

  35. Problems in treating Acinetobacterbaumannii • One of the biggest issues with treating Acinetobacter baumannii is that the bacterium is naturally resistant to a number of antibiotics,making it challenging to find a drug regimen which will effectively attack it in an infected patien

  36. Documented mechanisms of resistance in Acinetobacterbaumannii • Quantitative and/or qualitative changes in outer membrane porins. • Altered penicillin-binding proteins. • Aminoglycosides-modifying enzymes. • Broad-spectrum β-lactamases . • Efflux pumps .

  37. Treatment • Carbapenems (Imipenem and Meropenem) are the mainstay of treatment for antimicrobial-resistant gram-negative infections, though Carbapenems-resistant Acinetobacter is increasingly reported. • Resistance to the Carbapenems class of antibiotics makes multidrug-resistant Acinetobacter infections difficult, if not impossible, to treat.

  38. Multidrug Resistant strains a Global Concern • Multidrug-resistant A. baumanniiis a common problem in many hospitals in the US and Europe. First line treatment is with a Carbapenems antibiotic such as imipenem, but carbapenem resistance is increasingly common. Other treatment options include Colistin, tigecyclineand Aminoglycosides.

  39. Treating the Resistant Infections • Colistin and Polymyxin B have been used to treat highly resistant Acinetobacter infections. The choice of appropriate therapy is further complicated by the toxicity of colistin which is mainly renal. Acinetobacter isolates resistant to colistin and Polymyxin B have also been reported.

  40. Polymyxin -E antibiotics(Colistin) • History • Used extensivelyworldwide in topical oticand ophthalmic solutions fordecades • Intravenous Colistin wasinitially used inJapan and in Europeduring the 1950s, andin the United Statesin the form ofcolistimethate sodium in 1959 • The intravenousformulations of colistin andpolymyxin B were graduallyabandoned in most partsof the world inthe early 1980s becauseof the reported highincidence of nephrotoxicity • Colistin was mainlyrestricted during the past2 decades for thetreatment of lung infectionsdue to multidrug-resistant (MDR),gram-negative bacteria in patientswith cystic fibrosis

  41. Numerous recent clinical studies have confirmed that colistin is an efficient antimicrobial agent against nosocomial infections, including bacteremia, ventilator-associated pneumonia, urinary tract infection, and meningitis due to MDR GNB, such as P. aeruginosa, A.baumannii, and K. pneumonia, with an acceptable safety profile. Whereas colistin is mainly administered i.v. incritically ill patients, it can be safely be administered by inhalation in patients with pneumonia/VAP or intrathecally in patients with meningitis due to MDR GNB.

  42. Polymyxinantibiotics (Colistin):- • Mechanism of action: • Target: • Bacterial cellmembrane( Bactericidal). • Colistin binding with thebacterial membrane occurs throughelectrostatic interactions between thecationic polypeptide (colistin) andanionic lipopolysaccharide (LPS) moleculesin the outer membraneof the gram-negative bacteria • leads to a derangement ofthe cell membrane • The resultof this isan increase in thepermeability of the cellenvelope, leakage of cellcontents, and, subsequently, celldeath.

  43. Polymyxin antibiotics • Important pharmacokinetic parameters: • Colistinsulfate and colistimethate sodiumarenot absorbed bythe gastrointestinal tract withoral administration • Primary routeof excretion is throughglomerularfiltration • Experimental studieshave shown that colistinis tightly bound tomembrane lipids of tissues,including liver, lung, kidney,brain, heart, and muscles • Concentration of colistinin the CSF is 25% of the serumconcentration

  44. Polymyxinantibiotics (Colistin)

  45. ADMINISTRATION AND PHARMACOKINETICS: • Loading dose should be given as an IV infusion over 2 hours. • Maintenance dose should be given as IV infusion can be given over 30 minutes. • First maintenance dose should be given 24 hours after loading dose. • IM administration is not recommended. • Half-life is 3-4 hours in patients with normal renal function, and up to 2-3 days in • patients with renal impairment.

  46. Polymixin adverse effects

  47. Can Acinetobacter Infect Health care Workers ?

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