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Major Case Presentation Septic Shock
- 1. Pharmacotherapy of SepticShockMunzur Morshed, Pharm D. candidate 2011Arnold & Marie Schwartz College of Pharmacy and Health SciencesNorth Shore- Long Island Jewish Health SystemInfectious Diseases-Advanced Pharmacy Practice
- 2. Case PresentationIMA isa 59 Y/O female, who recently had a left urethral stent placed in her left ureter two weeks ago, came to the emergency room complaining of left-sided flank pain for 1-2 days. Patient was noted to have vomiting for oneday, with symptoms of headache, and anxiety. Patient had no hx. of URI, possible kidney stone is suspected. Patient was admitted to the ICU with septic shock secondary to left pyelonephritis, hypoxia and HOTN. Her BPdid not respond to the fluids given in the ER. Patient is currently intubated and is monitored on the ventilator. Past Medical/Surgical history: Patient had a left urethral stent placed a few weeks Family Hx: Patient has a family history of DM and CAD.Allg: NKAMeds on admission:IV Norepinephrine 2MG/250mL;Normal Saline 1000 ML; Lovenox 40MG SQ QD; Primaxin 500MG IVPB Q6H, Flagyl 1500 mg IVPB q6H STAT, Merrem 500mg IVPB Q8H, Regular Insulin Sliding Scale, Sodium Bicarb 7.5% 44.6MEQ, Gentamicin 100 MG IVPB one/time STAT, Protonix IVPB 40 mg PO q6h; Tylenol with Codeine #3 -1T PO Q4H PRN PE: Temp 102.6, Pulse 114, RR 18, BP 79/50,Laboratory Findings: WBC 20.6, Hg 8.5, Na 131, K 2.6, Cl 2.6, CO2 24, BUN 17, Scr 1.5, Glucose 217, Ca 6.5, Lactate 5.2, AST/ALT 61/91, MAP 59.67, PH 7.19, HCO3 17Urinalysis: Protein 150, Blood Urine- Large, Leuko Ester- Moderate, Nitrites (+), WBC 10-25, Bacteria-manyMicrobiology Blood Culture: Gram (-) Rods in aerobic Bottle. Urine Culture: Greater than 100,000 CFU/ML Pseudomona Less than 10,000 CFU/ML of other organismDiagnosis: Septic Shock and Pyelonephritis secondary to Stent placement
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- 4. Life threatening state,decrease in tissue perfusion of blood supply
- 5. Characterized by lackof nutrient and O2 rich blood to the organs resulting in inadequate perfusion
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- 7. HR < 20or > 150 bpm
- 8. SBP < 80mmHg, decrease by at least 40mmHg
- 9. MAP < 60mmHg
- 10. DBP > 120mmHg
- 11. RR > 35breaths/min
- 12. pH < 7.1or >7.7
- 13. low urine output(<0.5ml/kg/hr ) and confusion or loss of consciousnessTypes of ShockHypovolemic Shock
- 14. Loss of bloodvolume (plasma + RBCs)
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- 18. Hearts inability topump appropriate amount of blood
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- 20. Septic Shock- Discussedin detail
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- 23. Increase pressure ofthe jugular vein distended jugular vein
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- 25. Injury of thespine
- 26. Loss of cardiacnerve fibers from the sympathetic nerve fibers at T1-T4 resulting in profound bradycardia
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- 30. Large Eruptions orbumpy skin
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- 32. Constricted Airways; Swollenthroat; Breathlessness and cough
- 33. Weak or rapidpulseWhat is Septic Shock?Massive Systemic infection associated with arterial hypotension that is refractory to fluid resuscitation
- 34. It is asystemic inflammatory Response syndrome
- 35. Criteria must includethe following (2 out of 4)
- 36. WBC >12K or<4K or >10% bands
- 37. Temperature > 38Cor < 36C
- 38. Heart rate >90bpm
- 39. Respiratory Rate >22 breaths/min
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- 41. Systemic Infection- Anyetiology
- 42. Bacterial- Presence ofBacteria in the bloodstream
- 43. Fungemia- Presence ofFungus in the BloodstreamEpidemiologyDefined by site of infectionRespiratory Tract (21%-68%)Intraabdominal Space (14%-22%)Urinary Tract (14%-18%)PathogensGram-Positive bacteria (40% of patients)Gram-Negative bacteria (38% of patients)Fungi (17%)
- 44. PathogensGram-Positive Bacterial SepsisGram-NegativeBacterial SepsisMost predominant in Septic ShockStaph. Aureus Strep. Pneumoniae Coagulase-Negative StaphylococciEnterococcus Strep. Pneumoniae- Mortality rate of more than 25%Staph. Epidermidis- related to infected intravascular deviceSeverity depends on underlying comorbiditesFatal PrognosisAcute LeukemiaAplastic AnemiaBurn Injury- >70& BSANon-fatal prognosisDiabetes MellitusChronic Renal InsufficienciesMost predominantEscherichia coliPseudomonas aeruginosis
- 45. Pathogens Cont…Anaerobes andmiscellaneous bacterial Sepsis Fungal SepsisLow risk organism but can occurUsually seen with other common pathogens in sepsisMeningococci, gonococci, rickettsiae, chlamydiae, spirochetesRate of the infection doubled since the 2000
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- 47. Candida Albicans (Most Dominant)
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Editor's Notes
- #10 Once the bacteria invades the host, inflammatory mediators are produced which causes damage to the host tissue and activation of leukocytes. The balance to control the inflammatory mediators are lost and therefore a systemic inflammatory response develops which in turn converts the infection into sepsis, severe sepsis or septic shock. The key proinflammatory mediator is the tumor necrosis factor-α (TNF-α),interleukin-1 (IL-1), and interleukin-6 (IL-6) . The TNF-áa) is considered the primary mediator of sepsis. Once the TNFáa) is activated, it leads to the activation of IL-1 and IL-6. The TNFá also contributes to the production of Thrombaxane A2, and prostaglandins, which causes vascular endothelial damage, capillary leak, vasodilation, microvascular thrombi formation. Which in turn lead to disseminated intravascular coagulation and acute kidney injury.