1 / 33

Case Study: Sepsis

Case Study: Sepsis. Jill Collins, Dana Hogan, Louisa Golay, Krystal Morris & Wanda Schumacher December 16, 2010. History of Present Illness. 30 y/o pt presents to ED with increasing mental status changes and abdominal pain X 24 hrs per skilled nursing facility

hachi
Download Presentation

Case Study: Sepsis

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Case Study: Sepsis Jill Collins, Dana Hogan, Louisa Golay, Krystal Morris & Wanda Schumacher December 16, 2010

  2. History of Present Illness • 30 y/o pt presents to ED with increasing mental status changes and abdominal pain X 24 hrs per skilled nursing facility • Nursing home staff reports pt had unwitnessed fall last NOC • Patient appears diaphoretic, increased respiratory rate, thready pulses, flushed skin, hot to touch • Pt unable to verbalize pain rating; FACES score of 7-8 given from observed grimacing and moaning

  3. MEDICAL/SOCIAL HISTORY MEDICAL SOCIAL Patient single without children, previously lived alone Family denies pt using tobacco, alcohol, or recreational drugs Family unable to report if pt is currently sexually active Patient appears to have strong support system in place • Medical History • HIV • End Stage Liver Disease • Liver cirrhosis • Hepatic Encephalopathy • SIADH • Diabetes Mellitus Type 2 • Surgical History • Upper Gastrointestinal Endoscopy • Adenoidectomy

  4. Previous Admissions • Admitted 6 months ago with hepatic encephalopathy, acute kidney injury, hyperkalemia, EKG changes • Hepatic encephalopathy resolved with lactulose treatments, kidney function improved with short term dialysis • Patient was discharged after a 2 month hospitalization to a skilled nursing facility for rehabilitation

  5. Current Medications DM/ENCEPHALOPATHY HIV Lamivudine: 50 mg PO daily Ritonavir: 100mg PO daily Zidovudine: 300mg PO daily Darunavir: 400mg PO BID Truvada: 200/300 combination dose PO daily • Lactulose: 20g PO Q4hours • Rifaxamin: 400mg TID • Novolog: 2-14 U SQ per sliding scale with meals

  6. Initial Assessment • Vital signs: BP 65/32, HR 125, Resp 28, O2 sat 85% on RA, Temp 40C • Pt appears agitated and unable to follow basic instructions • Nursing home staff reports prior to ED arrival, pt was very lethargic and experiencing generalized weakness • Skin flushed pink warm

  7. Physical Examination • Neuro: Perrla, generalized weakness, oriented x1 to person, unable to answer questions appropriately • Cardio/Respiratory: Normal ST, hypotensive, weak pulses in all extremities, shallow/rapid breathing, lung sounds crackles bases bilaterally • GI/GU: Abdomen firm/distended, pt moans with RUQ palpation, BS absent, foley placed prior to pt arrival – no documentation of placement date; decreased urine output (10cc/hr; amber in color, cloudy with sediment)

  8. DIAGNOSES WORKING DIAGNOSES ALTERNATIVE DIAGNOSES Bowel perforation and/or bowel obstruction Abdominal appearance with absent bowel sounds Pyelonephritis Urine appearance and quantity Subdural hemorrhage Mental status changes (confusion) Recent fall at nursing home Generalized weakness • Hepatic encephalopathy secondary to ESLD • Altered mental status changes • Recent hospitalization for same diagnosis • Septic shock secondary to possible urosepsis • Vital sign presentation (meets 3 of the 4 criteria for hospital sepsis protocol) • Febrile • Unknown foley placement date and appearance of urine • Immune system compromised due to HIV

  9. OTHER DIAGNOSES • Pneumonia • Febrile, respiratory status, and recent hospitalization with d/c to nursing facility • Stroke • Altered mental status changes, generalized weakness, and recent fall • Abdominal Aortic Aneurysm • Abdominal assessment & severe hypotension

  10. DIAGNOSIS CONT. SEPSIS WORKING DIAGNOSES FINAL DIAGNOSIS SEVERE UROSEPSIS • Urosepsis • Sepsis caused by pneumocysitc pneumonia • Sepsis caused by bowel perforation or obstruction • SIRS from pancreatitis and ESLD

  11. UROSEPSIS • Definition: Severe Sepsis • Suspected or proven infection, plus a systemic inflammatory response (e.g. fever, tachycardia, tachypnea, elevated white blood cell count, altered mental state, and hyperglycemia in the absence of diabetes) with organ dysfunction (e.g. hypotension, hypoxemia, oliguria, metabolic acidosis, thrombocytopenia, or obtundation). (Porth, 628) • Epidemiology • Estimated that more that 750,000 cases of sepsis occur each year in the US ultimately leading to approximately 225,000 deaths. (Porth, 628) • Severe Sepsis is the leading cause of death in non-coronary ICU’s (www.acponline.org) • Sepsis has a mortality rate of about 40% currently in the US (www.merckmanuals.com)

  12. PATHOPHYSIOLOGY • Etiology • Most likely caused by bacterial organism in the urine which most likely developed as a result of a chronic indwelling foley catheter. Most cases of sepsis are caused by hospital-acquired gram-negative bacilli or gram positive cocci and often occur in immunocompromised patients and those with chronic and debilitating diseases (www.merckmanuals.com)

  13. PATHOPHYSIOLOGY CONT. • Mechanisms of the disease • Immunocompromised by HIV and diabetes mellitus • Chronic indwelling catheter is source for bacterial collection • Decreased food and fluid intake secondary to altered mental status from hepatic encephalopathy • Possible alteration in electrolytes secondary to medication for hepatic encephalopathy (lactulose)

  14. PATHOPHYSIOLOGY CONT. • Pathogenesis of disease • Starts with inflammatory trigger (bacteria) • Proinflammatory mediators are stimulated (tumor necrosis factor and IL-1) • Cytokines cause neutrophil-endothelial cell adhesion, activate the clotting mechanism, and generate microthrombi. • Other mediators released including leukotrienes, lipoxygenase, histamine, bradykinin, serotonin, and IL-2. • These are opposed by anti-inflammatory mediators like IL-4 and IL-10 which results in a negative feedback mechanism. • Vasoactive mediators cause blood flow to bypass capillary exchange vessels. • Poor capillary flow from the shunting along with capillary obstruction by microthrombi decreases the delivery of oxygen and impairs removal of carbon dioxide and waste products. • Decreased perfusion causes dysfunction and sometimes failure of one or more organs, including the kidneys,lungs, liver, brain, and heart. • Coagulopathy can develop because of intravascular coagulation with comsumption of major clotting factors. (www.merckmanuals.com)

  15. PATHOPHYSIOLOGY CONT. • Relation of pathology to history and clinical manifestations • Pt. immunocompromised by HIV, DM and cirrhosis • Indwelling catheter source of bacterial growth and proliferation • Bacteria in urinary tract eventually trigged the pathophysiologic process discussed in previous slide. • Processes eventually lead to decreased perfusion to organs which probably caused the altered mental status and possibly the abdominal pain (also caused by the UTI) • Hypotension occurs secondary to the vasodilation caused by the inflammatory response. Tachycardia then ensues in an attempt to keep blood pressure and cardiac output up. Tachypnea is an attempt of the body to remove excess acid buildup as well as the decreased availabilty of oxygen (hypoxemia)caused by the sepsis process. Fever occurs as a result of the energy expenditure needed to fight the bacterial invasion.

  16. SEPSIS TABLE

  17. DIAGNOSTIC TESTING FOR SEPSIS FOR ALTERNATE DX Subdural hemorrhage CT of head Hepatic encephalopathy secondary to ESLD Chemistry Liver functions • WBC with diff • Chemistry • Blood Cultures • Liver function • Cortisol • ABG • Lactic Acid • UA w/ C&S • CXR • Sputum C & S

  18. CBC with Differential

  19. Complete Chemistry

  20. ABG’s

  21. Cortisol and Liver Functions

  22. Urinalysis

  23. SURVIVING SEPSIS CAMPAIGN NATIONAL GOALS: TREATMENT • Immediately on arrival: • STAT lactate, random cortisol, SCO2, PT/PTT, fibrinogen, d-dimer, chemistry, CBC with Differential • Blood, urine, and sputum cultures • Prior to antibiotic administration if possible • Cultures preferably from 2 peripheral sites, cultures only from a line if line infection is a concern • Urine cultures should be obtained using clean catch technique or from a foley catheter

  24. SURVIVING SEPSIS CAMPAIGN NATIONAL GOALS: TREATMENT Start with ABC’s Establish a patent airway (patient lethargic) Insure proper oxygenation(sats were 85% on RA. ABG’s did not improve on NRB so patient was intubated on placed on ventilator) Insure proper circulation • Early Therapy • Start in ED • Focus on early recognition and TX • Studies show early, appropriate TX (within 6 hrs of ED admission) decreased 28 day mortality rates by 16% • Transfer to ICU

  25. SURVIVING SEPSIS: TREATMENT WITHIN 1 HOUR • Antibiotic Therapy • Standard-Broad spectrum therapy • Vancomycin 1000mg-1500mg IV Q 12 hours • Levaquin 500-750mg IV Q12 hours • Zosyn 2.25-4.5 mg IV Q 6 hours • If patient is allergic to any of these antibiotics, alternative medications can be used. • Random Vancomycin trough levels need to be obtained in order to appropriately dose this medication. Vancomycin can cause impaired renal function

  26. SURVIVING SEPSIS: WITHIN 6 HOURS • Central Venous Pressure (CVP) goal 8-12 • Optimization through Normal Saline fluid boluses • If less than 8, administer 500ml NS over 10 minutes • Recheck CVP Q15 minutes and repeat 500ml boluses until CVP is 8-12 • When goal is achieved, continue NS at 150ml/hr • 250ml 5% Albumin can be used for a CVP less than 4 • Lactate Monitoring • Redraw lactates Q4 hours until less than 2

  27. SURVIVING SEPSIS: WITHIN 6 HOURS • Mean Arterial Pressure (MAP) goal 65 • MAP is often optimized through fluid resuscitation with optimizing the CVP • If MAP remains less than 65, give vasopressor of choice: • Levophed (norepinepherine) • Begin with .01mcg/kg/min, titrate until MAP is 65 with a maximum dose of .3mcg/kg/min • Vasopressin • Consider at a set rate of 2.4 U/hr (standard) • Can also be ordered as a titration with a range of .6-3.6 U/hr

  28. SURVIVING SEPSIS: WITHIN 6 HOURS • ScV02 greater than 70 • Draw Q1 hour until optimized • Continuous Scvo2 monitoring can be obtained with the placement of a precept catheter • To optimize Scvo2: • If Hgb less than 10, transfuse 1 unit PRBCs, then recheck level • Consider dobutamine at 2.5mcg/kg/min if Hgb is greater than 10 • Increase Q30 minutes until Scvo2 meets goal. Do not exceed 20mcg/kg/min

  29. SURVIVING SEPSIS: WITHIN 24 HOURS • Evaluated and started on low dose steroids • Hydrocortisone 100mg Q8 after reviewing cortisol level on labs • If level is greater than 25mcg/dL, do not give steroids • Glucose less than 150 • Insulin drip initiated if patient’s glucose is greater than 150 • Keep in mind that steroid use and antibiotics will often can an increase in blood glucose levels • Evaluate for need of Activated Protein C (Xigris)

  30. Treatment • Activated Protein C (Xigris) • Costly • Decreased mortality by 20% • FDA approved • Early administration • Risk of increased bleeding • Steroids • Antibiotics • Remove sources of infection • Glycemic Control • Active cooling • Renal function (consider CRRT if needed)

  31. Treatment • WASH YOUR HANDS • Strict aseptic/sterile techniques • Safety • BSI • Frequent position changes • Inspect oral cavity QD • Support/Educate Pt and family

  32. References • Porth C., Matfin G. (2009). Pathophysiology: Concepts of Altered Health States. Philadelphia, PA. Lipppincott Williams & Wilkins. • Merck Manual Online. (2010). Retrieved December 4, 2010, from http://www.merckmanuals.com • Harkins M.D., M. (n.d.). ACP Online. Retrieved December 4th, 2010, from http://www.acponline.org/about_acp/chapters/nm/harkins/ppt • The University of Kansas Adult Severe Sepsis/Septic Shock Order Set • Dellinger, R. P., Levy, M. M., Carlet, J. M., Bion, J., Parker, M. M., Jaeschke, R., Vincent, J. L. (2008). Surviving sepsis campaign: International guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Medicine, 34, 17-60. • Institute for Healthcare Improvement. (2010). First steps and measures to reduce sepsis mortality. Retrieved from www.ihi.org/IHI/Topics/CriticalCare/Sepsis/ImprovementStories/FirstStepsan dMeasures.org • Institute for Health Care Improvement. (2010). Sepsis. Retrieved from www.ihi.org/Topics/Criticalcare/sepsis

  33. THANK YOU!!!QUESTIONS?????

More Related