Download - 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– 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
MEDICAL/SOCIAL HISTORY
MEDICAL• Medical History
– HIV– End Stage Liver Disease
• Liver cirrhosis• Hepatic Encephalopathy
– SIADH– Diabetes Mellitus Type 2
• Surgical History– Upper Gastrointestinal
Endoscopy– Adenoidectomy
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
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
Current Medications
DM/ENCEPHALOPATHY
• Lactulose: 20g PO Q4hours
• Rifaxamin: 400mg TID
• Novolog: 2-14 U SQ per sliding scale with meals
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
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
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)
DIAGNOSES
WORKING DIAGNOSES• 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
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
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
DIAGNOSIS CONT.
SEPSIS WORKING DIAGNOSES
• Urosepsis• Sepsis caused by
pneumocysitc pneumonia
• Sepsis caused by bowel perforation or obstruction
• SIRS from pancreatitis and ESLD
FINAL DIAGNOSIS
SEVERE UROSEPSIS
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)
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)
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)
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)
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.
SEPSIS TABLE
DIAGNOSTIC TESTING
FOR SEPSIS
• WBC with diff• Chemistry• Blood Cultures• Liver function• Cortisol• ABG• Lactic Acid• UA w/ C&S• CXR• Sputum C & S
FOR ALTERNATE DX• Subdural hemorrhage
• CT of head
• Hepatic encephalopathy secondary to ESLD
• Chemistry• Liver functions
CBC with DifferentialLab Normal Client
Hemoglobin 14-18 8.8
Hematocrit 42-52 23.5
Platelets 150-400 56
WBC 4.3-10 1.9
Neutrophils 55-70 76
Bands 8
Lymphocytes 20-40 13
Monocytes 2-8 3
PTT 20-45 67
PT (INR) <2 5
Complete ChemistryLab Normal Client
Sodium 136 - 145 125
Potassium 3.5 – 5.0 5.1
Chloride 98 – 106 99
CO2 23 – 30 15
Anion Gap 8 – 12 23
BUN 10 – 20 35
Creatinine .6 – 1.2 2.5
Glucose 60-110 205
Albumin 3.5 - 5 2.0
Lactate .5 - 2 7.28
Ammonia 15 - 45 96
Scvo2 Goal greater than 70
51
ABG’s
Lab Normal Client
PH 7.35 - 7.45 7.25
CO2 35 -45 55
HCO3 21 - 28 24
PO2 80 - 100 83
Cortisol and Liver Functions
Lab Normal Client
Total Bilirubin .3 – 1.0 30.8
AST 0 – 35 822
ALT 4 – 36 266
ALK Phos 30 - 120 47
Cortisol 5 – 20 15.7
UrinalysisLAB NORMAL CLIENT
Color Amber Amber
Turbidity Clear 1+
Specific Gravity 1.005 – 1.030 1.013
pH 4.6 – 8.0 6.5
Ketones Negative Negative
Protein Negative 1+
Blood Negative Trace
Bilirubin Negative Positive
Leukocytes Negative Trace
WBC 0 – 4 2-10
RBC 0 – 2 2-10
Sediment Few
Bacteria Packed
WBC Clumps Present
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
SURVIVING SEPSIS CAMPAIGN NATIONAL GOALS: TREATMENT
• 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
• 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
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
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
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
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
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)
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)
Treatment• WASH YOUR HANDS• Strict aseptic/sterile
techniques• Safety• BSI• Frequent position changes• Inspect oral cavity QD• Support/Educate Pt and
family
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/FirstStepsandMeasures.org
Institute for Health Care Improvement. (2010). Sepsis. Retrieved from
www.ihi.org/Topics/Criticalcare/sepsis
THANK YOU!!!
QUESTIONS?????