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?????