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morbidity and mortality
conference❀Antonio Chua, M.D.
❀Anne Marie Kathryn Ingente, M.D.❀Marizen Lim, M.d.
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ObjectivesTo present a case of an acute systemic infection that caused severe sepsis and disseminated intravascular coagulation in an immunocompetent patient
to present a case report of severe sepsis caused by a microorganism known only so far to cause disease in avian and bovine species
to briefly discuss on the recent guidelines on the management of sepsis
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Identifying Data
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History of Present Illness
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History of Present IllnessCBC
Urinalysis: NORMAL (rbc: 5.5, wbc 0, epith. cells 0, bacteria 13.62)
•ADMISSION
Hb HctWBC
Seg
Lym
Mono
Eos Met
aMyelo
Stabs
plt
5/19/09
12.5
39.6
2.42
70 20 2 2 1 - 5140
T
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General Survey: conscious, coherent, not in cardiorespiratory distress
VS: BP 90/60 HR: 102/min RR 20/min Temp 38.6C
HEENT: anicteric sclerae, pink palpebral conjunctivae, supple neck, no tonsillopharyngeal wall congestion
Skin: no pallor, no jaundice, no rashes
physical examination
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physical examination
CVS: adynamic precordium, tachycardic, regular rhythm, distinct heart sounds, no murmurs
Lungs: symmetrical chest expansion, clear breath sounds
Abdomen: Flabby, (+) infraumbilical scar, NABS, soft, non tender, no organomegaly
Extremities: no pedal edema, full and equal pulses
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Neurologic examination
Oriented to 3 spheres
CN intact
No cerebellar deficits
Motor 5/5 on all extremities
No sensory deficits
No neck rigidity
negative brudzinky and kernig’s sign
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SALIENT FEATURES
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ADMITTING IMPRESSION
SYSTEMIC VIRAL INFECTION
R/O DENGUE FEVER
HYPERTENSION, CONTROLLED
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Surviving Sepsis Campaign: International Guidelines for Management of Severe
Sepsis & Septic Shock: 2008
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COURSE IN THE WARDS
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PROBLEM #1: HYPOTENSION
DIFFERENTIAL DIAGNOSES
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ACUTE CORONARY SYNDROME
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INITIAL RESUSCITATIONS (1ST 6 HOURS)
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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INITIAL RESUSCITATIONS (1ST 6 HOURS)
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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PROBLEM #2: ACUTE RENAL FAILURE
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PROBLEM #3: ADRENAL INSUFFICIENCY & SEPSIS
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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PROBLEM #4: SKIN MANIFESTATIONS
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PROBLEM #4: SKIN MANIFESTATIONS
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COURSE IN THE WARDS
09:00 REPEAT BLOOD WORKS:
HbHct
WBC
Seg
Lym
Mono
Eos Met
aMyelo
Stabs
plt
5/19/09
12.539.6
2.42
70 20 2 2 1 - 5140
T
5/20/09
14.1
4512.55
74 18 1 - 1 4 2 43T
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5/20/09 (1AM)
5/20/09 (8 AM)
Na 140 145K 3.3 4
BUN 16.99 25.01↑Crea 1.7 2.7↑SGPT 63 91↑
TROP I 0.06 0.14↑CKMB 0.5 1.9TCPK 90 164
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PROBLEM #5: COAGULOPATHY
dengue duo, malaria, leptospira: negative
fdp: >80 ug/ml
LDH: 859 U/L
PBS: normocytic, normochromic RBC; leucocytosis w/ sl. shift to L; ↓ platelets
5/20/09 PT % ACT. 30.1% PTT Px>200 sec
INR 2.82 Control26 sec
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COURSE IN THE WARDS
Hematology Referral
8U FFP transfused
Vit. K OD
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BLOOD PRODUCT ADMINISTRATIONFFP: should not be used to correct lab clotting abnormality unless (+) bleeding or (+) plan of invasive procedure/s (2D)
platelet transfusion:
✓if with severe sepsis & plt count <5T/mm3;
✓ or plt count 5-10T/mm3 + significant risk of bleeding;
✓or goal platelet count ≥50T/mm3 if surgery or invasive procedures are contemplated (2D)
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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BLOOD PRODUCT ADMINISTRATION
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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VITAMIN Kcofactor required for the activity of coagulation factors VII, IX, X, and prothrombin, and regulatory proteins (proteins C & S), & proteins of mineralized tissue (bone Gla protein and matrix Gla protein)
depending on the cause of deficiency, it can be administered in doses of 1 to 25 mg PO, IM, SQ, or IV routes
www.uptodate.com Vitamin K, gamma carboxyglutamic acid, and the function of coagulation. Bruce Furie, MD, et al
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PROBLEM #6: HYPOXIA & METABOLIC ACIDOSIS
MVM 0.5
NaHCO3 drip
datetime
pO2 pHpC0
2HC0
3sat 02
B.ETCO
2FiO2
condition
5/20/09
0950H
69.1 7.18 25.3 9.3 89.9-
17.210.1
2 lpm/n
c
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BICARBONATE TX
Not recommended to improve hemodynamics or decreasing vasopressor requirements in patients w/ hypoperfusion-induced lactic acidosis with ph ≥ 7.15 (1B)
its effect for ph < 7.15 is unknown
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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LACTIC ACIDOSIS IN SEPSIS
plasma lactate conc: > 4 - 5 meq/l
due to marked tissue hypoperfusion in shock (e.g. sepsis, hypovolemia, cardiac failure)
prognosis is poor unless tissue perfusion can be readily restored
www.uptodate.com Causes of Lactic Acidosis. Burton D Rose, MD, et al
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COURSE IN THE WARDS
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PROBLEM #7: ACUTE RESPIRATORY FAILURE
CXR post Intubation
datetime
pO2 pHpC0
2HC0
3sat 02
B.ETCO
2FiO2
condition
5/20/090950H
69.1 7.18 25.3 9.3 89.9-
17.210.1
2 lpm/n
c
5/20/09(POST
INTUBATION
158.1
7.17 23.0 8.2 98.6-
18.48.9 1.0
AC MOD
E
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mechanical ventilation of sepsis-induced ALI/ARDS
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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GLUCOSE CONTROLIV insulin tx (1B)
➡ for severe sepsis w/ hyperglycemia & admitted in the icu
use a validated protocol for insulin dose adjustments (2C)
target glucose levels: < 150 mg/dl (2C)
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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Course in The Wards
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sedation, analgesia & NM blockade in sepsis
use sedation protocols in critically ill ventilated pxs to reduce duration of mech. vent. & icu stay (1B)
intermittent bolus sedation or continuous infusion sedation w/ daily interruptions (1B)
NM blocking agents: should be avoided, if possible (1B)
reduces tissue utilization of O2 thereby decreasing formation of lactic acid
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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other tests done
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COURSE IN THE WARDS
HbHct
WBC
Seg
Lym
Mono
Eos Met
aMyelo
Stabs
plt
5/19/09
12.539.6
2.42
70 20 2 2 1 - 5140
T5/20/0
914.1 45
12.55
74 18 1 - 1 4 2 43T
5/20/09
(1PM)
12.6
40.3
18.3
74 8 2 - 4 1 9 30T
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course in the wards
5/20/09 PT % ACT. 30.1% PTT Px>200 sec
INR 2.82 Control 26 sec
5/20/09(1 PM)
PT % ACT. 22.6% PTT Px>200 sec
INR 3.74 Control27.1 sec
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COURSE IN THE WARDS
datetime
pO2 pHpC0
2HC0
3sat 02
B.ETCO
2FiO2
condition
5/20/090950H
69.1 7.18 25.3 9.3 89.9-
17.210.1
2 lpm/n
c5/20/09(POST
INTUBATION
158.1
7.17 23.0 8.2 98.6-
18.48.9 1.0
AC MOD
E
5/20/09(5 hrs later)
74.2 7.14 34.7 11.7 90.5-
16.312.7 0.8
AC MOD
E
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Course in the wards
19:30
Anuric: HD not done (unstable hemodynamics; coagulopathy)
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Renal Replacement Therapy
continuous RRT & intermittent HD is suggested in severe sepsis and ARF (2b)
use of cont. rrt is suggested to facilitate management of fluid balance in hemodynamically unstable septic pxs (2b)
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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course in the wards27:00
✤ transferred to icu
✤ BP 60 palpatory
✤ Epinephrine drip started
✤ CP arrest 20 min CPR
✤ GCS 3, BP 40 palpatory (Quadruple vasopressors)
31:00 DNR signed
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consideration for limitation of support
advance care planning including communication of likely outcomes & realistic good treatments should be discussed with patients and families (1D)
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
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course in the wards
40:00
patient expired
autopsy done
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Preliminary autopsy report
Immediate cause of death: disseminated intravascular coagulation, 2° to septicemia
contributory cause of death:
★ hemorrhage, adrenals, lungs and pericardium
★ acute respiratory distress syndrome
★ acute bacterial meningitis
★ extensive tubular necrosis, bilateral kidneys
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preliminary autopsy report
non contributory cause of death:
hypertrophy of the heart, predominantly left ventricle
atherosclerosis of the aorta with calcification
micro and macrosteatosis, liver
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disseminated intravascular coagulation
consumption coagulopathy & defibrination syndrome
systemic process producing both thrombosis and hemorrhage
a complication of an underlying illness occurring in ~1% of hospital admissions
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dic: etiology
sepsis (40%)
trauma & tissue destruction
malignancy
ob complications
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blood CS result (case)
described by devriese et al (1999)
resembles strep.acidominimus
isolated from bovine mastitis, bovine vagina, cervix & tonsils; canary lung & lesions; tonsils of a goat & a cat
no human isolates have been confirmed (not until now??)
★Streptococcus pluranimalium, sensitive to ampicillin & penicillin
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Strep. pluranimalium
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Clin Microbiol Rev. 2002 October; 15(4): 613–630.doi: 10.1128/CMR.15.4.613-630.2002.
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DIC: pathogenesisuncontrolled and excessive production of thrombus
widespread & systemic intravasc. fibrin deposition
Disseminated intravascular coagulation (DIC)
tissue ischemia & consumption of coagulation & clotting factors
bleeding
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DIC: Pathogenesis2° fibrinolysis eventually occurs due to release of plasmin from plasminogen
release of fdp’s
further bleeding
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disseminated intravascular coagulation
Clinical manifestations:
Bleeding: petechiae, ecchymoses, purpura fulminans
Acute renal failure: 25 - 50%
✴due to microthrombosis of afferent arterioles & hypotension &/or sepsis that lead to ATN
Pulmonary disease: pulm. hge w/ hemoptysis & dyspnea due to damage of pulm. vasc. endothelium; ARDS may result due to sepsis & DIC
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disseminated intravascular coagulation
Clinical Manifestations:
Hepatic dysfunction: jaundice due to inc. bilirubin production due to hemolysis & the hepatocellular injury caused by sepsis & hypotension
CNS: coma, delirium, transient focal neuro’c sxs 2° to microthrombi, hemorrhage, or hypoperfusion
waterhouse-friderichsen syndrome:
✴ massive adrenal hemorrhage that can be caused by organisms other than meningococcus, which can induce dic and lead to adrenal hge
✴ causes: infectious and non-infectious
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waterhouse-frederichsen syndrome
early death is heralded by pyrexia, profound circulatory collapse, cyanosis, & confluent purpura
results in adrenal dysfunction
AKA critical illness-related corticosteroid insufficiency (CIRCI)
CORTICUS trial...
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CORTICUS TRIAL(European multicenter study)
a double-blind, randomized, placebo-controlled study
performed in 52 centers throughout Europe.
total of 500 p’ts (499 available to analyze) were enrolled
between March 2002 and November 2005.
Inclusion criteria:
✴ septic shock ( SBP < 90mm Hg, despite adequate fluid resuscitation or vasopressors)
✴ evidence of organ dysfunction attributable to sepsis.
✴ hydrocortisone (50 mg intravenously every 6 hrs for 5 days, then 50 mg intravenously every 12 hrs for 3 days, followed by 50 mg intravenously daily for 3 days) or matching placebo.
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CORTICUS TRIAL(European multicenter study)
P’ts did not receive fludrocortisone.
No difference in the 28-day all-cause mortality between those p’ts who received hydrocortisone as compared with placebo.
The p’ts who received hydrocortisone had more rapid resolution of shock (p= .001 for responders and p= .06 for nonresponders).
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DIC: Diagnosishistory (sepsis/trauma/ca) + clinical presentation + moderate to severe thrombocytopenia (<100T) + microangiopathic changes in PBS
↓fibrinogen (↑thrombin)
↑fibrinolysis (↑fdp & d-dimer)
prolonged pt, aptt
↑thrombin time, ↑reptilase time
↓endogenous coag. inhibitors (anti-thrombin, protein c, protein s)
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Dic: treatment
correct the underlying disease and initiating factors
hemodynamic support is essential
supportive tx: platelet and clotting factors
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dic: prognosisacute dic: serious complication with ↑mortality rate (40-80%) in pxs with severe sepsis, burns, trauma
risk factors for death:
✤ advance age
✤ severity of organ dysfunction
✤ hemostatic abnormalities
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final diagnoses
cardiopulmonary arrest 2° to multiorgan failure, 2° to severe sepsis
hypertensive cardiovascular disease
fatty liver disease
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thank you for your kind
attention ❦