morbidity and mortality conference

morbidity and mortality

conference❀Antonio Chua, M.D.

❀Anne Marie Kathryn Ingente, M.D.❀Marizen Lim, M.d.

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

Identifying Data

History of Present Illness

History of Present IllnessCBC

Urinalysis: NORMAL (rbc: 5.5, wbc 0, epith. cells 0, bacteria 13.62)

•ADMISSION

Hb Hct WBC

Seg

Lym

Mono Eos Met

aMyelo

Stabs plt

5/19/09

12.5

39.6

2.42 70 20 2 2 1 - 5 140

T

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

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

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

SALIENT FEATURES

ADMITTING IMPRESSION

SYSTEMIC VIRAL INFECTION

R/O DENGUE FEVER

HYPERTENSION, CONTROLLED

Surviving Sepsis Campaign: International Guidelines for Management of Severe

Sepsis & Septic Shock: 2008

COURSE IN THE WARDS

PROBLEM #1: HYPOTENSION

DIFFERENTIAL DIAGNOSES

ACUTE CORONARY SYNDROME

INITIAL RESUSCITATIONS (1ST 6 HOURS)

Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008

INITIAL RESUSCITATIONS (1ST 6 HOURS)


PROBLEM #2: ACUTE RENAL FAILURE

PROBLEM #3: ADRENAL INSUFFICIENCY & SEPSIS


PROBLEM #4: SKIN MANIFESTATIONS

PROBLEM #4: SKIN MANIFESTATIONS

COURSE IN THE WARDS

09:00 REPEAT BLOOD WORKS:

Hb Hct

WBC

Seg

Lym

Mono Eos Met

aMyelo

Stabs plt

5/19/09 12.5 39.

62.42 70 20 2 2 1 - 5 140

T

5/20/09

14.1 45 12.

55 74 18 1 - 1 4 2 43T

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

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 Control 26 sec

COURSE IN THE WARDS

Hematology Referral

8U FFP transfused

Vit. K OD

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)


BLOOD PRODUCT ADMINISTRATION


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

http://www.uptodate.com/

PROBLEM #6: HYPOXIA & METABOLIC ACIDOSIS

MVM 0.5

NaHCO3 drip

datetime pO2 pH pC0

2HC0

3sat 02 B.E TCO

2FiO2

condition

5/20/09

0950H

69.1 7.18 25.3 9.3 89.9 -17.2 10.1

2 lpm/n

c

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


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

http://www.uptodate.com/

COURSE IN THE WARDS

PROBLEM #7: ACUTE RESPIRATORY FAILURE

CXR post Intubation

datetime pO2 pH pC0

2HC0

3sat 02 B.E TCO

2FiO2

condition

5/20/090950H 69.1 7.18 25.3 9.3 89.9 -

17.2 10.12

lpm/nc

5/20/09(POST

INTUBATION

158.1 7.17 23.0 8.2 98.6 -

18.4 8.9 1.0AC

MODE

mechanical ventilation of sepsis-induced ALI/ARDS


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)


Course in The Wards

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


other tests done

COURSE IN THE WARDS

Hb Hct

WBC

Seg

Lym

Mono Eos Met

aMyelo

Stabs plt

5/19/09 12.5 39.

62.42 70 20 2 2 1 - 5 140

T5/20/0

9 14.1 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

course in the wards5/20/09 PT % ACT. 30.1% PTT Px >200

secINR 2.82 Control 26 sec

5/20/09(1 PM) PT % ACT. 22.6% PTT Px >200

sec

INR 3.74 Control 27.1 sec

COURSE IN THE WARDS

datetime pO2 pH pC0

2HC0

3sat 02 B.E TCO

2FiO2

condition

5/20/090950H 69.1 7.18 25.3 9.3 89.9 -

17.2 10.12

lpm/nc

5/20/09(POST

INTUBATION

158.1 7.17 23.0 8.2 98.6 -

18.4 8.9 1.0AC

MODE

5/20/09(5 hrs later)

74.2 7.14 34.7 11.7 90.5 -16.3 12.7 0.8

AC MOD

E

Course in the wards

19:30

Anuric: HD not done (unstable hemodynamics; coagulopathy)

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)


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

consideration for limitation of support

advance care planning including communication of likely outcomes & realistic good treatments should be discussed with patients and families (1D)


course in the wards

40:00

patient expired

autopsy done

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

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

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

dic: etiology

sepsis (40%)

trauma & tissue destruction

malignancy

ob complications

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

Strep. pluranimalium

Clin Microbiol Rev. 2002 October; 15(4): 613–630.doi: 10.1128/CMR.15.4.613-630.2002.

DIC: pathogenesisuncontrolled and excessive production of thrombus

widespread & systemic intravasc. fibrin deposition

Disseminated intravascular coagulation (DIC)

tissue ischemia & consumption of coagulation & clotting factors

bleeding

DIC: Pathogenesis2° fibrinolysis eventually occurs due to release of plasmin from plasminogen

release of fdp’s

further bleeding


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


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

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...

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.

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).

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)

Dic: treatment

correct the underlying disease and initiating factors

hemodynamic support is essential

supportive tx: platelet and clotting factors

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

final diagnoses

cardiopulmonary arrest 2° to multiorgan failure, 2° to severe sepsis

hypertensive cardiovascular disease

fatty liver disease

thank you for your kind

attention ❦

morbidity and mortality conference

Documents

hourssurviving sepsis

case report of severe

international guidelines

recent guidelines

supple neck

normal rbc

intravascular coagulation

skin manifestationscourse