Post Operative Management

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PULMONARY ENDARTERECTOMY: POST-OPERATIVE MANAGEMENT F. MOJOLI Cattedra di Anestesiologia e Rianimazione Università degli Studi di Pavia Servizio di Anestesia e Rianimazione I IRCCS Policlinico San Matteo - Pavia

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Transcript of Post Operative Management

Page 1: Post Operative Management

PULMONARY ENDARTERECTOMY:

POST-OPERATIVE MANAGEMENT

F. MOJOLICattedra di Anestesiologia e Rianimazione

Università degli Studi di PaviaServizio di Anestesia e Rianimazione IIRCCS Policlinico San Matteo - Pavia

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POSTOPERATIVE MANAGEMENT

- Weaning from Mechanical Ventilation

- Weaning from Inotropes, Vasopressors

and Pulmonary Vasodilators

- Effective Anticoagulation

- Management of Complications

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RESPIRATORY CHANGES AFTER PEA

Anesthesia Sternotomy CPB Bed Rest

Hypoventilation of DEPENDENT

pulmonary regions

Hyperperfusion of DEPENDENT

pulmonary regionsPulmonary Artery StealPEA

V’ / Q mismatchPostoperative Hypoxemia

Functional Residual Capacity decreaseAtelectasis formationExtraVascular Lung Water increasePulmonary Compliance decrease

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Post PEA Mechanical Ventilation

To mantain adequate ventilation of dependent pulmonary parenchyma, two different STRATEGIES:

A protective approach limits pulmonary STRESS (transpulmonary pressure), STRAIN (pulmonary overdistention) and ATELECT TRAUMA (opening and closing of alveoli), therefore also VILI (Ventilation induced Lung Injury)

HIGH VOLUMES

VENTILATION

PEEP 5 cmH20

TV 12 -15 ml/Kg

PROTECTIVE

VENTILATION

PEEP 10 cmH20

TV ≈ 8 ml/Kg

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WEANING FROM MECHANICAL VENTILATION

• PEEP, “normal” TV

• Forced diuresis, negative fluid balance

• Rapid switch from controlled to assisted modes

• Rapid extubation, irrespective of moderate-severe hypoxemia

• Eventually, post-extubation C-PAP (helmet) and respiratory physiotherapy

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RATIONALE FORACCELERATED WEANING FROM

INVASIVE MECHANICAL VENTILATION

• CTEPH are “used” to severe hypoxemia

• A gradual improvement of gas exchange is expected

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CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: SURGICAL TREATMENT

ARTERIAL BLOOD GASES

• Gas exchanges returned to normal values in the majority of pts already at the 3-month control

Pa O2

50

60

70

80

90

100

Before PEA 3 months 1 year 2 years 3 years 5 years

mm

Hg

Before PEA vs 3m, 1y, 2y, 3y and 5y p < 0.01

Pa CO2

25

30

35

40

45

Before PEA 3 months 1 year 2 years 3 years 5 years

mm

Hg

Before PEA vs 3m, 1y, 2y, 3y and 5y p < 0.02

O2-Sat

90

92

94

96

98

100

Before PEA 3 months 1 year 2 years 3 years 5 years

%

Before PEA vs 3m, 1y, 2y, 3y and 5y p < 0.02

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RATIONALE FORACCELERATED WEANING FROM

INVASIVE MECHANICAL VENTILATION

• CTEPH are “used” to severe hypoxemia

• A gradual improvement of gas exchange is expected

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RATIONALE FORACCELERATED WEANING FROM

INVASIVE MECHANICAL VENTILATION

• CTEPH are “used” to severe hypoxemia

• A gradual improvement of gas exchange is expected

• Prolonged Invasive MV increases ICU stay and infections

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WEANING FROM MV:The accelerated approach

0

2

4

6

8

10

12

14

MV lenght (days) ICU stay (days)

before 03

03-05

P = 0.02P = 0.07

R2 = 0,9436

0

10

20

30

40

50

60

70

80

0 10 20 30 40 50 60

MV lenght (days)

ICU

sta

y (d

ays)

0

5

10

15

20

25

30

VAP (%) Infections (%)

before 03

03-05

P = 0.03P = 0.04

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WEANING FROM MV:The accelerated approach

0

100

200

300

400

PaO

2 / F

iO2

(mm

Hg

)

PRE-EXTUBPRE-OP

POST-EXTUB

PRE-DISC

POST-OP

PRE-EXTUBATION PARAMETERS

PaO2/FiO2 246 ± 110 mmHg (113–491)

PEEP 7.5 ± 2 cmH2O (4–10)

FiO2 0.5 ± 0.1 (0.3–0.7)

POST-EXTUBATION C-PAP

2 / 3 patients

PEEP 9 ± 1 cmH2O (8 – 10)

Lenght 2.2 ± 1.4 days

INITIAL MVPARAMETERS

TV 666 ± 168 ml

TV / Kg 8.5 ± 2.2 ml/Kg

PEEP 9.7 ± 2.9 cmH2O

(5–14)

FiO2 0.7 ± 0.2

(0.4–1)

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HEMODYNAMIC MANAGEMENT AFTER PEA

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Weaning from CPB

Eventual SUPPORT to

RV

function

InotropesDobutamine

Ph 3 Inhibitors

Epinephrine

Systemic

circulation

Systemic

VasopressorsNorepinephrine

Pulmonary

VasodilatorsiNO

Prostanoids

Nitroprusside

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HEMODYNAMIC MANAGEMENT

• Rapid weaning from Inotropes and iNO

• Diuretics• Gradual weaning

from vasopressors

• No persistent PH• Good RV function• CO increase limit.

• Intraop. Overload• Hypoxemia• Rapid MV weaning

• Need for negative fluid balance

• Effective surgery• Cardiac protection

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HEMODYNAMIC MANAGEMENTRESULTS

Dobut.5.9 ± 2.7

(2-12)

1.3 ± 0.8

(1 – 4)

Norep.0.2 ± 0.1

(0.01-0.5)

4.1 ± 3.7

(1 – 13)

2

3

4

5

6

7

8

CO

(l/m

in)

0

250

500

750

1000

1250

1500

PV

R (

dy

ne

s/s

*cm

-5)

Dosemcg/Kg/min

Lenghtdays

1 2 3 4 5

0

20

40

60

80

100

% p

ati

en

ts

postoperative days

Dobutamine

Norepinephrine

PRE-OP

POST-OP

POST-OP

PRE-OP

Mean ∆PVR -68 %

Mean ∆CO +37 %

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ANTICOAGULATION

• Prevention of local re-thrombosis:- Early start of SC heparin- Early resumption of Vit. K antagonism• PLT count daily monitoring (high risk HIT)

In our experience:1° dose SC Heparin: 15 ± 9 hours (6 – 36)

1° dose VKA: 2.4 ± 1.3 days (1 – 6)after ICU admission

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POSTOPERATIVE COMPLICATIONS OF PEA

• Persistent PH and RH failure

• Reperfusion pulmonary edema

• Pulmonary hemorrhage

• Neurologic disturbances

• Infections

• Heparin induced thrombocytopenia

• Arrhythmyas

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CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: SURGICAL TREATMENTOPERATIVE MORTALITY

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Survivors 95.6 %

Deaths 4.4 %500 patients

Low postoperative PVR

Deaths 0.9 %

High residual PVR

Deaths 30,1 %

90 % 10 %

CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: SURGICAL TREATMENT

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Patients at risk for PPH?

- Distal disease

- Inhomogeneous disease (unilateral!)

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Pervious branches

Obstructedbranches

normal

plexiformlesions

muscularthickening

CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: SURGICAL TREATMENT

Secondary Small Vessel Disease

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PREOPERATIVE EVALUATION

PAC

Prediction of responsiveness to

surgery

Outcome

Pulm.Angiography

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Treatment of PPH

• Pulmonary vasodilators

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PULMONARY VASODILATORS

Which agent?To decrease right ventricle afterload without

systemic vasodilation and arterial oxygen desaturation, use a

SUPER-SELECTIVE AGENT:Inhaled Nitric Oxide

- Effective decrease of Pulmonary Vascular resistance- No effect on systemic circulation (pulmonary selective)- Vasodilates only ventilated lung areas (super-selective)- Decrease of V’/Q mismatch- Blunted reperfusion injury?

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Ghofrani et al,JACC 2004; 44 (7): 1488-96

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Treatment of PPH

• Pulmonary vasodilators

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Treatment of PPH

• Pulmonary vasodilators

• Inotropic support

• Systemic vasopressors

• Preload optimization

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Treatment of PPH

• Pulmonary vasodilators

• Inotropic support

• Systemic vasopressors

• Preload optimization

• Control of O2 consumption

• Gas exchange optimization

• Acidosis treatment

• (ECMO)

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PVR (last)

< 500 dynes*s*cm-5 > 500 dynes*s*cm-5 Functional group Persistent group

35 % 65 %

PVR (114 ICU admission)

< 500 dynes*s*cm-5 > 500 dynes*s*cm-5

Control Group Study group

77 % 23 %

High residual PVR after PEA:outcome in the Pavia experience

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High residual PVR after PEA:

Postoperative

management

Control Group(n = 88)

Study group(n = 26)

p

ICU stay (days) 7.7 ± 9.1 18.2 ± 16.9 < 0.0005

Dobutamine (mcg/Kg/min) 5.9 ± 2.5 7.6 ± 2.9 < 0.01

Norepinephrine (days) 2.7 ± 2.6 4.8 ± 6.1 < 0.05

Fluid balance (ml) -1772 ± 2253 -875 ± 1231 < 0.05

Inhaled NO (n, %) 10 (16.1 %) 10 (41.7 %) < 0.05

Mech. Ventilation (days) 4.2 ± 6.0 11.5 ± 11.7 < 0.0001

PEEP (cmH2O) 7.7 ± 1.9 8.9 ± 2.1 < 0.01

FiO2 (%) 58.6 ± 14.3 68.5 ± 14.9 < 0.005

CPAP (days) 1.8 ± 1.2 3.8 ± 4.7 < 0.02

Tracheotomy (n, %) 2 (3.2 %) 5 (20.8 %) < 0.02

Sedation (days) 3.0 ± 3.5 4.8 ± 5.2 < 0.05

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High residual PVR after PEA:Postoperative complications

Study group(n = 26)

Control group(n = 88)

p

Hemorrhage (n, %) 2 (8.3 %) 7 (11.3 %) ns

RPE (n, %) 10 (41.7 %) 10 (16.1 %) < 0.05

Arrhythmia (n, %) 9 (37.5 %) 16 (25.8 %) ns

Pneumonia (n, %) 12 (50.0 %) 11 (17.7 %) < 0.01

Extubation failure (n, %) 10 (41.7 %) 7 (11.3 %) < 0.01

Pneumothorax (n, %) 2 (8.3 %) 7 (11.3 %) ns

Neurologic disturbances (n, %) 5 (20.8 %) 7 (11.3 %) ns

HIT (n, %) 1 (4.2 %) 3 (4.8 %) ns

Mortality (n, %) 3 (11.5%) 5 (5.7%) ns

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RAMI PERVI

RAMI OCCLUSI

REPERFUSION PULMONARY EDEMACHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: SURGICAL TREATMENT

Massive blood flow diversion from “remodeled” areas to those cleared by surgery

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• First described by Utley and Moser in 1982

• 5-25 % incidence• Rarely life-treatening

REPERFUSION PULMONARY EDEMA

0

5

10

15

20

25

MV lenght (days) ICU stay (days)

RPE

no RPE• Lenghten Invasive Mechanical Ventilation and ICU stay

p<0.001 p<0.001

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Reperfusion Pulmonary Edema

• Prevention:

CO increase limitation? Protective MV?

Negative Fluid Balance?

• Treatment:

- iNO

- aggressive diuretic therapy

- PEEP, post-extubation C-PAP

- postural changes

- (ECMO)

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PULMONARY HEMORRHAGE

• O.5 – 5 % incidence• 3° cause of perioperative mortality• Soon after CPB weaning• Experience and skill of the surgeon• Advanced age• Residual PH

Main Goals of Treatment

Hemodynamic

Stability

Adequate

Gas Exchange

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Massive Pulmonary Hemorrhage After Pulmonary Thromboendarterectomy

Gerard R. Manecke et al.Anesth Analg 2004;99:672-5

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Treatment of pulmonary hemorrhage

• PEEP

• Topical vasoconstrictors

• Treatment of coagulopathy

• Control of Pulmonary Artery Pressure

• Bronchial blockade

• Surgical repair

• Lung resection or embolization

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INFECTION• In our series, the most frequent

complication of postoperative period• Blood Stream, Urinary tract, Wound

infections, but especially

(Ventilator Associated) Pneumonia• Risk factor: prolonged MV

Management:

Distal and protected pulmonary specimens

Empiric antibiotic therapy

Eventual down escalation

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Pulmonary Samples

BronchoAlveolarLavage

PluggedTelescopicCatheter

TrachealAspirate

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NEUROLOGIC DISTURBANCES

Typical manifestations:- Prolonged Drowsiness- Temporary Delirium- Hallucinations- Agitation •Lower cardiac arrest times

•Effective local cooling

•Cerebral continuous monitoring

Post-operative neurologic disorders rarely prevent extubation, maintenance of spontaneous breathing and

normal patient recovery

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HEPARIN INDUCED THROMBOCYTOPENIA

Antibodies vs Heparin-PF4 complexes

Platelet activation

Thrombocytopenia Venous and ArterialThrombosis

Typical features

• Seroconversion and initial PLT count fall

(5-10 days after Heparin exposure)

• PLT < 50% or < 150 109/L

(7-14 days after Heparin exposure)

•25% pts: Rapid Onset HIT

(Heparin exposure within the previous 100 days and residual circulating antibodies)

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HIT in cardiac surgery patients

Teatment of HIT• Alternative, Non-Heparin

Anticoagulation:- Direct Thrombin Inhibitors

- Factor Xa Inhibitors• Routine ultrasonography• VKA after PLT recovery

(PLT > 100-150 109/L)

• Vit K Antagonism reversal (pts receiving VKA at HIT diagnosis)

• PLT transfusion (High bleeding risk or overt bleeding)

• 1-5 % incidence• DD with po PLT decrease:- secondary to CPB, hemodilution- nadir day 2 after surgery