Embolia polmonare in obstetrics

Servizio di Anestesia e Rianimazione Ospedale di Faenza(RA)
Embolia polmonare in ostetricia;
dal punto di vista dell’anestesista-rianimatore
Claudio Melloni
Direttore Servizio di Anestesia e
Rianimazione Ospedale di
Faenza(RA)

Report on Confidential enquiries into maternal deaths in
England and Wales 1970-1996
0
5
10
15
20
25
30
19
70-
72
73-
75
76-
78
79-
81
82-
84
85-
87
88-
90
91-
93
94-
96
Frequenza per milione di gravid.stimate
emb.polm
ipertens
anest
emb.fluido amniotico
aborto
gravid.ectopica
emorragia
sepsi
rottura utero
altre cause dirette
Entrata in vigore della nuova classificazione

Morti materne associate con l’anestesia in milioni di
gravidanze stimate per England & Wales
0
5
10
15
20
25
30
35
40
45
50
70-
72
73-
75
76-
78
79-
81
82-
84
85-
87
88-
90
91-
93
94-
96
morti associate
direttamente
freq.per milione
% delle morti dirette
decessi per PE/per
milione
decessi per PE
(num.ass.)

Da Parker,J,Schiffer,MA,Nelson,F.“Maternal and perinatal
mortality”in Clinical management of mother and newborn,GF
Marx ed.,Springer,New York 1979,pag 241-274.
0
5
10
15
20
25
30
Num %
Maternal mortality,New York 1973-76;122 morti.
emb.polm
precl-eclampsia
anest

Da Parker
0
5
10
15
20
%
Maternal mortality,New York 1980
gravid.ectopica
ipertens
emb polm
accid cerebrovasc
anestesia

Maternal Mortality in The USA
(Koonin et al.Maternal mortality surveillance,United yatetes,1980-85.MMWR 1989;37:19)
0
2
4
6
8
10
12
14
16
18
%
embolism
Hypertension
Hemorrhage
infection
anesthesia
ectopc pregnancy
CVA
cardiomyopathy
other(& indirect)

Incidence of venous thromboembolism during
pregnancy
0
0,05
0,1
0,15
0,2
0,25
0,3
0,35
Letsky 1984
Aaro 1971
Henderson 1972
Weiner 1985
Moore 1967
PE 12-25%
untreate
d
Isotopic perfusion lung
scanning and pulm
angiography
with clinical suspicion of PE

PE(CEMDUK)
PE come causa maggiore di morte
mort per TEB:2.1/100.000 gravid.
48 decessi,30 nel prec triennio
46 PE e 2 trombosi cerebrali
15 morti prenatali,25 postpartum

Intervallo fra parto e PE(dati UK 1994-96)
0
1
2
3
4
5
6
gg
0-7 8_14 15-28 29-42 ??
parto vag
C/S
Ma la maggior parte delle DVT
accadono antepartum;il 51% ver
la 15 settimana….(Rutherford et al.Am J O

Fattori di rischio(CEMDUK)
Gravidanza come stato ipercoagulabile
riposo a letto prolungato
disidratazione
chirurgia pelvica
obesità
fumo
età materna > 35(5/100.000….)
multiparità
trombofilia(resist alla prot C attiva,mutaz nel coding del fatt V);deficit AT III,della
prot C ,della prot S…...
emorragia
sepsi

Gravidanza come fattore di
rischio
Puerperio * 6
C/S *10-20

Gravidanza come fattore di rischioGravidanza come fattore di rischio
Triade di VirchowTriade di Virchow
IpercoagulabilitàIpercoagulabilità
Stasi venosaStasi venosa Danno della
parete venosa
Danno della
parete venosa

Fattori di rischio per PE(Salonen H et al.Pulmonary
embolism and stroke in relation to pregnancy:how can high risk women be identified?
Am.J.Obstet.Gunecol 2002;186:198-203.)
Età materna
parità
fumo
preeclampsia;III trim RR 7 vs 3 non
preeclamptic;puerperiumRR 8 ;stroke 12 RR
gravid multipla,stroke risk 12
diabete
C/S;parto e puerperio 7 RR vs vag;stroke risk 4 RR

Prediction indexes for patients with DVT:(Wells et al.Value of
assesment of pretst probability of deep vein thrombosis in clinical management.Lancet
1997;350:1795-98)
Presence of active
cancer
presence of paralysis
presence of a cast
no alternative
diagnosis(??)
recent immobilization
recent surgery
tenderness along deep
veins
swelling of entire leg
difference in calf
circumference > 3 cm
pitting edema
presence of superficial
veins

Dehring DJ, Arens JF: Pulmonary thromboembolism: Disease
recognition and patient management. ANESTHESIOLOGY
73:146-64, 1990
Segni e sintomi
>50%:dispnea,tachipnea,tachicardia,apprensione,rant
oli,tosse, II tono polm accentuato,dolore
toracico(pleuritico/anginoso)
<40%emottisi,febbre di grado medio,cianosi,diaforesi,
segni di aumentata PVC, DVT clinica,
sincope,alterato stato mentale.
<10%wheezing,DIC,dolore addominale

73:146-64, 1990
Tests di lab:
non esiste un
esame singolo o
una associazione
che sia predittiva
EGA:ipossiemia,ip
ocapnia(ma non si
può escludere PE
con EGA normale)
ECG:
anormalità ST e T
disturbi del
ritmo:Exs
atriali,ventric,tachi
c atriale..
modificaz ventric
dxsovracc atriale
dx,RBB,R(L)AD,S1Q
3T3

73:146-64, 1990
Modificazioni RX
atelectasis
elevaz emidiaframma
versam pleurico
oligemia focale
“knuckle sign”
infarto polmonare

Indagini diagnostiche( Toglia MR, Weg JG. Venous
thromboembolism during pregnancy. N Engl J Med 1996; 335:108-14.)
DVT:
Pletismografia ad impedenza
ultrasonografia real time B-mode
ultrasonografia doppler Duplex
PE:
scan V/Q
angiografia polm.

Miron et al. Clinical assesment of suspected deep vein
thrombosis:comparison between a score and empirical
assessment.J.Intern.Med. 2000;247:249-254.
..overall accuracy higher for the empiric
asessment ,especially in patients
categorized as high risk.

H.Treatment of Pulmonary Embolism during Cesarean Section
with Recombinant Tissue Plasminogen
activator.Anesthesiology 89:1027-8, 1998
abruptio placenta and preeclampsia
GA for C/S
intraop life-threatening pulmonary
embolism
recombinant tissue plasminogen
activator (rt-PA).

Treatment of Pulmonary Embolism during Cesarean Section
Activator.Anesthesiology 89:1027-8, 1998
35-yr-old woman at 29 weeks' and 4 days' gestation
admitted from an outside institution for the treatment of
abruptio placenta and preeclampsia
no external vaginal bleeding
the patient had undergone previous C/S for preeclampsia and
prematurity;no history of pulmonary disease or DVT
Ultrasonography revealed an estimated fetal weight of 1,212
g, and the fetal HR was > 100 beats/min.
Results of blood tests performed at admission showed
» HB: 7.6 g/dl (11.8 < normal < 13.0)
» erythrocyte count: 3.30 106
/ml (3.74 106
< normal < 4.29 ´ 106)

GA+ETT induced using a rapid-sequence technique with
cricoid pressure. Bilateral breath sounds were normal:SpO2
99% , ETCO2 26–28 mmHg.
Just after delivery of a neonate, methylergometrine maleate
was administered iv . A few min later, ETCO2 decreased
suddenly to 9 mmHg. Simultaneously, it became difficult to
ventilate the lungs, and 3 min later, SpO2 decreased from
99% to 19%. (FIO2 = 1.0) SBP progressively decreased from
140 to 80 mmHg, and the HR increased to 142 beats/min. 8
mg ephedrine was administered iv ;SBP recovered to 120
mmHg. 15 min after the decrease in blood pressure, an
intraarterial catheter was inserted, EGA: pH = 6.93; PO2 =

Dopamine infusion was started at a rate of 10 micro
g×kg-1×min-1 and increased to 17 microg×kg-1×min-
1. Nevertheless, SBP decreased to 62 mmHg, and
the HR decreased to 38 beats/min. Epinephrine was
started at a rate of 0.133 microg×kg-1×min-1, with an
increase in BP to 100/60 mmHg. SpO2 and ETCO2
monitoring showed 0% and 16 mmHg,
respectively…….per 40 min…. .

Nishimura et al.
Based on a provisional diagnosis of pulmonary
embolus, 5,000 u heparin followed by 5,000 u/h was
administered. SpO2 increased to 50–60%. However,
the patient continued to be hypoxic for 1 h, and her
condition gradually deteriorated…..
. A bolus of 1,800,000 units followed by 12,000,000
units/h rt-PA was then administered.
10 minutes later…. SpO2 dramatically increased to
100%. EGA pH: 7.328, PO2: 451.1 mmHg; PCO2:
49.2 mmHg; BE: -0.5 (FIO2 = 1.0).

Chest RX performed in the OR was unremarkable.
The patient was transferred to the ICU. 3 hours later,
she recovered consciousness without neurologic
compromise. However, her abdomen gradually
became distended. There was external evidence of
severe ongoing coagulopathy with bleeding from the
vagina and the abdominal incision. Multiple
transfusions of blood components were transfused for
the next 35 h. Exploratory laparotomy for hemostasis
of bleeding was performed through a midline incision
the next day.

Although postoperative transfusions were necessary,
coagulation test results returned to normal levels and
bleeding decreased gradually. 14 days after delivery
of a neonate, the patient was transferred to the
obstetric ward. Pulmonary ventilation/perfusion scan 2
weeks after the operation was compatible with a large
embolism to the left upper lobe; the patient eventually
made a complete recovery.

Warning!!
Obstetric delivery and major surgery
within 7–10 days were classified as
major relative contraindications by the
National Institutes of Health (NIH)
Consensus Conference because
thrombolytic therapy also lyses other
tissue clots…..

Woodward DK,Birks R, Granger KA.Massive pulmonary
embolism in late pregnancy .Clinical Report
Can J Anaesth 1998 ; 45: 888-892
A case of massive pulmonary embolism is described in a
woman who presented in early labour at thirty-eight weeks
gestation. Immediate management involved the
administration of oxygen and intravenous heparin, and
transfer to the regional cardiothoracic centre. Pulmonary
angiography confirmed the diagnosis of massive pulmonary
embolism, but attempts at percutaneous catheter disruption
of the clot were of only temporary benefit. The patient
subsequently underwent Caesarean section under general
anaesthesia, followed minutes later (because of an abrupt
deterioration in her condition) by surgical pulmonary
embolectomy. The outcome was successful for both mother

Woodward & Granger.Massive pulmonary
embolism in late pregnancy . Can J Anaesth
1998 ; 45: 888-892
A 25 yr old Caucasian woman in the 38th week of her 2nd
pregnancy
presented to the ante-natal ward of a local district general
hospital with a two hour history of an abrupt onset of severe
dyspnoea, chest tightness, and dizziness.
Examination demonstrated central cyanosis and tachycardia,
although she was normotensive (blood pressure (BP) 110/70
mmHg). A clinical diagnosis of pulmonary embolism was
made, and, following initiation of treatment with oxygen and
intravenous heparin, she was transferred immediately to the
cardiothoracic unit at this hospital.

Woodward & Granger.Massive pulmonary embolism in late
pregnancy . Can J Anaesth 1998 ; 45: 888-892
On arrival on the CCU (4 hr after initial presentation), the
patient was found to be conscious, tachypnoeic and
cyanosed, with an SpO2 of 89% breathing oxygen by face
mask (nominal FIO2 of 0.9). She was tachycardic (pulse rate
140 bpm) but remained normotensive (BP 125/75 mmHg).
EGA: pH of 7.44, PaCO2 of 3.5 kPa, PaO2 of 7.7 kPa and BD
of 5.3 mmol×l-1. An ECG demonstrated sinus tachycardia
with partial RBB and right ventricular strain. Cardiotocography
indicated fetal well-being (with a baseline rate of 150 bpm and
good variability). The presence of regular `tightenings' and
vaginal examination confirmed that the patient was in early
labour.

1998 ; 45: 888-892
The immediate management of the patient was discussed
with obstetrics, cardiothoracic surgery, cardiology,
anaesthetics and radiology. In view of the evidence of early
labour, it was considered that to provide the best chance of
survival for both mother and child, delivery by urgent C/S was
indicated. The need for surgical pulmonary embolectomy was
a distinct possibility, and pulmonary angiography was
required to confirm the diagnosis; attempts at mechanical clot
disruption during this investigation also held the possibility of
improving the patient's haemodynamic status. As the patient
was at term and in early labour, and an active surgical
approach to management had been selected,
pharmacological thrombolysis to supplement percutaneous

1998 ; 45: 888-892
The patient subsequently underwent pulmonary
angiography (2 hr after arrival at our hospital), which
confirmed bilateral large proximal pulmonary emboli, with
preserved perfusion only of the left upper lobe. Attempts at
mechanical disruption of the proximal thrombus using a
pigtail catheter were met with some improvement in her
symptoms and arterial oxygen saturation, and radiologically
improved perfusion to the right lung. An infra-renal caval
filter was inserted.

1998 ; 45: 888-892
However, the initial improvement in the patient's
condition was not maintained, and re-examination
within the hour confirmed progression of labour; the
FHR remained satisfactory. It was, therefore, decided
to proceed to delivery of the baby by C/S under GA
with full preparation being made to proceed to
emergency surgical pulmonary embolectomy if
indicated.

1998 ; 45: 888-892
She received premedication with sodium citrate and
50 mg ranitidine iv, and a radial arterial cannula for
blood pressure monitoring was secured. She was
transferred to theatre 3 hrs 10 min after admission.
Following pre-oxygenation, GA was induced with 500
mg alfentanil and 20 mg etomidate, and 100 mg
succinylcholine was given to facilitate tracheal
intubation after cricoid pressure was applied and
tracheal intubation was easily performed.
Maintenance of anaesthesia was by means of

A pre-induction BP of 140/70 mmHg decreased to 95/70
mmHg post-induction, and increased to 140/95 mmHg during
delivery. A live but asphyxiated 3.8 kg male infant was
delivered within ten minutes of induction of anaesthesia (and
just under four hours after the patient had been admitted to
this hospital). Apgar scores: 1 at 1 min; 2 at 5 min; 6 at 10
min; 8 at 15 min). Following administration of 10 IU
syntocinon and fentanyl post-delivery, the BP decreased to
80/60 mmHg. A sinus tachycardia of 140–160 bpm persisted
throughout this period. However, approximately 10 min after
delivery, and while the uterus was being closed, the patient's
BP decreased suddenly to 50/30 mmHg.

1998 ; 45: 888-892
On suspicion of a further massive PE, median
sternotomy was performed, and normothermic, non-
cardioplegic cavoaortic cardiopulmonary bypass was
instituted following full heparinisation. A 20 cm length
of embolic thrombus was extracted from the main
pulmonary artery bifurcation. An innominate vein
central line was inserted by the surgeon following
embolectomy, (as attempts at internal jugular line
insertion following delivery had been interrupted by
the need to institute CPB); the CVP after separation
from CPB was 10 cmH2O.

1998 ; 45: 888-892
Pre-operatively, Hb was 98 g×l-1 and platelet count 87 x l-1.
Following delivery, perop Hb was 82 g×l-1, and decreased to
55 g×l-1 during cardiopulmonary bypass The patient received
3 units of blood (packed cells or SAG-M) in theatre and,
subsequently, a further 3 units overnight in the CICU. In view
of the pre-operative thrombocytopenia, period of CPB, and six
unit blood transfusion, she was also given 5 units each of
platelets and FFP in CICU. However, there was no evidence
of excessive obstetric haemorrhage either in theatre or post-
operatively. The patient's arterial blood gas values are
recorded in the table.()
Following extubation, she continued an uneventful post-

conclusion, recent case reports support the use of
thrombolysis and percutaneous catheter fragmentation in
cases of massive P.E. occurring in pregnant women not
in labour; furthermore, this should be performed early, and arguably
does not require cardiac catheterisation facilities. Use of thrombolytic
agents during labour and delivery can be expected to be
associated with peri-partum haemorrhage, and the risks
and benefits of conservative management vs
thrombolysis or surgical embolectomy must be made on
an individual basis in these patients. However, some maintain that
thrombolysis should be strongly contraindicated in the peri-partum
period until evidence from controlled trials is available. It may be that
increasing experience with `clot specific' thrombolytic agents (e.g. rt-PA)

Flobdorf Th, Breulmann M, Hopf H-B. Successful treatment
of massive pulmonary embolism with recombinant tissue
type plasminogen activator (rt-PA) in a pregnant woman
with intact gravidity and preterm labour. Intensive Care
Med 1990; 16:454-56.
27 y,31st week
preterm labour & tachypnea
immobilization * preterm labour;2 weeks
of tachypnea
BP 80/50,HR 130,cyanosis (PaO2
72,PaCO2 28).

Flobdorf et al. Successful treatment of massive pulmonary embolism
with recombinant tissue type plasminogen activator (rt-PA) in a
pregnant woman with intact gravidity and preterm labour. Intensive
Care Med 1990; 16:454-56.
R.HEART CATH;Mpap 36,RVp 50/20 :
pulm angiography ;lack of perfusion of R upper &
middle & lower lfet lobe
dobutamine 5 microgr/kg/min
urokinase 200.000 + heparin;obst objection…...
further deterioration;BP 75/45,CVP 17, Mpap 39 ;HR
132,RAD+ST depression,neg T;paO2 72,PaCO2
25,O2 10 lt/min mask

Care Med 1990; 16:454-56.
2 hr without improvement;new consultation..
RTPA 10 mg/hr*4 hr,followed by 2 mg/hr * 1.30
hr,discontinued for slight bleeding from a puncture side(+
marked improvement)---300 UI heparin/kg/24 hr)
“ subsequent” angiography;complete reperfusion RUL/RML &
partial reperfusion LLB:
coag tests normal;
after 24 hr_transferred to ob ward;IInd day spont delivery of a
male preterm infant(2100 gr);
2 weeks later heparin subst by oral coumarin:discharged at 4

Care Med 1990; 16:454-56.
Haemodynamics time course
0
20
40
60
80
100
120
140
0 1 2 3 4 5 6 7 8 9 10 11 12
hr
mmHG
Mpap
CVP
HR
MAP
Rtpa
Dobutamine

M,Furuya H.In Situ Pulmonary Thrombolysis Using
Recombinant Tissue Plasminogen Activator after Cesarean
Delivery .Anesthesiology, 91:578-9, 1999
. We successfully gave lower doses of recombinant
tissue plasminogen activator (rt-PA) via a pulmonary
artery catheter for thrombolysis in a 20-yr-old woman
2 days after a cesarean section. She was referred to
us after an urgent CS at 34 weeks' gestation because
of a suspected pulmonary embolism with concomitant
fetal distress. Pulmonary embolism was suspected
because of the sudden occurrence of
consciousness troubles (confusion and
disorientation), dyspnea, cyanosis, hypotension,

Aya et al In Situ Pulmonary Thrombolysis Using
She was treated prophylactically with subcutaneous
low molecular weight heparin for 1 week. Heparin
(5,000 units bolus and 1,000 units/h) was
administered, but collapse and hypoxia persisted
throughout the cesarean section despite the
administration of fluids (2,500 ml) and mechanical
ventilation with 100% oxygen. When she was
admitted to our intensive care unit, the patient's
systolic blood pressure varied from 50—100 mmHg,
and hypoxia persisted (blood gas analysis with 100%

The pulmonary artery wedge pressure could never be
measured. Echocardiography showed a strongly
dilated and hypokinetic right ventricle, with bulging of
the interventricular septum into the left ventricle.
Epinephrine and heparin administration and
ventilation with a positive end-expiratory pressure (14
cm water) improved the patient's hemodynamic status
(blood pressure, 140/90 mmHg; urine output, >0.5 ml
× kg-1 × h-1; lactic acid, <2 mM/l; partial pressure of
arterial oxygen, 135 mmHg with 80% oxygen),
allowing further investigation.

Pulmonary angiography confirmed the pulmonary
embolism and venocavography showed a
compression on the left iliac vein (Cockett
syndrome). Because of hemodynamic instability
during the following 2 days, 60 mg rt-PA was
administered over 6 h in situ via the pulmonary
artery catheter but stopped at a cumulative dose of
57 mg because of bleeding on vascular puncture
sites. No bleeding occurred from the wound or the
uterus. Nevertheless, we obtained satisfactory

Aya et al. Pulmonary Thrombolysis Using Recombinant
Tissue Plasminogen Activator after Cesarean Delivery
.Anesthesiology, 91:578-9, 1999

Fine
More cases following…..

Kramer WB, Belfort M, Saade G, Surani S, Moise KJ Jr.
Successful urokinase treatment of massive pulmonary
embolism in pregnancy. Obstet Gynecol 1995; 86:660-2
A 20-year-old woman at 21 weeks' gestation
presented to the ER
history of worsening dyspnea and dizziness, and an
episode of loss of consciousness lasting 1-2 min.
family history of thromboembolic disorder, and her
mother died at age 37 of a suspected PE
admission: lethargic and had clinical evidence of
respiratore distress;vital signs were: BP 82/58 mmhg,
HR 132 RR 27,SaO2 90% on room air.

Kramer WB, Belfort M, Saade G, Surani S, Moise KJ Jr.
Successful urokinase treatment of massive pulmonary
embolism in pregnancy. Obstet Gynecol 1995; 86:660-2
Cardiac exam. was remarkable for an accentuated
pulmonary component of the second heart sound, a strade 2
(of 6) systohc ejection murmur , and a right ventricular
heave. The FHR was 150 beats per minute; no evidence of
thrombophlebitis or edema. Apart from her lethargy, the
neurologic examination was nonfocal. Abdominal
ultrasound confirmed a singleton intrauterine pregnancy at
21 weeks' gestation.
ECG revealed sinus tachycardia with S1Q3; chest RX
showed no vascular markings over the left lung field.

Kramer et al. Successful urokinase treatment of massive
pulmonary embolism in pregnancy. Obstet Gynecol 1995;
86:660-2
A PE was diagnosed, and the patient was admitted to the obstetric
intensive care unit and started on intravenous (IV) heparin. An
emergency radionuclide ventilation perfusion lung scan indicated a high
probability for pulmonary embolism. The echocardiogram revealed
severe right ventricular and right atrial enlargement, right ventricular wall
hypokinesia, and bulging of the interatrial septum into the left atrium.
These fìndings were believed to be consistent with increased right
ventricular end-diastolic pressure. Right heart catheterization was
performed via the left antecubital v. VVhile we attempted to float
the inflated balloon into the pulmonary artery, circulatory
collapse occurred with a sudden loss of consciousness.
Immediate defiation of the balloon resulted in rapid recovery,
and the patient regained conscious ness…..

86:660-2
During this episode, the FHR decreased to 100
beats/min and required 30 min.to return to baseline.
Initial data obtained using the pulmonary artery
catheter are presented in Figure 1,
The patient continued to show hemodynamic and
respiratory deterioration despite heparin therapy,
repeated fluid boluses of normal saline, and a
dopamine infusion. Therefore, we instituted
thrombolytic therapy with IV urokinase and
discontinued the heparin infusion. An IV priming dose

86:660-2
Six hours after discontinuing the urokinase, the patient experienced an
episode of dyspnea with sudden deterioration in her hemodynamic
status. She responded to a fluid bolus and 100% oxygen through a
non rebreather mask. This episode was thought to be secondary to‑
further pulmonary embolism, and the urokinase infusion was restarted
after the priming dose was repeated. She experienced no further
episodes of dyspnea or hemodynamic instability (Figure 1). Twelve
hours later, urokinase was discontinued and IV heparin was restarted.
Repeat echocardiogram showed a decrease in the size of the right
atrium and ventricle with less bulging of the interatrial septum to the left.
Impedance plethysmography and venography of the lower extremities
were normal.
The patient experienced no further episodes of hemodynamic instability,
and her dyspnea improved every day. After 7 days of a continuous IV

Discussion …..1
Considerable problems with obstetric haemorrhage
have occurred, however, in a case reported in 1972 in
which streptokinase was infused throughout labour
and delivery, only being discontinued in the third
stage due to persisting blood loss which was finally
controlled with aminocaproic acid. In a more recent
report, streptokinase was commenced for massive PE
at 28 wk gestation, but was stopped after 10 hrs for
the duration of a pre-term labour and delivery. It was
recommenced eight hours later, but discontinued after

Discussion 2….
The technique of percutaneous transvenous
fragmentation of pulmonary emboli may be performed
using catheters specifically designed for the purpose,
or with conventional cardiac catheters. A case report
of acute massive P.E. involving three non-obstetric
cases demonstrated this to be a rapid and relatively
non-invasive method of improving cardiac output in
very sick patients. Two cases subsequently also
received an infusion of streptokinase via a pulmonary
artery catheter, although the dramatic haemodynamic
improvement occurred prior to this, and was

Discussion ….3
A case report in 1985 discussed a woman presenting
at 35 wk gestation with a massive PE, in active
labour. Despite cardiorespiratory compromise, labour
was allowed to proceed and resulted, eight hours
later, in the spontaneous vaginal delivery of a 2.3 kg
live infant. Caesarean section was rejected as it was
felt that the maternal risk was too great; any surgical
intervention should be for `maternal indications' only
(such as embolectomy for worsening status).
Thrombolytic therapy was also rejected as carrying
too high a risk. However, following delivery, elective

Discussion….4
A case bearing some similarity to ours
was reported in 1989, in which a woman
presented with cardiorespiratory
compromise due to acute PE, at 32 wk
gestation. She was not in labour.
Heparin was commenced four hours
after admission, but there is no record of
whether thrombolytic agents were
considered. Five hours after admission,
emergency Caesarean section was

Marples IL, Heap M , Suvarna SK,Mills G H Acute right-to-
left inter-atrial shunt; an important cause of profound hypoxia
Br. J. Anaesth. 2000; 85:921-925
Three patients presented to our
intensive care unit over a 3-yr period
with profound hypoxia resulting from
acute right-to-left inter-atrial shunt
(RLIAS). Patient I was a 67-yr-old male
with an atrial septal defect who became
hypoxic and developed the rare sign of
platypnoea following elective repair of
an abdominal aortic aneurysm
(breathlessness made worse when

Skinner, Sean C., BAAnesth
Analg 1996; 83:247–53
Patients with severe pulmonary embolism can suffer progressive
hypercapnia refractory to supramaximal mechanical ventilation, and
may require open-thoracic or transvenous emergency embolectomy in
addition to anticoagulation and/or thrombolysis. The functional recovery
of gas exchange would be signaled by an increase in pulmonary CO2
elimination and decrease in CO2 retention; such data could guide the
course of operative embolectomy. Accordingly, we studied five
chloralose-urethane anesthetized, mechanically ventilated dogs with
open thoraces in which the right pulmonary arteries (RPAs) were
reversibly occluded with cloth snares. After waiting for steady state, we
abruptly released the snare to restore RPA perfusion and experimentally
simulate resolution of pulmonary embolism. For 70 min we serially
measure the CO2 volume exhaled per breath (VCO2,br), arterial, mixed
venous, and end-tidal PCO2 (PaCO2, PCO2, PETCO2), cardiac output

embolism in pregnancy treated with streptokinase and
percutaneous catheter fragmentation.Eur.Heart J. 1994;15:1281-
1283
We report a patient who suffered
massive pulmonary embolism with
circulatory collapse in the second
trimester and who was treated with
intravenous streptokinase followed by
percutaneous mechanical dispersion of
thrombus using a catheter and guide
wire. She made an excellent recovery
despite complicating anteparturn
haemorrhage.

P. K. MAZEIKA, C. M. OAKLEY .Massive pulmonary
1283
In life threatening circumstances‑
pharmacological thrombolysis is
mandatory particularly for hospitals
without a cardiac catheterization
laboratory on site…..

MAZEIKA PK,OAKLEY , C. M. .Massive pulmonary embolism
in pregnancy treated with streptokinase and percutaneous
catheter fragmentation.Eur.Heart J. 1994;15:1281-1283
A 34 year old w.,25 weeks ,Ist pregnancy‑ ‑
admitted with worsening exertional dyspnoea over 2 weeks.
no past history of venous thromboembolism,pregnancy
uncomplicated.
On examination she was mildly breath less,centrally
cyanosed with a raised jugular venous pressure.
HR 124 beats/ min,BP 110/70 mmHg.
no clinical evidence of deep vein thrombosis.
RX unremarkable ;ECG S,Q,T, pattern. P02 8.7 kPa,
PC02 3,2 kPa.

MAZEIKA PK,OAKLEY , C. M. .Massive pulmonary embolism
in pregnancy treated with streptokinase and percutaneous
catheter fragmentation.Eur.Heart J. 1994;15:1281-1283.
Following transfer to the intensive care unit and after
discontinuing streptokinase (total dose 1400 000 U)
she began bleeding from the os cervix. Prothrombin
time was 26 s, partial thromboplastin time 42 s and
fibrinogen I g. I Heparin was stopped, FFP and
cryoprecipitate were administered and she required 4
u blood under cvp monitoring. The FHR remained
stable throughout and an ultrasound scan of the
uterus showed intact membranes and no evidence of
retroplacental haemorrhage. Iv heparin was

MAZEIKA PK,OAKLEY , C. M. .Massive pulmonary
1283.

Data from reports on fetal and maternal outcome after
thrombolytic treatment for PE in pregnancy
Author ca
se
s
wee
ks
stage Mat
erna
l Ko
Fetal
outco
me
Ther
Hall 1972 1 32 labour PPH ok streptk
Fagher
1990
1 28 labour PPH ok streptk
Ludwig
1973
24 14-40 antepartum none Ok streptk
Pfeifer
1970
12 No
data
antepartum none Ok streptk
Mc
Taggart
1977
1 34 antepartum none Death in
utero
streptk
Mazeika
1994
1 25 antepartum none Ok (CS) Streptk +
cath.frag

Author cas
es
weeks stage Maternal Ko Foe
tus
Ther
Hall 1972 1 32 labour PPH ok streptk
Fagher 1990 1 28 labour PPH ok streptk
Ludwig 1973 24 14-40 antepartum none Ok streptk
Pfeifer 1970 12 No data antepartum none Ok streptk
Mc Taggart 1977 1 34 antepartum none Death
in
utero
streptk
AYA 1999 1 34+2 Post C/S none ok RTPA
Flossdorf 1990 1 31 Preterm
labour
none ok Urok--RTPA
Kramer 1995
1 21 antepartum none Ok urok
Woodward 1998 1 38 antepartum haemorrhage Ok
but
rian
Cath fragm +
pulm embolect
Mazeika 1995 1 25 antepartum No Ok,C/ Sterpt+cath
Data from reports on fetal and maternal outcome after thrombolytic
treatment for PE in pregnancy

Amniotic fluid embolism (AFE)

We read with interest the article by
Bastien et al. describing the occurrence
of a rare case of amniotic fluid embolism
(AFE). They elegantly addressed the
clinical features and the treatment of
AFE, but we would like to emphasize
some recent information that could lead
to better treatment of this critical
condition. Although the pathophysiologic
responses seen with AFE are not

Anesth Analg 1998; 87:124

Shechtman M,Ziser A,Markovits R, Rozenberg B. Amniotic
Fluid Embolism: Early Findings of Transesophageal
echocardiography . Anesth Analg 1999; 89:1456–8

Evitare:
ipossia,ipercapnia,stress
PG,ERGOT,KETAMINA,N2O
BRADICARDIA
DEPRESSIONE MIOCARDICA
RIDUZIONE DELL’AFTERLOAD
RIDUZIONE DEL PRELOAD(RITORNO
VENOSO)

Coagulazione in gravidanza:
Piastr norm o dim
fatt
VII,VIII,IX(=),X,XII +
fibrinog +
XI dim 62%
protc C =
prot S dim 40-50%
AT III =
PT dim
APTT dim
TT dim

trombofilie
fAm,acquis
storia di DVT,PE
ricerca continua con avanzamenti rapodi
trombosi art e ven
storia di aborti
rciorrenti,IUGR,preeclampsia
episodi trombotici on the pill”

Trombofilie congenite
19210079

Tromboflie acquisite
19210080

Disordini delle piastrine
19210081

Preeclampsia & HELLP

Dosrdini dei fattori delal
coagulazione

Esami di laboratorio
Formazione del coagulo(coinvolge le
pareti dei vasi,piastrine e sist.
coagulativo…..)
storia clinica,es obb
consulto ematologico
conta piastrinica
tempo di sanguinamento
PT,PTT,INR,fibrinogeno

Problemi anestesiologici
Raccomandazioni di Vandermeulen
1994
piastr> 80.000
INR non < 1.5
APTT limiti sup della norma
tempo di sang = o > 8 min
no storia di sanguinam anormale o
bruising

Raccomandaz per anest
reg(Vandermeulen)
Inserz adattata al trattamento
spi> epid
inserim atraumatico
4 cm catet nello spazio
monitorizzazione vigile post partum

LMWH
Horlocker 1997:
ritarda inserz 10-12 h dopo LMWH
ritarda rimoss catetere 10-12 h
dall’ultima dose
in caso di inserz traumatica,ritarda la
dose successiva
controlla coag prima della rimoss del
catetere
dopo rimoss del catetere ritarda la

I.V. heparin(Horlocker 1997)
Ritarda inserim o rimoss 1 ora dalla
dose

farmaci
Eparina i.v.
streptokinasi:streptase 250.000 0
750.000 u.;250.000/30 min poi
100.000/h sec.TT;*24-72 h?
urokinasi;urokinase,actosolv,persolv,pur
ochin,alfachinasi,ukidan 100.000 u
persolv,alfachinasi e urokinasi anche da
1.000.000 :dosaggi 4400 U/kg /10 min
poi /ogni h *12 h

Eparina s.c.
Ritarda inserz o rimoss 4 ore dalla dose
con tutti gi agenti;usa misture
oppioidi/LA

Antepartum deaths from PE

Antepartum deaths from PE:
II

Deaths from PE following C/S:
I

Deaths from PE following C/S

Deaths from PE following vaginal delivery:
I

Daeths from PE following vaginal delivery

trattamento
Rapido
prima della dg definitiva???
Piena anticoagulaz con iv eparina
LMW heparin
filtri ilio-femorali

Prevenzione
Tromboprofilassi iniziata nel periodo
prenatale………
identificazione dei gruppi a rischio:
» valvole cardiache prostetiche
» trombofilie
» pregresse DVT e PE familiari
» gli anestesisti hanno un ruolo da
giocare….....

Non private le pazienti dei benefici della
tromboprofilassi (e dei blocchi
centrali……..)

Embolia polmonare in obstetrics

Recommended

Recommended

More Related Content

Similar to Embolia polmonare in obstetrics

Similar to Embolia polmonare in obstetrics (20)

More from Claudio Melloni

More from Claudio Melloni (20)

Recently uploaded

Recently uploaded (20)

Embolia polmonare in obstetrics