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

1970-72

73-75

76-78

79-81

82-84

85-87

88-90

91-93

94-96

Frequenza per milione di gravid.stimate

emb.polmipertens

anestemb.fluido amnioticoaborto

gravid.ectopicaemorragiasepsi

rottura uteroaltre cause dirette

Entrata in vigore della nuova classificazione


Morti materne associate con l’anestesia in milioni di gravidanze stimate per England & Wales

05

101520253035404550

70-72

73-75

76-78

79-81

82-84

85-87

88-90

91-93

94-96

morti associatedirettamente

freq.per milione

% delle morti dirette

decessi per PE/permilione

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

%

embolismHypertensionHemorrhageinfectionanesthesiaectopc pregnancyCVAcardiomyopathyother(& 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%

untreated

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% verso

la 15 settimana….(Rutherford et al.Am J Ob Gyn 1991)


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 rischioTriade di VirchowTriade di Virchow

IpercoagulabilitàIpercoagulabilità

Stasi venosaStasi venosaDanno dellaparete venosaDanno 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




Tests di lab: non esiste un

esame singolo o una associazione che sia predittiva

EGA:ipossiemia,ipocapnia(ma non si può escludere PE con EGA normale)

ECG: anormalità ST e T disturbi del ritmo:Exs

atriali,ventric,tachic atriale..

modificaz ventric dxsovracc atriale dx,RBB,R(L)AD,S1Q3T3




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.


Nishimura K,Kawaguchi M,Shimokawa M,Kitaguchi M,Furuya 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).


Nishimura et al. Treatment of Pulmonary Embolism during Cesarean Section with Recombinant Tissue

Plasminogen 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)» HCT: 23% (35 < normal < 45).» platelet counts: 92 .000/ml (131 ´ 103 < normal < 362 ´ 103)» prothrombin activity: 56.5%» FDP> 70




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 = 20.7 mmHg; PaCO2 = 67.3 mmHg; BE= -19.1.




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…. .




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

ReportCan 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 and child.


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.




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 mechanical clot fragmentation was considered too dangerous because of the attendant risks of bleeding.




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.




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.




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 ventilation with oxygen, isoflurane 1%, with vecuronium for relaxation. Alfentanil 500 mg, followed by 300 mg fentanyl, were given after delivery of the baby.



45: 888-892 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.




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.

An adrenaline infusion (0.1 – 0.2 mg×kg-1×min-1) was required to support separation from cardiopulmonary bypass, and this was continued throughout a ten hours of post-operative ventilation. The heparin was reversed with 200 mg protamine when CPB was discontinued, and a syntocinon infusion of 20 IU over five hours was commenced in theatre.




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-operative course, with good oxygenation on an FIO2 of 0.4. She was discharged to the post-natal ward 24 hr later. Sc heparin (5,000 IU bd) was commenced on the 1st post-op day, for 2 days, and warfarin on the 2nd postop day. She was discharged home 7 days after admission, and she and the baby were progressing well. The caval filter was removed on the 10th postop day, as an outpatient procedure.



45: 888-892 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) in pregnancy will further reduce the indications for surgical pulmonary embolectomy. Finally, after surviving a 40 min inter-hospital

transfer, the management of the patient at this unit was greatly facilitated by having both cardiothoracic and obstetric facilities on the same site.


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




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

weeks.normal




Haemodynamics time course

0

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140

0 1 2 3 4 5 6 7 8 9 10 11 12

hr

mm

HG

Mpap

CVP

HR

MAP

Rtpa

Dobutamine


Aya AGM, Saissi G,Eledjam JJ, Nishimura K,Kawaguchi 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, and tachycardia combined with a swollen left leg with a decreased venous blood flow shown on Doppler echography.


Aya et al In Situ Pulmonary Thrombolysis Using Recombinant Tissue Plasminogen Activator after

Cesarean Delivery .Anesthesiology, 91:578-9, 1999

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% oxygen; partial pressure of arterial oxygen, 66 mmHg; and arterial oxygen saturation, 89%). The patient had a sinus tachycardia with incomplete right bundle branch block shown on an electrocardiograph, and decreased vascular marks were evident over the right lung on a chest radiograph. Blood tests showed lactic acidosis (pH 7.23, lactic acid, 6 mM/l), anemia (9 g/dl), and thrombopenia (87,000/mm3). Pulmonary and radial artery catheters were placed for hemodynamic monitoring. Cardiac output, mean blood pressure, and mean pulmonary artery pressure were 3 l × min-1 × m2, 48 mmHg, and 33 mmHg, respectively.




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 hemodynamics and oxygenation and could reduce the epinephrine dosage, the fraction of inspired oxygen, and the positive end-expiratory pressure (partial pressure of arterial oxygen, 130 mmHg; arterial oxygen saturation, 98% with 40% oxygen; and positive end-expiratory pressure, 8 cm water). The cardiac output increased (7 l × min-1 × m2), and the pulmonary arterial pressure decreased (23 mmHg). Two days later, a second angiography confirmed the lung reperfusion (). Epinephrine was discontinued 3 days later. The patient left the hospital on day 27 of admission with instructions to take an oral anticoagulant therapy.

Although we used low doses, our case and others illustrate the reduced bleeding complications associated with the perioperative use of rt-PA. However, the intraoperative use and the underlying coagulopathy may have increased the risk of bleeding in the case by Nishimura et al.


Aya et al. Pulmonary Thrombolysis Using Recombinant Tissue Plasminogen Activator after



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…..



Obstet Gynecol 1995; 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 of 4400 ITJ/kg was infused over 10 minutes, followed bv a constant infusion of 4400 IU/kg per hour. During this time, the woman's hemodynamic status improved markedly (Figure 1), and she felt her symptoms had improved. The dopamine infusion was discontinued 8 hours after starting urokinase. The urokinase was discontinued after 12 hours, and an IV beparin infusion was restarted. A repeat ventilation perfusion scan showed an improvement of flow to the left lung.



Obstet Gynecol 1995; 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 heparin infusion, she was converted to subcutaneous heparin at anticoagulant doses. She was discharged on 10,000 IU of heparin subcutaneously every 8 hours and was followed‑up in our anteparturn clinic to term. There were no further complications, and she delivered a healthy male infant (3122 g). Heparin was restarted 6 hours postpartum, and warfarin was initiated the next day. She was discharged on daily warfarin.


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 a total of 29 hr and substituted with heparin. The total post-partum blood loss reached 8900 ml by the 5th day.


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 maintained in the third case in whom thrombolysis was contra-indicated. The authors questioned whether the streptokinase conferred any additional benefit over and above fragmentation. A combination of streptokinase and percutaneous catheter fragmentation has also been used successfully in pregnancy at 25 wk gestation.


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 ventilation was instituted to maximise oxygen delivery and avoid maternal exhaustion. The patient underwent a V/Q scan, which was positive. Before angiography and caval filter insertion could be performed, she decompensated and required surgical embolectomy. Both mother and baby subsequently fared well.


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 performed because of fetal bradycardia. The technique used involved awake intubation, prior to induction with ketamine. Following delivery of an asphyxiated 1.86 kg infant, pulmonary artery catheter insertion was attempted, but abandoned after a brief episode of ventricular tachycardia. Blood pressure subsequently decreased to 40/20 mmHg, following which pulmonary embolectomy on cardiopulmonary bypass was performed. Separation from CPB required 5 mg×kg-1×min-1 dopamine, .3 mg×kg-1×min-1 isoproterenol, and 0.8 mg×kg-1×


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 upright and relieved by lying flat). Patient 2 was a 38-yr-old female who developed platypnoea and hypoxia secondary to a patent foramen ovale (PFO) and pericardial effusion. Patient 3 was a 46-yr-old male with a PFO who developed hypoxia without platypnoea because of multiple pulmonary emboli following right hemicolectomy. These case reports illustrate the need to consider RLIAS as a cause of hypoxia of sudden onset. Early use of bubble contrast echocardiography is indicated.


Carbon Dioxide Elimination Measures Resolution of

Experimental Pulmonary Embolus in Dogs

CRITICAL CARE AND TRAUMA

AUTHOR(S): Breen, Peter H., MD, FRCPC; Mazumdar, Bhaskar, MBBS, FFARCSI;

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 (T), and the alveolar dead space fraction (VDalv/VTalv = [PaCO2 - PETCO2]/PaCO2). RPA reperfusion caused VCO2,br to significantly and abruptly increase from 8.9 ± 2.7 to 11.6 ± 3.6 mL; 70 min later VCO2,br had returned to baseline. PaCO2 and PCO2 steadily decreased during 70 min of RPA reperfusion. PETCO2 increased from 25 ± 5 to 33 ± 5 mm Hg immediately after RPA reperfusion, as VDalv/VTalv decreased from 54% ± 10% to 32% ± 12%, but PETCO2 was still significantly greater than baseline at 70 min of RPA reperfusion. T did not significantly change. We conclude that intraoperative measurement of VCO2,br should immediately detect and follow the resolution of CO2 retention in the lung and peripheral tissues after RPA reperfusion. PETCO2 could not detect the decrease of VCO2,br back to baseline because PETCO2 does not measure exhaled volume or the PCO2 waveform.


P. K. MAZEIKA, C. M. OAKLEY .Massive pulmonary 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 embolism in pregnancy treated with

streptokinase and percutaneous catheter fragmentation.Eur.Heart J. 1994;15:1281-1283

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. A diagnosis of pulmonary embolism was made and heparin and oxygen were administered but

shortly afterwards she suddenly collapsed with syncope and severe dyspnoea. On examination she was profoundly cyanosed, peripherally shut down and had a rapid weak pulse. After initial resuscitation 200 000 U of streptokinase was given intravenously over 20 min followed by a 100 000 U . h ‑ 1 infusion and emergency transfer to Hammersmith Hospital was arranged. She improved considerably over the next 2 h and subsequent pulmonary arteriography showed no central thrombus but complete occlusion of the left lower lobe pulmonary artery, which was opened using a 6F headhunter catheter and 0‑035 inch guide wire


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 cautiously restarted without incident 8 h after cessation of bleeding. Assays on a pre‑heparin blood sample showed normal levels of antithrombin III, protein C, protein S and anticardiolipin antibodies and no evidence of lupus anticoagulant. A Doppler scan of the leg veins was normal and an echocardiogram showed a dilated hypokinetic right ventricle. She made an excellent recovery and was discharged home on warfarin.

After an uneventful third trimester she had a C/S at term for obstetric indications and delivered a healthy baby boy.


MAZEIKA PK,OAKLEY , C. M. .Massive pulmonary embolism in pregnancy treated with

streptokinase and percutaneous catheter fragmentation.Eur.Heart J. 1994;15:1281-1283.


Data from reports on fetal and maternal outcome after thrombolytic treatment for PE in pregnancy

Author cases

weeks

stage Maternal Ko

Fetaloutcome

Ther

Hall 1972 1 32 labour PPH ok streptk

Fagher1990

1 28 labour PPH ok streptk

Ludwig1973

24 14-40 antepartum none Ok streptk

Pfeifer1970

12 Nodata

antepartum none Ok streptk

McTaggart1977

1 34 antepartum none Death inutero

streptk

Mazeika1994

1 25 antepartum none Ok (CS) Streptk +cath.fragm


Author cases

weeks stage Maternal Ko Foetus

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 Deathinutero

streptk

AYA 1999 1 34+2 Post C/S none ok RTPA

Flossdorf 1990 1 31 Pretermlabour

none ok Urok--RTPA

Kramer 19951 21 antepartum none Ok urok

Woodward 1998 1 38 antepartum haemorrhage Okbutrian

Cath fragm +pulm embolect

Mazeika 1995 1 25 antepartum No Ok,C/S

Sterpt+cathfragm

Data from reports on fetal and maternal outcome after thrombolytic treatment for PE in pregnancy


Amniotic fluid embolism (AFE)


Inhaled Nitric Oxide and Amniotic Fluid Embolism LETTER TO THE EDITOR

AUTHOR(S): Tanus-

Santos, Jose Eduardo, MD; Moreno, Heitor, Jr., MD,

PhD; Bastien, John L., MD

Anesth Analg 1999; 88:691

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 completely understood, amniotic fluid has an injurious effect on endothelial cells , probably mediated by endothelin 1 (ET-1). Additionally, ET-1 causes pulmonary hypertension, not only in AFE , but also in air embolism . The potent vasoconstrictor effects of ET-1 result in coronary constriction and cardiodepression seen in both conditions. Thus, any therapeutic attempt to relieve pulmonary vasospasm without decreasing cardiac output would probably increase the low survival rate after AFE. Inhaled nitric oxide (NO) is a selective pulmonary vasodilator and was proposed as a therapeutic option in pulmonary embolism . In agreement with this suggestion, NO attenuated the increase in pulmonary vascular resistance and blunted the decrease of cardiac output after a massive air embolism in dogs . Although the relevance of these findings remains to be elucidated, we suggest that NO therapy could partially reverse the circulatory collapse caused by an AFE.


Atypical Presentation of Amniotic Fluid Embolism

CASE REPORT

AUTHOR(S): Bastien, John L., MD; Graves, Jeffrey R., MD; Bailey, Steven, MD

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 TEG fatt X(eparina)


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

tromboprofilassi 2 h


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,purochin,alfa

chinasi,ukidan 100.000 u persolv,alfachinasi e urokinasi anche da

1.000.000 :dosaggi 4400 U/kg /10 min poi /ogni h *12 h

R.TPA:recombinant plasminogen activator


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……..)

Health & Medicine

Embolia polmonare in obstetrics