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Print version ISSN 0034-7094
Rev. Bras. Anestesiol. vol.52 no.2 Campinas Mar./Apr. 2002
Pulmonary embolism in the operating room. Case report*
Embolia pulmonar en sala operatoria. Relato de caso
Karina Bernardi Pimenta, M.D.I; Beatriz do Céu Nunes, TSA, M.D.II
Hospital do Câncer; Intensivista da Clínica São Vicente da Gávea,
Rio de Janeiro
IIInstrutora do CET/SBA do Hospital do Câncer, Rio de Janeiro
BACKGROUND AND OBJECTIVES:
Pulmonary embolism is a common postoperative complication. This report aimed
at presenting a case of pulmonary embolism in the operating room and at calling
the attention to the importance of venous thrombosis prophylaxis in surgical
CASE REPORT: The authors describe a case of a male patient, 55 years of age and 83 kg submitted to radical prostatectomy for prostate cancer. At the end of the surgery and already extubated, patient presented hemodynamic instability and a decrease in SpO2 to 80%. Patient was re-intubated and sent to the ICU. CT images suggested pulmonary embolism. Patient died in the 5th postoperative day.
CONCLUSIONS: A high suspicion rate is not enough to establish a diagnosis because pulmonary embolism is a silent disease and its investigation routine is not highly sensitive. Early prophylaxis is the best strategy.
Key words: COMPLICATIONS: pulmonary embolism; SURGERY, Urologic: prostatectomy
JUSTIFICATIVA Y OBJETIVOS:
Embolia pulmonar es una complicación frecuente en el período pós-operatorio.
El objetivo de este relato es presentar un caso de embolia pulmonar ocurrida
en la sala de operación y llamar la atención para la importancia de la profilaxis
de trombosis venosa en pacientes cirúrgicos.
RELATO DE CASO: Se trata de un paciente del sexo masculino, 55 años y 83 kg con diagnóstico de cáncer de próstata, sometido a prostatectomia supra-púbica bajo anestesia general. Al final de la cirugía, el paciente ya entubado y luego después de pasar para la camilla de transporte presentó inestabilidad hemodinámica y diminución de la SpO2 para 80%. Fue reintubado y encaminado para la UTI. La tomografía computadorizada mostró imágenes con aspecto de embolia pulmonar. El paciente evolucionó para óbito en el 5º día de pós-operatorio.
CONCLUSIONES: El elevado índice de sospecha no es suficiente para firmar el diagnóstico pues la embolia pulmonar es una enfermedad silenciosa y la rutina de investigación no posee elevada sensibilidad. La profilaxis precoz y adecuada es la mejor estrategia.
In spite of recent epidemiological advances, pulmonary embolism (PE) diagnosis, treatment and prevention is still a challenge for our clinical skills. PE is accountable for approximately 50 thousand deaths per year in the USA, with an annual incidence of 300 thousand cases 1. Mortality during the first hour is 12% and reaches 30% when not diagnosed. A third of those patients suffer recurrent episodes. For every 10-year increment in age, venous thrombosis incidence doubles 2,3. Future seems promising, with advances in molecular biology, imaging techniques and treatment with low molecular weight heparin 4.
Primary embolization sources are deep thigh and pelvic thrombotic veins 4. Thrombosis-triggering events are not totally explained and the classic Virchow Triad (venous stasis, endothelial injury and hypercoagulation) does not explain all mecahnisms 1.
This report aimed at calling the attention for the importance of early and adequate pulmonary embolism prophylaxis according to patients risk stratification.
Caucasian male patient, 55 years of age, 1.78 m, 83 kg, submitted to supra-pubic radical prostatectomy for prostate cancer.
Previous history included hepatitis A, minor thalassemia and conventional cholecystectomy. Physical and lab exams were normal and ECG presented left anterior hemiblock. Physical status was defined as ASA II. Patient was premedicated with sublingual 15 mg midazolam with satisfactory response. Patient reached the operating room relaxed and cooperative. After venous puncture with 14G and 16G catheters, lactated Ringers was started. Initial monitoring consisted of cardioscope, non-invasive blood pressure and pulse oximetry. Baseline parameters were blood pressure = 130 x 85 mmHg, heart rate = 90 bpm, oxygen saturation = 98% and regular heart rhythm.
Epidural puncture in L2-L3 interspace was performed with the patient in the lateral position and a cephalad catheter was inserted after four attempts. Patient received 4 mg epidural morphine. Preoxygenation was performed with 100% oxygen for 3 minutes, after which anesthesia was induced with propofol (2 mg.kg-1), atracurium (0.5 mg.kg-1) and 1% lidocaine (1 mg.kg-1) followed by tracheal intubation with a 36G tube, metal guide and Sellicks maneuver. Pulmonary auscultation and capnography were normal. Anesthesia was maintained with 6-10 mg.kg-1 propofol continuous infusion, 0.3 mg.kg-1 bolus atracurium and 100% oxygen. Immediately after intubation patient received 0.5% epidural bupivacaine. A 20G teflon catheter was inserted in the left radial artery. Mean blood pressure throughout the procedure was maintained between 60 and 55 mmHg 5 and bolus ephedrine (10 mg) was administered whenever pressure got below those values.
Arterial blood gases, hemoglobin and hematocrit were controlled throughout the procedure and adjustments were made according to the results. There was a discrepancy between capnography and arterial blood gases analysis. At the end of the surgery, patient received one unit of autologous red blood cells concentrate.
After anesthetic recovery and NMB reversion, patient returned to spontaneous ventilation maintaining PETCO2 between 29 and 35 and SpO2 of 99%. Patient was extubated after receiving flumazenil. Patient was easily awakened and maintained a good saturation. When transferred to the stretcher, there was a sudden saturation decrease and severe hemodynamic instability associated to tachycardia of 155 bpm. Patient was immediately re-intubated and ventilated with 100% O2 while maintaining a saturation of 80%. Norepinephrine was infused in increasing doses up to 80 µg.min-1 to maintain stability and patient was transferred to the ICU.
Test results were as follows:
- After 3 hours of surgery:
pH 7.31 PaO2 412 PaCO2 47 HCO3 23.3 EB - 3.0 SatO2 99.8 % Ht % 35.8
Hb 13.3 g, Lactate 25.8 mg % (ref: 4.5 to 20.00)
- After 3 hours of surgery:
pH 7.30 PO2 384 PCO2 50 HCO3 24.3 EB - 2.0 SatO2 99,8 Ht 32.4%
Hg 12.3 g, Lactate 20.0 mg % (ref: 4.5 to 20.00)
- Blood Gases Analysis before intubation:
pH 7.50 PO2 19 PCO2 81 HCO3 22.3 EB - 8.2 SatO2 15.7
Lactate 65.9 mg% (ref: 4.5 to 20.00)
- Blood gases analysis at admission
to ICU with FiO2 100%:
pH 7.17 PO2 414 PCO2 52 HCO3 20.3 EB - 9.7
ECG revealed acute right branch block.
Transesophageal echocardiogram showed increased right cavities with signs of pressure overload and right ventricle systolic dysfunction, systemic venous congestion, interatrial septum shifted to the left, estimated pulmonary artery pressure of 68 mmHg with dilated pulmonary artery and branches.
Lower limbs duplex scan has not shown evidences of venous thrombosis in both limbs.
Computerized chest angiotomography has shown condensations in the bases to the right, bilateral pleural effusion, normal pulmonary artery and central branches, right interlobar branch filling failure and posterior basal segments to the right and to the left, characterizing pulmonary embolism.
Patient died in the 5th postoperative day.
Post mortem findings have shown that 73% of pulmonary embolisms are not clinically diagnosed 6. Pulmonary embolism diagnosis is not always easy and its first manifestation may be fatal. Patients may be totally asymptomatic or present mild symptoms such as dyspnea, tachypnea or central or pleuritic chest pain. In general patients present with hypoxemia and hypocapnia secondary to hyperventilation 6. They may also show nonspecific signs such as tachycardia and right ventricular overload at ECG or echocardiogram 1. Massive embolism may present with sudden cardiovascular collapse and pulseless electric activity. Surgery predisposes to pulmonary embolism up to one month after the intervention 6 and is one of the most significant risk factors together with prolonged immobilization and trauma.
The association between malignity and thrombotic phenomena has been described by Arnoud Trousseau. Any neoplasia, (especially in pancreas, lung, breast and genito-urinary tract) will increase deep venous thrombosis (DVT) risk as a consequence of pro-coagulating and platelet activating factors release by neoplastic cells 3.
Additional risk factors are burns, contraceptives, heart failure, nephrotic syndrome, mieloproliferative syndrome, auto-immune diseases, pregnancy, hyperhomocystein, post-menopausal hormone replacement, anti-phospholipid antibody, endogenous coagulation proteins deficiency (anti-thrombin III, proteins C and S) 4.
According to DVT and pulmonary trhombosis (PT) risk, patients may be classified as follows:
Patients below 40 years of age submitted to minor surgeries and without additional risk factors are at low risk for thrombotic diseases with a DVT incidence of 0.4% and 0.2% for PT.
Patients between 40 and 60 years of age have a 10-fold increase in PT risk even without additional risk factors when submitted to medium or major surgeries. The same is true for patients below 40 years of age submitted to major surgeries or patients with additional risk factors submitted to minor surgeries.
Patients above 60 years of age and patients between 40 and 60 years of age with additional risk factors and submitted to major surgeries. In these cases, the incidence of DVT is 4% to 8% and of PE of 2% to 4%.
VERY HIGH RISK
Patients with additional risk factors, such as malignancy, hypercoagulation and major orthopedic surgeries, spinal-medullary trauma and multiple trauma, with an incidence of DVT of 10% to 20% and of PT of 4% to 10%.
Pulmonary embolism may be diagnosed by computerized pulmonary angiography, pulmonary angioresonance or pulmonary arteriography, but sometimes there might be logistic transportation problems or immidiate unavailability of radiologists. In these cases, and as part of the investigation, a transesophageal echocardiogram and a Duplex Scan of lower limbs should be performed. Nuclear venography may be performed to detect pelvic clots 7.
This case report reminds us that pulmonary embolism is difficult to diagnose and treat, with high morbidity and costs and occasionally fatal evolution.
Identification and stratification of patients at risk for DVT are very important for an adequate prophylaxis which is often underutilized.
According to the 5th consensus of the American College of Chest Physicians on anti-thrombotic therapy, Clagget et al. 8 have emphasized the rational use of deep vein thrombosis prophylaxis with 40 mg sc/day subcutaneous enoxiparin, with a low associated bleeding risk 8.
Suggestions for thrombo prophylaxis with low molecular weight heparin are shown in table I.
To minimize the risk for epidural hematoma, catheter may be inserted 10 to 12 hours after the last dose or low molecular weight heparin should be administered 2 hours after catheter insertion. Blood in the needle or catheter does not prevent surgery, however, thrombo-prophylaxis should only be started 24 hours later 9,10. Traumatic epidural puncture may represent an increased risk for epidural hematoma 9,10. The catheter should be removed only 10 to 12 hours after the last dose and the subsequent dose should be administered 2 hours after catheter removal 9. This strategy, however, does not prevent epidural hematoma and one must be alert for early symptoms, such as muscle weakness and numbness 6.
A high suspicion level is not enough to establish a diagnosis because pulmonary embolism is a silent disease and its investigation routine is not highly sensitive. Early and adequate prophylaxis is the best strategy.
01. Knobel E, Baruzzi AC - Condutas no Paciente Grave. 2ª Ed, Rio de Janeiro, Atheneu, 1999; 197-210. [ Links ]
02. Nakano T, Goldhaber SZ - Pulmonary Embolism. Springer-Verlag, Tokyo, 1999;1-14. [ Links ]
03. Levitan N, Dowlati A, Remick SC et al - Rates of initial and recurrent thromboembolic disease among patients with malignancy versus those without malignancy. Medicine, 1999;78;285-291. [ Links ]
04. Goldhaber ZS - Pulmonary Embolism, em: Braunwald - Heart Disease a Textbook of Cardiovascular Medicine. 6th Ed, Philadelphia, W.B.Saunders Company, 2001;52:1886-1907. [ Links ]
05. Whalley GD, Berrigan JM - Anesthesia for radical prostatectomy, cystectomy, nephrectomy, pheochromocytoma, and, laparoscopic procedures Anesthesiology Clinics of North America, 2000;18;889-917. [ Links ]
06. De Wet CJ, Pearl RG - Perioperative use of anticoagulants and thrombolytics. Anesthesiology Clinics of North America 1999;17:895-917. [ Links ]
07. Krivec B, Voga G, Zuran I et al - Diagnosis and treatment of shock due to massive pulmonary embolism. Chest, 1997;112;1310-1316. [ Links ]
08. Clagett GP, Anderson FAJ, Geerts W et al - Prevention of venous thromboembolism. Chest, 1998;114:531S-560S. [ Links ]
09. Neuraxial Anesthesia and Anticoagulation, Consensus Statements. American Society of Regional Anesthesia Consensus Conference Chicago, Illinois, 1998;2-3. [ Links ]
10. Horlocker TT, Heit JA - Low molecular weight heparin: biochemisty, pharmacology, perioperative prophylaxis regimens and Guidelines for Regional Anesthetic Management. Anesth Analg, 1997;85:874-885. [ Links ]
Submitted for publication July 10, 2001
Accepted for publication October 16, 2001