Option 4 is not indicated.

The clinical case is a typical pulmonary thromboembolism. In this case it is associated with persistent arterial hypotension. Option 2 would be correct if the patient were not hypotensive. Option 3 is not correct since diagnostic confirmation is not necessary to initiate anticoagulant therapy in case of PTE without hypotension. Option 4 is not indicated. Option 5 would be correct only if the patient had a contraindication to fibrinolysis. Persistent hypotension in PTE is the most widely accepted indication for fibrinolysis, so the correct option is 1.

The clinical case is a typical pulmonary thromboembolism. In this case it is associated with persistent arterial hypotension. Option 2 would be [HIDDEN] if the patient were not hypotensive. Option 3 is [HIDDEN] since diagnostic confirmation is not necessary to initiate anticoagulant therapy in case of PTE without hypotension. Option 4 is [HIDDEN]. Option 5 would be [HIDDEN] only if the patient had a contraindication to fibrinolysis. Persistent hypotension in PTE is the most widely accepted indication for fibrinolysis, so [HIDDEN].

A 37-year-old man with no past history of interest comes to the emergency department for syncope while walking. He had started two days earlier with dyspnea on exertion. Examination: weight 75 kg, BP 75/50 mm Hg. SatO2 89%. Pulmonary auscultation was normal. Cardiac auscultation: rhythmic tachycardic tones at 130 bpm. Abdomen normal. Extremities: no alterations. Normal hemogram. Troponin 1.2 ng / ml. ECG: Sensual tachycardia at 130 bpm. Inverted T in V1-V4. Thoracic CT angiography: repletion defect in both main pulmonary arteries. One hour after arrival at the emergency room, BP 70/55 mm Hg persists. What would be the most appropriate initial treatment?

Unfractionated heparin, 10,000U iv on clinical suspicion. Fibrinolysis with tPA 100 mg iv once the diagnosis is confirmed.

Enoxaparin: 80 mg sc every 12 hours, starting upon diagnostic suspicion.

Enoxaparin; 80 mg sc every 12 hours, starting upon diagnostic confirmation.

ANESTHESIOLOGY, CRITICAL CARE AND EMERGENCIES

Case 294.

History A 50-year-old woman presented to the emergency department of our hospital with a 2-day history of lower limb pain associated with unusual asthenia and diffuse arthralgia over the past 3 weeks. She was a native of Guinea and had lived in France for most of her life, working as a personal care assistant. Her only medical history of note was an occurrence of fetal death at 12 weeks gestation when she was 35 years old. She had bilateral lower limb swelling, without changes in skin temperature or color. All proximal and distal arterial pulses were felt. General physical examination findings were otherwise unremarkable. Her laboratory tests showed a decreased hemoglobin concentration of 8.9 g/dL (normal range, 12-16 g/dL), a decreased platelet count of 45 × 10<sup9</sup/L (normal range, 150-400 × 10<sup9</sup/L), a C-reactive protein level of 158 mg/L (normal range, <5 mg/L) and a d-dimer level of 2000 mg/L (normal range, <500 mg/L). Compression US of the lower limbs revealed bilateral calf vein thrombosis involving the fibular and posterior tibial veins. Curative anticoagulation using low-molecular-weight heparin (enoxaparin, subcutaneous injection of 100 units per kilogram of body weight twice a day) was started. The day after the start of anticoagulation therapy, the patient reported dyspnea and acute chest and abdominal pain. Her vital signs were assessed, and she had elevated blood pressure and increased heart rate and respiratory rate, but she remained afebrile. Her cardiac auscultation was unremarkable, besides tachycardia. Skin examination revealed small areas of necrosis on the fingertips of her right hand. Laboratory studies were repeated and showed an increase in serum creatinine level from a baseline value of 0.49 mg/dL to a new value of 1.01 mg/dL (normal range, 0.6-1.1 mg/dL), an apparition of low-grade proteinuria of 0.43 g per day (normal range, <0.3 g/day), and a high serum troponin level of 1066 ng/L (normal range, <14 ng/L), whereas electrocardiography showed no ST segment modification and echocardiography revealed a moderately altered left ventricular ejection fraction (45%). There was no coronary occlusion seen at emergency coronarography. Contrast-enhanced CT of the chest, abdomen, and pelvis was performed (Figs 1, 2) together with cardiac MRI (Figs 3, 4).

[Pulmonary thromboembolism. A clinical case with unusual presentation].

The authors describe a rare case of pulmonary thromboembolism with unusual clinical findings and emphasized the large difficulty encountered in formuling a correct diagnosis in a reasonable time. A man, 60 years old, was admitted to a Medical Division of our hospital for the appearance of chest pain and epigastric pain during effort in the last year. He smoked 20 cigarettes a day and drank wine (1 or 2 litres a day). He was affected by hypercholesterolemia and in the past reported relapsed thrombophlebitis in the left leg. Four years before admission to our hospital he underwent large and small left saphenectomy. He had no cardiac events in the past. After a non significant exercise stress test the patient was treated with nitrates and asa and was discharged from the hospital. At home the symptoms increased and after 8 months the patient was admitted again to the Cardiologic Division of the hospital. At admission he reported dyspnea and chest pain at rest, not only during effort and the ECG showed negative T waves in anterior and inferior leads. Intravenous heparine, nitrates and calcium antagonists stabilized the clinical picture. The following examinations revealed: reduction of the T wave negativity at the ECG registered during chest pain; mild enlargement of the heart at the chest roentgenogram; normal value of the left ventricle and apical and midseptal by ipokinesia at the transthoracic echocardiogram; normal coronary artery at the coronary arteriography. "Vasospastic angina" was diagnosed and the patient was discharged after 20 days, asymptomatic. After 15 days he returned to the hospital again for chest pain, dyspnea, hypotension and syncope despite therapy. At physical examination he showed a painful left tibio-tarsal tumefaction, an increased and splitting second heart sound in the pulmonary area and a systolic murmur in the third and fourth left interspace. The ECG showed a severe anterior ischemia, while a new transthoracic echocardiogram revealed a considerable dilatation of the right atrium, right ventricle and the main pulmonary artery with severe tricuspid regurgitation and pulmonary hypertension (mean PAP about 50 mmHg). The following pulmonary perfusion scintigraphy confirmed the diagnosis of pulmonary embolism and the selective right and left pulmonary arteriography exhibited multiple thrombi and large intravascular filling defects. The right heart catheterization confirmed a chronic precapillary pulmonary hypertension (mean PAP = 55 mmHg). About 24 hours after these examinations the patient died because of a cardiac arrest with electromechanical dissociation. Pulmonary thromboembolism is a potentially fatal disease characterized by a largely variable clinical presentation. Frequently pulmonary embolism diagnosis is difficult especially when clinical findings are unusual. In the case observed the "typical" chest and epigastric pains associated with the electrocardiographic findings directed diagnosis towards myocardial ischemia. Also after the coronary arteriography that showed normal coronary artery, the erroneous diagnosis persisted. Pulmonary embolism was correctly diagnosed too late to begin an effective therapy. These unusual clinical findings and diagnostic mistakes are stressed and critically reviewed in the article.

High-risk pulmonary embolism assessed by transthoracic echocardiography: A case report.

Acute pulmonary embolism (APE) as a life-threatening illness may present with a wide range of manifestations. APE was diagnosed using computed tomographic pulmonary angiography (CTPA); however, transthoracic echocardiography (TTE) can reveal hemodynamic status. Early thrombolysis is the most effective therapy for the treatment of massive pulmonary embolism. Herein, we report a case of high-risk APE with a wide range of manifestations, including chest pain, dyspnea, low-blood pressure, and syncope. A 55-year-old, previously healthy woman, complained of dyspnea and pleuritic chest pain for 40 days, along with transitory (10 minutes) episodes of syncope that had occurred 2 days previously. Because of the high-risk APE, the patient received intravenous thrombolytic therapy with low-dose recombinant tissue plasminogen activator (rt-PA, 50 mg over 30 minutes) and an anticoagulant (subcutaneous low-molecular-weight heparin, once every 12 hours for 5 days). Five days after thrombolysis, bedside TTE revealed RV diastolic dimension decreased to 22 mm. Color ultrasonography revealed a significant decrease in systolic and mean pulmonary artery pressure. TTE may provide initial suspicion of APE and may help identify patients with unstable hemodynamic status before the onset of shock. Moreover, concomitant TTE signs of decreased RV load may predict better prognosis for high-risk APE patients.

Anatomy_Gray

A 53-year-old man presented to the emergency department with a 5-hour history of sharp pleuritic chest pain and shortness of breath. The day before he was on a long haul flight, returning from his holidays. He was usually fit and well and was a keen mountain climber. He had no previous significant medical history. On physical examination his lungs were clear, he was tachypneic at 24/min, and his saturation was reduced to 92% on room air. Pulmonary embolism was suspected and the patient was referred for a CT pulmonary angiogram. The study demonstrated clots within the right and left main pulmonary arteries. There was no pleural effusion, lung collapse, or consolidation. He was immediately started on subcutaneous enoxaparin and converted to oral anticoagulation over the course of a couple of days. The whole treatment lasted 6 months as no other risk factors (except immobilization during a long haul flight) were identified. There were no permanent sequelae.

Acute venous thromboembolism.

To review the recent advances in management of acute venous thromboembolism. Articles and published reviews on venous thromboembolism, pulmonary embolism and deep vein thrombosis. Acute venous thromboembolism describes a group of disorders that include venous thrombosis (usually deep vein thrombosis) and pulmonary thromboembolism. Ultrasound supplemented by Doppler flow detection imaging has become the investigation of choice in the diagnosis of deep vein thrombosis and spiral volumetric computed tomography or ventilation perfusion scan (if the patient is haemodynamically stable) or bedside echocardiography (if the patient is hypotensive) are often the initial investigations in a patient who has a suspected pulmonary thromboembolism. Magnetic resonance venography has only recently been evaluated and may prove in future to be a valuable diagnostic test for both deep vein thrombosis and pulmonary thromboembolism. Treatment requires immediate anticoagulation using either subcutaneous low molecular weight heparin (e.g. enoxaparin 1 mg/kg 12-hourly or dalteparin 100 IU anti Xa/kg twice daily) or intravenous unfractionated heparin (80 U/kg as a bolus then 18 U/kg/hr and adjusted to keep the APTT 1.5-2x the control value). Oral anticoagulation using warfarin is started simultaneously with heparin. Fibrinolytic therapy is considered in all patients with pulmonary thromboembolism in whom there are no contraindications, as the improvement in right ventricular function is greater and the pulmonary artery perfusion defect is less compared with patients treated by anticoagulation alone. Fibrinolytic therapy is usually only considered in patients with deep vein thrombosis if severe limb oedema is present. While streptokinase, urokinase and alteplase have been recommended, alteplase (100 mg over two hours with heparinisation) may be the treatment of choice as alteplase has a shorter half life, has a more rapid effect and may be more effective in lysing older clots, when compared with streptokinase or urokinase. Reteplase (10 U over 2 minutes followed by 10 U 30 minutes later) may be as effective as alteplase. Acute venous thromboembolism is a disorder that carries a high morbidity and mortality. Anticoagulation with or without fibrinolysis is the treatment of choice.

EkoSonic™ Endovascular System-Directed Thrombolysis in a Patient With COVID-19 Infection Presenting With Bilateral Large Pulmonary Embolism Causing Right Ventricular Strain: A Case Report.

We discuss a case of a 31-year-old male patient who presented to the accident and emergency department with shortness of breath and chest pain since the morning of the day of presentation. His polymerase chain reaction (PCR) test had returned positive for severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2), which causes coronavirus disease 2019 (COVID-19), two weeks ago and his main symptoms had been shortness of breath, dry cough, generalized body pain, and fever. He was not vaccinated against the COVID-19 virus. He had not required hospitalization for COVID-19 and his symptoms had improved on day 10 from the date of diagnosis; however, he developed pleuritic chest pain with shortness of breath on the day of presentation. He was found to have tachypnoea, hypoxia, and tachycardia on assessment. His electrocardiogram showed a right bundle branch block with sinus tachycardia. He underwent a CT pulmonary angiography (CTPA) that showed bilateral large pulmonary emboli extending from the main pulmonary arteries bilaterally extending to the sub-segmental level. There was evidence of right heart strain on the scan. He also had a bedside echocardiogram performed after the CT scan, which showed an enlarged right ventricle but no left ventricular thrombus. His blood results showed D-dimer levels of 14,000 ng/mL and troponin T of 255 ng/L. He received treatment with low molecular weight heparin (LMWH) and underwent emergency EkoSonic™ Endovascular System (EKOS) thrombolysis (Boston Scientific, Marlborough, MA). He remained on ultrasound-accelerated thrombolysis (USAT) for the next 12 hours and showed significant improvement and was taken off oxygen post-EKOS thrombolysis. He was discharged home on oral rivaroxaban after 48 hours of hospital stay; follow-up after two months showed normal-sized right ventricle with no evidence of pulmonary hypertension.

Impending paradoxical embolism presenting as a pulmonary embolism, transient ischemic attack, and myocardial infarction.

A 25-year-old man presented with complaints of nonpleuritic, substernal chest pain, dyspnea, and decreasing exercise tolerance. His vital signs were normal, with the exception of an oxygen saturation level of 93% while breathing room air. During his assessment, he developed transient left facial droop, left arm and leg weakness, and an ataxic gait, which lasted 15 min then resolved spontaneously. Cardiac enzyme levels were elevated, and an ECG revealed T-wave inversion in leads III, aVF, V1, and V2 with evolving ST-segment elevation in leads V3 through V5. The findings of a CT scan and MRI of the head were negative; a Doppler ultrasound of the right lower extremity revealed a thrombus extending from the common femoral vein to the popliteal vein. Cardiac catheterization revealed no evidence of epicardial coronary artery disease. CT pulmonary angiography revealed bilateral pulmonary emboli. Transesophageal echocardiography (TEE) showed a 4-cm, dumbbell-shaped mass lodged in a patent foramen ovale, confirming the diagnosis of an impending paradoxical embolism. The patient was started on therapy with unfractionated heparin, and his thrombus resolved spontaneously by hospital day 5. An impending paradoxical embolism is rare but should be suspected in anyone presenting with evidence of both venous and arterial emboli. The therapeutic options include anticoagulation, thrombolysis, and surgical embolectomy. We would propose that initial treatment with anticoagulation therapy and following with serial TEEs may be appropriate therapy in an otherwise stable patient, with surgical embolectomy or thrombolysis reserved for the treatment of thrombi that do not resolve with anticoagulation therapy or for patients with clinical deterioration.

Anteroseptal Myocardial Infarction -- Treatment / Management

Enoxaparin is given as an initial intravenous dose of 30 mg in all patients followed by 1 mg/kg subcutaneously every 12 hours dosing (can be used as 1 mg/kg SC once daily dose if creatinine clearance is less than 30 mL/min). It is given for the duration of hospitalization or until PCI is completed. Unfractionated heparin is dosed at an initial loading dose of 60 IU/kg (maximum 4000 IU) followed by infusion of 12 IU/kg per hour (maximum 1000 IU/h) with close monitoring of the activated partial thromboplastin time, continued for 48 hours or until PCI is performed. Fondaparinux administration is a 2.5 mg SQ daily dose that is usually maintained for the duration of hospitalization or until PCI. Fondaparinux should always be used in addition to another anticoagulant such as intravenous heparin or bivalirudin to reduce the risk of catheter thrombosis. Bivalirudin is administered as 0.10 mg/kg initial loading dose, followed by 0.25 mg/kg per hour (only to be used in patients managed with an early invasive strategy) and is continued until diagnostic angiography or PCI. The anticoagulant effect of bivalirudin is monitored by measuring the activated clotting time.

[The cardiologist facing pulmonary embolism. The experience of 160 cases of acute cor pulmonale].

The results of recent multicenter studies dealing with pulmonary embolism often reveal remarkable discrepancies in terms of diagnosis, prognosis and treatment, partly due to the heterogeneity of study patients and of evaluation criteria. Our prospective study focused exclusively on patients affected by pulmonary embolism with a hemodynamic pattern of acute cor pulmonale, investigated at a single center. Particular attention was paid to in-hospital mortality, embolic recurrences, major bleeding and underlying pathologies. This study includes 160 cases (103 women with a median age of 71 years and 57 men with a median age of 65 years) in whom the clinical and echocardiographic findings suggestive of acute pulmonary embolism were confirmed by lung perfusion scan, pulmonary angiography, techniques for the detection of deep vein thrombosis and/or autopsy. The most common clinical manifestations were: dyspnea (92% of cases), tachycardia (80%), syncope (44%), cardiac arrest (22%), and shock (20%). Thoracic pain was present in only 27% of patients. None of the patients showed a normal ECG; a right bundle branch block was found in 47% of cases. T-wave inversion in the precordial leads (32%) was not related to the severity and outcome of pulmonary embolism. Present or previous deep vein thrombosis was found in 53 and 26% of cases, respectively. Only in 2 patients pulmonary embolism was secondary to a deep vein thrombosis of the upper limbs. Intravenous heparin alone was used in 36% of cases, whereas 56% were treated with thrombolytic agents + heparin. Major bleeding occurred in 9% of patients treated with heparin alone, and in 16% of those who received heparin + thrombolytic drugs. Death occurred in 17% of the former, and in 27% of the latter patients. The in-hospital mortality rate was related not only to the presence of cardiac arrest and--to a lower degree--of shock, but also to the recurrence of pulmonary embolism and to the underlying heart disease. No relationship was found between mortality and age, intracardiac thrombi or malignancy. Prognosis was quite different depending on clinical presentation, with a death rate ranging from 11% in the absence of systemic hypertension, and 77% in the presence of cardiac arrest. Even the "massive" pulmonary embolism that is observed in a cardiac department represents a true "spectrum" of pathological conditions, a spectrum that should be taken into account not only in order to evaluate prognosis and treatment in a particular case, but also when meta-analyses are performed.

Case 294: Catastrophic Antiphospholipid Syndrome.

History A 50-year-old woman presented to the emergency department of our hospital with a 2-day history of lower limb pain associated with unusual asthenia and diffuse arthralgia over the past 3 weeks. She was a native of Guinea and had lived in France for most of her life, working as a personal care assistant. Her only medical history of note was an occurrence of fetal death at 12 weeks gestation when she was 35 years old. She had bilateral lower limb swelling, without changes in skin temperature or color. All proximal and distal arterial pulses were felt. General physical examination findings were otherwise unremarkable. Her laboratory tests showed a decreased hemoglobin concentration of 8.9 g/dL (normal range, 12-16 g/dL), a decreased platelet count of 45 × 10<sup9</sup/L (normal range, [150-400] × 10<sup9</sup/L), a C-reactive protein level of 158 mg/L (normal range, <5 mg/L), and a d-dimer level of 2000 mg/L (normal range, <500 mg/L]). Compression US of the lower limbs revealed bilateral calf vein thrombosis involving the fibular and posterior tibial veins. Curative anticoagulation using low-molecular-weight heparin (enoxaparin, subcutaneous injection of 100 units per kilogram of body weight twice a day) was started. The day after the start of anticoagulation therapy, the patient reported dyspnea and acute chest and abdominal pain. Her vital signs were assessed, and she had elevated blood pressure and increased heart rate and respiratory rate, but she remained afebrile. Her cardiac auscultation was unremarkable, besides tachycardia. Skin examination revealed small areas of necrosis on the fingertips of her right hand. Laboratory studies were repeated and showed an increase in serum creatinine level from a baseline value of 0.49 mg/dL to a new value of 1.01 mg/dL (normal range, 0.6-1.1 mg/dL), an apparition of low-grade proteinuria of 0.43 g per day (normal range, <0.3 g/ day), and a high serum troponin level of 1066 ng/L (normal range, <14 ng/L), whereas electrocardiography showed no ST segment modification and echocardiography revealed a moderately altered left ventricular ejection fraction (45%). There was no coronary occlusion seen at emergency coronarography. Contrast-enhanced CT of the chest, abdomen, and pelvis was performed (Figs 1, 2) together with cardiac MRI (Figs 3, 4).

Case 290.

History A 26-year-old man presented with a 1-month history of chest pain, a palpable and painful right inguinal mass, and edema in the right lower extremity. One month earlier, he started to experience left chest pain with no cough. Pulmonary CT angiography (CTA) revealed a left lower lobe segmental pulmonary embolus. The local hospital made a diagnosis of pulmonary embolism (PE). He received anticoagulants, and his chest pain was gradually relieved. At the time of current presentation, the patient was experiencing right lower extremity swelling and pain. Physical examination revealed a 4 × 3 cm palpable right inguinal mass with no redness. His medical history and family history were negative. The results of laboratory work-up were normal, with a D-dimer level of 0.16 mg/L fibrinogen equivalent units (reference range, <0.46 mg/L) and an international normalized ratio of 2.45 (therapeutic range, 2.0-3.0 for a patient taking warfarin), except the prothrombin time was 28.2 seconds (reference range, 9.6-12.8 seconds) and the activated partial thromboplastin time was 52.2 seconds (reference range, 24.8-33.8 seconds). Echocardiography, chest radiography, chest CT, and contrast-enhanced CT revealed no abnormalities. The patient underwent right lower extremity vascular conventional US (Philips IU22; Philips) with an L9-3 probe (3-9 MHz, venous condition) and contrast-enhanced US (1.5-2.0 mL, SonoVue; Bracco) with an intravenous bolus injection at the initial evaluation. Two days later, noncontrast and contrast-enhanced CT images of the lower abdomen (1.5 mL per kilogram of body weight, 300 mg/mL iomeprol, Iomeron; Bracco) were acquired for further evaluation (Figs 1-3).

[Extracorporeal membrane oxygenation treatment of a neonate with severe low cardiac output syndrome following open heart surgery].

To summarize the experience of extracorporeal membrane oxygenation (ECMO) to rescue a neonate with severe low cardiac output syndrome following open heart surgery. The patient was a male, 2 d, 2.8 kg, G3P2 full-term neonate with gestational age 40 weeks, born by Cesarean-section with Apgar score of 10 at 1 min. He was admitted due to severe dyspnea with oxygen desaturation and heart murmur on the second day after birth. Physical examination showed clear consciousness, cyanosis, dyspnea, RR 70 bpm and a grade II/6 heart murmur. Bp was 56/45 mm Hg (1 mm Hg = 0.133 kPa) and SpO2 around 65%. Blood WBC 13.1 x 10(9)/L, N 46.1%, Hb 238 g/L, Plt 283 x 10(9)/L, CRP < 1 mg/L. Echocardiographic findings: TGA + ASD + PDA with left ventricular ejection fraction (LVEF) of 60%. After supportive care and prostaglandin E1 (5 ng/kg/min) treatment, his condition became stable with SpO2 85 - 90%. On the 6(th) day of life, the baby underwent an arterial switch procedure + ASD closing and PDA ligation. The time of aorta clamp was 72 mins. The cool 4:1 blood cardioplegia was given for 2 times during aortal clamp. Ultrafiltration was used. The internal and external volumes were almost equal and the electrolytes and blood gas and hematocrit (36%) were normal during extracorporeal bypass. Due to a failure (severe low cardiac output) to wean from cardiopulmonary bypass (263 min) with acidosis (lactate 8.8 mmol/L), low blood pressure (< 39/30 mm Hg), increased LAP (> 20 mmHg), bloody phlegm, decreased urine output [< 1 ml/(kg.h)], a V-A ECMO was used for cardio-pulmonary support. ECMO setup: Medtronic pediatric ECMO package (CB2503R1), carmeda membrane oxygenator and centrifugal pump (bio-console 560) were chosen. Direct cannulation of the ascending aorta (Edward FEM008A) and right atrium (TF018090) was performed using techniques that were standard for cardiopulmanory bypass. The ECMO system was primed with 400 ml blood, 5% CaCl(2)1g, 5% sodium bicarbonate 1.5 g, 20% mannitol 2 g, albumin 10 g, and heparin 5 mg. The blood was re-circulated until the temperature was 37 degrees C and blood gases and the electrolytes were in normal range. The patient was weaned from bypass and connected to V-A ECMO. Management of ECMO: the blood flow was set at 150 - 200 ml/kg/min. Venous saturation (SvO2) was maintained at the desired level (75%) by increasing and decreasing extracorporeal blood flow. Systemic blood pressure was maintained at 76/55 - 80/59 mm Hg by adjusting blood volume. Hemoglobin was maintained between 120 - 130 g/L. Platelet count was maintained at > 75,000/mm3 and ACT was maintained at 120 - 190 s. The mechanical ventilation was reduced to lung rest settings (FiO2 35%, RR 10 bpm, PIP 16 cm H(2)O, PEEP 5 cm H2O) to prevent alveolar collapse. Inotropic drug dosages were kept at a low level. The patient was successfully weaned from ECMO following 87 hours treatment. LVEF on day 1, 2 and 3 following ECMO were 20%, 34% and 43% respectively. The circulation was stable after weaning from ECMO with Bp 75/55 mm Hg, HR 160 bpm and LAP 11 mm Hg under inotropic drug suppor with epinephrine [(0.2 microg/(kg.min)], dopamine [(8 microg/(kg.min)], milrinone [(0.56 microg/(kg.min)]. The blood gases after 1 h off-ECMO showed: pH 7.39, PaO2 104 mm Hg, PaCO2 45 mm Hg, lactate 3.8 mmol/L, Hct 35%, K(+) 3.8 mmol/L, Ca(++) 1.31 mmol/L. The serum lactate was normal after 24 h off-ECMO. On day 22 off-ECMO, the baby was successfully extubated and weaned from conventional ventilator. On day 58, the patient was discharged. Serial ultrasound imaging studies revealed no cerebral infarction or intracranial hemorrhage during and after ECMO. At the time of hospital discharge, the patient demonstrated clear consciousness with good activity, normal function of heart, lung, liver and kidney. However, more subtle morbidities, such as behavior problems, learning disabilities should be observed ria long term follow-up. The main ECMO complications were pulmonary hemorrhage, bleeding on the sternal wound, tamponade, hemolysis and hyperbilirubinemia. ECMO is an effective option of cardio-pulmonary support for neonate with low cardiac output syndrome following open heart surgery.

Pulmonary embolism hotline 2012. Recent and expected trials.

Management of acute pulmonary embolism (PE) has advanced considerably in the past year, and progress is expected to continue in 2013. To help determine the optimal management strategy for normotensive patients with intermediate-risk PE, the Pulmonary Embolism Thrombolysis (PEITHO) study completed enrolment of 1006 patients with evidence of right ventricular dysfunction (by echocardiography or computed tomography) plus a positive troponin test. Patients have been randomised to thrombolytic treatment with tenecteplase versus placebo, and the effects on clinical end points (death or haemodynamic collapse) assessed at 7 and 30 days. The results are expected in spring 2013; long-term follow-up is also being performed. The results of a randomised trial on ultrasound-enhanced low-dose catheter-delivered thrombolysis will also become available soon. While optimisation of treatment with vitamin K antagonists incorporating pharmacogenetic testing is still being pursued, new oral anticoagulants are entering the field of PE treatment and secondary prophylaxis. Following the successful use of rivaroxaban as single oral drug therapy in the EINSTEIN-PE trial, the approval of this drug has recently been extended to cover, apart from deep vein thrombosis, PE as well. The apixaban (AMPLIFY) and edoxaban (HOKUSAI) trials have finished recruitment of PE patients, and their results will become available shortly. In the meantime, the AMPLIFY-EXT trial showed that both the therapeutic (5 mg twice daily) and the prophylactic dose (2.5 mg twice daily) of apixaban are effective and safe for long-term secondary prophylaxis after PE. For the extended prophylaxis (after the reommended initial anticoagulation period) of the (few) patients who are unable to tolerate any form of anticoagulation, low-dose asprin may be a safe albeit moderately efficacious option, as indicated by two recent investigator-initiated trials with a total of 1224 patients.

An 88-year-old man with syncope and an alternating axis.

An 88-year-old man, admitted to the emergency room (ER) after three episodes of syncope within 1 day, reported a precursory of syndrome of light-headedness with rapid palpitations that led to an abrupt loss of consciousness. After undergoing percutaneous and surgical revascularisation, he started complaining of chest and back discomfort for the past 20 years and searching for help from Chinese medicine, Fuzi. He had history of chronic renal failure and heart failure, but denied neither taking digitalis nor having family history related to sudden death.On arrival, heart rate was 150 bpm and blood pressure (BP) by cuff was 91/81 mm Hg (non-invasive BP could not be accurately obtained during tachycardia) plus oedema on both lower extremities. There were diffuse crackles and indistinct heart sounds on auscultation.The admission ECG was performed in the ER (figure 1). His serum creatinine was 139.7 mmol/L, serum K(+) was 4.7 mmol/L, N-terminal of the prohormone brain natriuretic peptide was highly elevated (12 000 pg/mL) and troponin I was negative. What is the most likely diagnosis suggested based on the patient's ECG and history? Aconite poisoningDigitalis toxicityCatecholaminergic polymorphic ventricular tachycardia (CPVT)Andersen-Tawil syndrome (ATS).

[Acute pulmonary embolism emergency. Confirming diagnosis, administering heparin, begin thrombolysis].

In suspected acute pulmonary embolism, the measurement of the d-dimer is now an established screening method. Further diagnostic measures include the electrocardiogram, echocardiography and conventional chest radiography, as well as the analysis of blood gases. The specific demonstration of a pulmonary embolism is achieved with a helical CT of the thorax, pulmonary angiography and ventilation/perfusion scanning. Apart from continuous (infusion) of unfractionated heparin, the low molecular weight heparins also are of potential value in the treatment of pulmonary embolism. A larger percentage of patients benefit from the use of fibrinolytic agents than was previously thought, so that the indication for fibrinolytic therapy should not be made dependent on the presence of hemodynamic instability.

Low-molecular-weight heparin in thrombotic disease in children and adolescents.

The use of unfractionated heparin (UFH) in children is problematic. In adults, subcutaneous low-molecular-weight heparin (LMWH) is as effective as UFH in the treatment of thrombosis. Because pediatric data are limited, the authors studied the use of enoxaparin in children. Nineteen children (ages 18 days to 19 years; median age, 40 months) with indications for thrombosis treatment or prophylaxis were studied. Six patients (median age, 33 months), treated on a protocol that included pharmacokinetic studies, initially received enoxaparin 1 mg/kg subcutaneously every 12 hours; doses then were adjusted until target plasma levels of 0.5 to 1.2 anti-Xa U/mL were achieved. The records of 13 additional patients treated with enoxaparin off study were reviewed. In the first six patients, enoxaparin pharmacokinetics was found to be similar to that in adults; once targeted levels were achieved, these remained stable. Among all 19 subjects, 14 had treatment of active thrombosis and 5 underwent thrombosis prophylaxis. For treatment of thrombosis, enoxaparin 1 mg/kg initially was administered subcutaneously every 12 hours. Target anti-Xa levels were achieved with 0.55 to 1.5 mg/kg every 12 hours (mean, 0.98 mg/kg; median, 1.0 mg/kg) in 1 to 7 days (median, 1 day). All patients in the treatment group had clinical improvement within 2 to 5 days, and 12 had follow-up radiological studies that confirmed this. For prophylaxis, enoxaparin was given at 1 mg/kg subcutaneously every 24 hours. No new thrombi were clinically evident in this group. There was no major bleeding with enoxaparin; one patient had transient mild mucosal oozing. In this limited population, enoxaparin seems to be a safe, effective, and convenient alternative to UFH in children and adolescents. The adult therapeutic target range of 0.5 to 1.2 anti-Xa U/mL is readily achievable with a starting dose of 1 mg/kg every 12 hours in most children. Initial close monitoring with plasma anti-Xa activity should be done and doses adjusted to achieve target range, particularly in neonates. In the population of this study, enoxaparin seems as effective as UFH in the period immediately thrombotic episode. These results should be confirmed in the ongoing randomized trial comparing LMWH with UFH in children.

Acute Pulmonary Embolism: A Review.

Pulmonary embolism (PE) is characterized by occlusion of blood flow in a pulmonary artery, typically due to a thrombus that travels from a vein in a lower limb. The incidence of PE is approximately 60 to 120 per 100 000 people per year. Approximately 60 000 to 100 000 patients die from PE each year in the US. PE should be considered in patients presenting with acute chest pain, shortness of breath, or syncope. The diagnosis is determined by chest imaging. In patients with a systolic blood pressure of at least 90 mm Hg, the following 3 steps can be used to evaluate a patient with possible PE: assessment of the clinical probability of PE, D-dimer testing if indicated, and chest imaging if indicated. The clinical probability of PE can be assessed using a structured score or using clinical gestalt. In patients with a probability of PE that is less than 15%, the presence of 8 clinical characteristics (age <50 years, heart rate <100/min, an oxygen saturation level of > 94%, no recent surgery or trauma, no prior venous thromboembolism event, no hemoptysis, no unilateral leg swelling, and no estrogen use) identifies patients at very low risk of PE in whom no further testing is needed. In patients with low or intermediate clinical probability, a D-dimer level of less than 500 ng/mL is associated with a posttest probability of PE less than 1.85%. In these patients, PE can be excluded without chest imaging. A further refinement of D-dimer threshold is possible in patients aged 50 years and older, and in patients with a low likelihood of PE. Patients with a high probability of PE (ie, >40% probability) should undergo chest imaging, and D-dimer testing is not necessary. In patients with PE and a systolic blood pressure of 90 mm Hg or higher, compared with heparin combined with a vitamin K antagonist such as warfarin followed by warfarin alone, direct oral anticoagulants such as apixaban, edoxaban, rivaroxaban, or dabigatran, are noninferior for treating PE and have a 0.6% lower rate of bleeding. In patients with PE and systolic blood pressure lower than 90 mm Hg, systemic thrombolysis is recommended and is associated with an 1.6% absolute reduction of mortality (from 3.9% to 2.3%). In the US, PE affects approximately 370 000 patients per year and may cause approximately 60 000 to 100 000 deaths per year. First-line therapy consists of direct oral anticoagulants such as apixaban, edoxaban, rivaroxaban, or dabigatran, with thrombolysis reserved for patients with systolic blood pressure lower than 90 mm Hg.

Contrast-induced nephropathy

Roxana Mehran score The Roxana Mehran score is a clinical prediction rule to estimate probability of nephropathy (increase ≥25% and/or ≥0.5 mg/dl in serum creatinine at 48 h): Risk Factors: Systolic blood pressure <80 mm Hg - 5 points (if systolic BP less than 80 mmHg for at least one hour requiring inotropic support) Intra-arterial balloon pump - 5 points Congestive heart failure, counting as NYHA class III (marked limitation in activity due to symptoms, even during less-than-ordinary activity) or worse, or history of pulmonary edema - 5 points Age >75 y - 4 points Hematocrit level <39% for men and <35% for women - 3 points Diabetes mellitus- 3 points Contrast media volume - 1 point for each 100 mL Decreased kidney function: Serum creatinine level >1.5 g/dL - 4 points or Estimated Glomerular filtration rate (online calculator) 2 for 40–60 mL/min/1.73 m2 4 for 20–40 mL/min/1.73 m2 6 for < 20 mL/min/1.73 m2

[Pulmonary embolism].

Acute pulmonary embolism is an important differential diagnosis of acute chest pain. The clinical signs are often non-specific. However, diagnosis and therapy must be done quickly in order to reduce morbidity and mortality. The new (2014) European guidelines for acute pulmonary embolism (PE) focus on risk-adapted diagnostic algorithms and prognosis adapted therapy concepts. According to the hemodynamic presentation the division in a high-risk group (unstable patient with persistent hypotension or shock) or in non-high-risk groups (hemodynamically stable) was proposed. In the high-risk group the immediate diagnosis is usually done by multidetector spiral computed tomography (MDCT) and primarily the medical therapy of right ventricular dysfunction and thrombolysis is recommended.In the non-high-risk group, this is subdivided into an intermediate-risk group and low-risk group, the diagnosis algorithm based on the PE-pretest probability--determined by validated scores. Moreover, the diagnosis is usually secured by MDCT--the new gold standard in the PE-diagnosis, scores, or it can be primarily ruled out due to the high negative predictive value of D-dimer determination. To improve the prognostic risk stratification in non-high-risk group patients the additional detection of right ventricular dysfunction (MDCT, echocardiography), cardiac biomarkers (troponin, NT proBNP) and validated scores (e.g. Pulmonary Embolism Severity Index) is recommended. Therefore, the intermediate-risk group can be further subdivided. For treatment of non-high-risk group patients, the initial anticoagulation (except those with severe renal insufficiency) using low molecular weight heparin/fondaparinux and conversion to vitamin-K antagonists or alternatively with direct oral anticoagulants (DOAK) is recommended. Hemodynamically stable patients with right ventricular dysfunction and myocardial ischemia (Intermediate-high-risk group patients) but with clinically progressive hemodynamic decompensation may benefit from systemic thrombolysis as well. Due to the high risk of bleeding in the PEITHO study, however, a critical individual risk-benefit evaluation should be done. A dose reduced systemic or local ultrasound-assisted thrombolysis could gain importance in the future. For very selected patients in the low-risk group early outpatient treatment could be considered.The diagnosis and treatment of pulmonary embolism remains complex. Improved algorithms support the diagnosis procedures and therapy decisions. Direct oral anticoagulants are a new first-line therapy alternative for hemodynamically stable non-high-risk patients.

Enoxaparin -- Administration

Treatment of Acute Deep Vein Thrombosis with or without Pulmonary Embolism: The recommended dose of enoxaparin is 1 mg/kg SC every 12 hours or 1.5 mg/kg SC daily. Anticoagulation should be started immediately in the case of suspected or proven pulmonary embolism. Patients with pulmonary embolism usually require inpatient therapy, according to the PERT Consortium. [14] [15]

Infectious disease capsules: a pox on your house.

A 31-year-old, previously healthy white man presented to the emergency department with complaints of malaise, fevers, shortness of breath, a non-productive cough, and a "rash." His physical exam revealed a temperature of 100.2F, a pulse of 129 bpm, respiratory rate of 14 BPM, and blood pressure of 140/74 mm Hg. He was alert, oriented, and in no distress. His oropharynx was dry, his neck was supple, and cervical lymphadenopathy was absent. He had tachycardia, bilateral wheezes, and rhonchi with prolonged expirations. There was a diffuse vesicular eruption enveloping his entire body with involvement sparing his palms and soles (Figures 1 and 2). Laboratory values showed a hemoglobin of 16.0 g/dL and a white blood cell count of 7100 cells/pL, with 39%neutrophils, 23% bands, and 35% lymphocytes. His platelet count was mildly decreased to 86,000 x 103/pL. Chest radiograph revealed bilateral diffuse interstitial infiltrates. A diagnosis of acute varicella-zoster virus pneumonia (varicella pneumonia) was made, and the patient was started on IV acyclovir (10 mg/kg every 8 hours). Upon further questioning, the patient stated that his daughter had been diagnosed with "chickenpox" 7 days ago. The patient had numerous exposures to chickenpox in the past but had never developed clinical expressions of varicella. He was not at risk for HIV infection, not having multiple sexual partners, IV drug abuse, or blood transfusions. During the 1 day of in-hospitalization, his fever abated and the pulmonary signs diminished. Following discharge, IV acyclovir was replaced by valacyclovir to complete a 7-day course of therapy.

[Role of thrombolysis in massive pulmonary embolism].

Massive pulmonary embolism is a life threatening pathology with a high mortality over 20%. Thrombolysis is one of therapy ways that leads to a lower rate of death. The aim of the study is to show interest, limits and complications of thrombolytic therapy in massive pulmonary embolism. This descriptive study presents 8 cases of pulmonary embolism admitted to the Cardiology Division of Grand-Yoff from March 2003 to March 2006. All cases confirmed by Tomodensitometry (TDM) with massive pulmonary embolism were included in this study. We used thrombolytic only in 8 cases of massive pulmonary embolism about 32. In-hospital prevalence was 25%. The average age was 49.8 ± 19.1 (from 15 to 72) and sex-ratio 0.33. Seven patients had a moderate clinical probability Well's score and one of them 1 had a high clinical probability. The clinical signs were: cardio-vascular collapse (7 cases), syncope (1) and cardio-vascular arrest. The electrocardiogram showed a sub-epicardial ischemia (4 cases), a right bundle branch block and a Mac Ginn White's sign. Two patients had a right-basal opacification at the chest X ray. The echocardiography found 5 cases of right ventricular dilatation, 1 case of paradoxal septum, 1 case of multiple thrombi in the right ventricule. The TDM confirmed diagnosis with 3 cases of bilateral pulmonary embolism, 1 case of pulmonary aneurysm. The treatment used thrombolytic : 1,500,000 IU of streptokinase, sympathomimetic drugs, anticoagulation with heparins and vitamin K antagonists.

Miliary tuberculosis in an immunocompetent male with a fatal outcome.

A man aged 33 years, born in Nepal, but resident in the UK for 7 years presented to the emergency department with a 4-day history of general malaise, fever (temperature 38.6°C) and a non-productive cough. His medical history was unremarkable and no high-risk behaviour was identified. Clinical examination confirmed decreased air entry bilaterally with bibasal crackles. He was tachycardic, with a heart rate of 120 bpm. Further investigation with a 12-lead ECG confirmed supraventricular tachycardia (SVT) which was terminated with vagal manoeuvres. His chest radiograph demonstrated left basal consolidation. His white cell count was 11×10<sup9</sup/L and his C reactive protein was 43.2 mg/L. His blood cultures revealed no growth. He was diagnosed with community-acquired pneumonia and started treatment with amoxicillin and clarithromycin. 3 days post admission, he was intubated for 24 hours in the Department of Intensive Care Medicine. Further episodes of SVT were observed and an ECHO showed a severely dilated and impaired left ventricle. Further chest radiographs illustrated diffuse consolidation with evidence of pulmonary oedema. HIV serology was negative. He developed transaminitis and thrombocytopenia. An ultrasound scan of his liver showed no obvious liver pathology. He remained tachypnoeic and due to worsening pulmonary oedema and extensive consolidation, he was readmitted to the intensive care unit. A CT abdomen with contrast showed an unusual pattern of lymphadenopathy with disproportionately enlarged coeliac axis nodes (5×7×5 cm) and minor para-aortic adenopathy, suspicious for lymphoma. On inserting his central venous catheter in his right internal jugular vein, pus was inadvertently aspirated from his right neck. Acid alcohol fast bacilli (AAFFB) were isolated from the pus and was subsequently identified as Mycobacterium tuberculosis He started treatment with antitubercular medication rifater: a combination of rifampicin 720 mg od, isoniazid 300 mg po od and pyrazinamide 1750 mg. In addition, he received ethambutol 1000 mg po od and pyridoxine 5 mg. He developed worsening metabolic acidosis, pH 7.19, loss of respiratory compensation and pancytopenia. Right heart strain was evident on his Focused Intensive Care Echo. He developed an increased oxygen requirement and respiratory distress on the ventilator. An erect chest radiograph showed bilateral pneumothoraces and bronchopleural fistulae. A chest drain was inserted. Following discussion with the Cardiothoracic Surgeons, pleurodesis was not deemed possible. He developed inotropic-dependent shock with worsening lung compliance. As a result of his deteriorating ventilation, acidosis and hyperkalaemia, he started treatment with continuous veno-venous haemofiltration. With a diagnosis of miliary tuberculosis and SVT causing cardiogenic pulmonary oedema, this man sadly died with his family at his bedside 10 weeks following initial hospital presentation.

[Massive pulmonary embolism--echocardiographic diagnosis and thrombolytic therapy].

Thrombolysis is widely accepted as the treatment of choice for acute massive life-threatening pulmonary embolism. Several trials have shown that thrombolytic treatment has reduced morbidity and mortality in this condition, compared to heparin therapy. Rapid diagnosis and treatment start is mandatory for improving the prognosis. Clinical presentation, ECG, arterial blood gas analysis and D-dimer are non-specific tests. Additional tests like ventilation/perfusion lung scan, spiral-computed tomography or pulmonary angiography are needed. In an emergency situation a non-invasive and bedside technique is preferred, and several studies have demonstrated the accuracy of echocardiography in pulmonary embolism. Acute right ventricular overload is indicated by different echocardiographic findings. Three cases with the echocardiographic method as the initial technique for the diagnosis of massive pulmonary embolism are described as well as the treatment consequence and practical administration of thrombolysis. Our patients had presenting features suggestive of massive pulmonary embolism, a clinical situation where an echocardiographic evaluation is appropriate. All presented with typical echocardiographic features. Thrombolytic treatment was initiated immediately after echocardiographic diagnosis. Different thrombolytic regimens were used. Echocardiography may be used as the initial imaging technique for the diagnosis of massive pulmonary embolism. The advantages are obvious, and thrombolytic treatment can be initiated without delay.

Acute coronary syndrome

NSTEMI and NSTE-ACS If the ECG does not show typical changes, the term "non-ST segment elevation ACS" is applied. The patient may still have suffered a "non-ST elevation MI" (NSTEMI). The accepted management of unstable angina and acute coronary syndrome is therefore empirical treatment with aspirin, a second platelet inhibitor such as clopidogrel, prasugrel or ticagrelor, and heparin (usually a low-molecular weight heparin), with intravenous nitroglycerin and opioids if the pain persists. The heparin-like drug known as fondaparinux appears to be better than enoxaparin. A blood test is generally performed for cardiac troponins twelve hours after onset of the pain. If this is positive, coronary angiography is typically performed on an urgent basis, as this is highly predictive of a heart attack in the near-future. If the troponin is negative, a treadmill exercise test or a thallium scintigram may be requested.

Obstentrics_Williams

TABLE 52-5. Anticoagulation Regimen Definitions Prophylactic LMWHa Enoxaparin,n40 mg SC once daily Dalteparin, 5,000 units SC once daily Tinzaparin, 4,500 units SC once daily Therapeutic LMWHb Enoxaparin, 1 mg/kg every 12 hours Dalteparin, 200 units/kg once daily Tinzaparin, 175 units/kg once daily Dalteparin, 100 units/kg every 12 hours May target an anti-Xa level in the therapeutic range of 0.6-1.0 units/mL for twice daily regimen; slightly higher doses may be needed for a once-daily regimen. Minidose prophylactic UFH UFH, 5,000 units SC every 12 hours Prophylactic UFH UFH, 5,000-10,000 units SC every 12 hours UFH, 5,000-7,500 units SC every 12 hours in first trimester UFH 7,500-10,000 units SC every 12 hours in the second trimester UFH, 10,000 units SC every 12 hours in the third trimester, unless the aPTI is elevated Therapeutic UFHb UFH, 10,000 units or more SC every 12 hours in doses adjusted to target aPTI in the therapeutic range (1n.5-2.5) 6 hours after injection

Anaphylactic shock due to intravenous amiodarone.

A 24-year-old male patient was admitted to the coronary intensive care unit with atrial fibrillation with rapid ventricular response. He was given amiodarone (Cordarone 150 mg i.v., Sanofi-Aventis) intravenous loading dose of 300 mg in 100 mL dextrose 5% in water (D5W) over 1 hour, followed by a maintenance dose of 900 mg in 500 mL D5W for infusion up to 24 hours. At the emergency department, the patient was conscious and cooperative; his pretreatment arterial blood pressure was 120/80 mm Hg, and the arrhythmic tachycardia was 145 per minute. After intravenous amiodarone loading and half an hour into maintenance infusion, extreme perspiration, hypotension (blood pressure immeasurable), and mild cyanosis developed. The patient was conscious; his auscultation and pulse were normal. He was given physiologic serum and dopamine support. Approximately an hour later, the blood pressure was measurable. Infusion was terminated because of suspicion of an allergic reaction to acetylsalicylic acid or amiodarone. The allergic reaction observed was attributed to acetylsalicylic acid and amiodarone; infusion was resumed when the clinical situation worsened during the maintenance infusion. Once again, the patient was given physiologic serum (2000 mL), dopamine (20 mg/kg per minute), and, additionally, 250 mg of methyprednisolone sodium succinate intravenous, whereby the clinical condition improved within 20 minutes. Anaphylactic shock cases due to amiodarone are rare; it is important to take a history of drug-mediated anaphylaxis before prescribing amiodarone. An addition to a review of the literature regarding treatment of amiodarone-related anaphylactic shock cases had not been reported before.

Diagnosis and management of carbon monoxide poisoning in the emergency department.

An 89-year-old female is found by her family, lying unconscious on her kitchen floor after they had been unable to reach her by phone for several hours. EMS is activated and when the paramedics arrive, they note that the gas oven is on, and there is thin, gray smoke coming from around the door. The house gas supply is turned off, windows are opened, and the family and the patient are immediately evacuated from the home. En route to the hospital, the patient is placed on high-flow oxygen at 15 liters per minute by non-rebreather mask. Her bedside glucose determination is 229 mg/dL. Vital signs are within normal limits during transport. She opens her eyes to sternal rub, and makes spontaneous movements of all extremities. Upon arrival to the ED, the patient becomes more alert and is able to respond to your questions. She tells you that she remembers putting a tray of calzones into the oven, after which she has no recall of the day's events. She has a past medical history of "well-controlled" hypertension, hyperlipidemia, and non-insulin-dependent diabetes. Her medications include hydrochlorothiazide 25 mg daily, lisinopril 10 mg daily, simvastatin 20 mg daily, and metformin 1000 mg twice daily. On physical examination, weight is 65 kg, blood pressure is 97/50 mm Hg, heart rate is 113 beats per minute, respiratory rate is 22 breaths per minute, temperature is 37.1 degrees C (98.8 degrees F), and oxygen saturation is 99% on 15 liters per minute via non-rebreather mask. She appears her stated age. Cardiopulmonary examination is remarkable only for tachycardia. Her abdomen is soft and non-tender with normal bowel sounds. Her skin is warm and dry, and there is no peripheral edema. Her cranial nerves are intact, with briskly reactive, symmetric pupils. Motor and sensory examination is non-focal, and cerebellar testing is notable only for an intention tremor on finger-nose-finger test. Gait is normal and speech is fluent and without errors. Laboratory testing shows a hemoglobin of 10.3 g/dL and a leukocyte count of 11.7 x 10(9)/L. Electrolyte results fall within the normal range, and her serum creatinine is 1.7 mg/dL. Qualitative CK-MB and troponin I tests are positive, and the sample has been sent to the STAT lab for quantitative testing. Serum carboxyhemoglobin level is 15% with normal serum pH on an arterial blood gas. An ECG reveals deep, down-sloping inferior and lateral ST-segment depressions which were not present on a routine cardiogram 1 month prior. You have many questions about this patient's care. What symptoms and physical signs need to be addressed and treated? What additional diagnostic testing should be performed? What treatment regimen is appropriate and what should be avoided? What are the risks or delayed complications from her illness? Are there special considerations for this or other patient populations?

[Diagnosis and treatment of acute pulmonary embolism in 2010].

Diagnostic approaches in acute pulmonary embolism include evaluation of clinical likelihood, D-dimers, echocardiography and spiral CT angiography and pulmonary scintigraphy. Determination of D-dimers is only meaningful in patients with low or intermediate clinical likelihood. It is safe not to initiate anticoagulation treatment (or to discontinue such treatment) in patients with low clinical likelihood of acute pulmonary embolism and negative D-dimer test (only if methods with 99-100% sensitivity are used). Duplex sonography and pulmonary scintigraphy are only necessary at the centres with a first generation spiral CT and not those with multidetector devices. Investigations in normotensive patients should include echocardiography that should also include assessment of the right ventricular function using echocardiography and determination of biomarkers of pulmonary embolism. Right ventricular dysfunction together with elevated troponins identifies a normotensive group at an increases risk. Highly sensitive troponin T (hsTnT) appears to be particularly valuable. Echocardiography reading might the decisive factor for treatment initiation in patients with massive acute pulmonary embolism. Negative or unclear echocardiography finding warrants spiral CT angiography (CTA). Ventilation/perfusion scan or pulmonary arteriography are recommendable in patients with unclear CTA finding and patients with high clinical likelihood of pulmonary embolism and negative CTA finding. A combination of CTA and CTV also appears useful as it increases the overall sensitivity of the investigation and enables imaging of pelvic veins. Thrombolytic treatment is indicated in haemodynamically unstable patients, patients with a high risk of a massive pulmonary embolism associated with cardiogenic shock or hypotension (systolic pressure below 90 mmHg or a decrease in systolic pressure by > 40 mmHg) or symptoms of acute right-sided heart failure. Thrombolytic treatment is also indicated in pulmonary embolism not receding following heparin treatment, in recurring or expanding pulmonary embolism, in the presence of thrombi in the right heart and in patients with right-to-left shunting through patent foramen ovale. This treatment should also be considered in patients with submassive pulmonary embolism associated with a dysfunction of the right ventricle and increased troponins, and particularly in patients lacking even a relative contraindication of thrombolytic treatment. A thrombolytic of choice is alteplase. Embolectomy or catheterization should be used if thrombolytic treatment is contraindicated or ineffective. Long-term monitoring of massive and submassive acute pulmonary embolism is highly recommended. Low molecular weight heparins or unfractioned heparin or fondaparinux are used in haemodynamically stable patients.

Myocarditis in a patient treated with Nivolumab and PROSTVAC: a case report.

Immune checkpoint inhibitors have revolutionized treatment and improved survival in many cancers. However, since immune-related adverse events (irAEs) are potentially fatal, early recognition and prompt treatment are warranted. One of the rarest but most dramatic irAE is myocarditis, which has significant morbidity and mortality if not recognized and treated early. To report the first case of myocarditis in a patient with metastatic castration-resistant prostate cancer (mCRPC) treated with a combination of nivolumab, an anti-programmed cell death protein 1 antibody, and PROSTVAC, a vector-based therapeutic prostate cancer vaccine. A 79-year-old man with mCRPC metastatic to bone and lymph nodes and a history of atrial fibrillation presented with blurred vision and pain and stiffness in the upper back after 8 weeks on a clinical trial with nivolumab (1 mg/kg) and PROSTVAC, both given every 2 weeks. Eye exam was within normal limits, while musculoskeletal exam revealed tenderness in trapezius muscles and decreased motor strength in arms (III/V) and neck (IV/V). The rest of the physical exam was within normal limits, with the exception of an irregular heart rhythm. Laboratory tests were as follows: creatinine kinase (CK) 3200 U/L (normal: 39-308 U/L), CK-MB 65.7 mcg/L (normal: 0-7.6 mcg/L), troponin I 0.209 ng/mL (normal: 0-0.056 ng/mL). Electrocardiogram (ECG) revealed atrial fibrillation with QT prolongation (QTc 514 msec) and left anterior fascicular block, unchanged from baseline. 2D-echocardiogram showed a left ventricular ejection fraction of 65% with an enlarged left atrium, dilated right ventricle, and increased pulmonary artery pressure (45 mmHg). ProBNP was elevated at 1463 pg/mL and peaked at 3066 pg/mL one day after hydration. With a presumed diagnosis of autoimmune myositis and possible myocarditis, the patient was admitted and started on methylprednisolone 1 mg/kg/day. Cardiac MRI showed elevated native myocardial T1 values consistent with myocarditis (Fig. 1). The patient was discharged on a prednisone taper after normalization of cardiac enzymes on day 4. Treatment with PROSTVAC continued for three more months; nivolumab was discontinued. Six months later, patient is doing well, with no residual cardiac damage. Cardiovascular irAEs are relatively rare (< 1%) and have a variety of clinical presentations. Myocarditis is potentially life-threatening and can range from subclinical to fulminant. Therefore, clinical suspicion, early detection, and prompt treatment are imperative (1). The initial diagnostic workup should include cardiac enzymes, ECG, and 2D-echocardiogram. The most commonly observed ECG changes are generalized repolarization abnormalities, prolonged QT interval, and conduction abnormalities (2). An elevated troponin I in the absence of overt coronary artery disease is suggestive of myocarditis and should be evaluated further. Myocardial biopsy is the standard diagnostic procedure; however, a cardiac MRI can achieve a diagnosis when biopsy is not feasible (3). Advancements in parametric mapping techniques have allowed the use of native myocardial T1 in the detection of myocarditis, as it has superior diagnostic performance and higher sensitivity than older parameters (3). Our patient had been treated with an immune checkpoint inhibitor and a therapeutic cancer vaccine to induce effective antitumor activity through immunogenic intensification and presented with muscle stiffness and elevated CK. Although he had no new cardiovascular symptoms, cardiac enzymes were tested to rule out myocardial involvement. MRI with gadolinium confirmed the diagnosis of myocarditis. To date, none of the 1360 patients treated with PROSTVAC as a single agent have developed myocarditis, while myocarditis has been rarely reported in patients treated with nivolumab (< 1%) (1). Whether the combination of PROSTVAC and nivolumab presents an additional risk of myocarditis is unclear. To our knowledge, this is the first case of myocarditis in a patient with mCRPC receiving simultaneous treatment with an immune checkpoint inhibitor and a prostate cancer vaccine. Our experience highlights the importance of suspicion and early intervention in patients who present with cardiac abnormalities after receiving cancer immunotherapy. We propose following protocol: baseline troponin, ECG, and 2D-echocardiogram prior to treatment, then repeated troponin at 2, 4, and 12 weeks post-treatment, then monthly. If troponin becomes positive without alternative explanation, myocarditis should be ruled out with cardiac MRI or myocardial biopsy, and patient should be admitted for treatment with high-dose steroids as early intervention may minimize myocardial injury.

Is it a pheochromocytoma?

The patient is a 44-year-old man with a 4-year history of intermittently elevated blood pressure (BP) controlled by diet and exercise. Three months before evaluation he described daily "spikes" of BP with sharp unilateral headaches. He was seen in the emergency department with a BP of 212/106 mm Hg and was started on hydrochlorothiazide 25 mg daily. He denied palpitations, diaphoretic episodes, pallor, and tremor. The patient did not want to take medication and specifically requested an evaluation to rule out pheochromocytoma. Results from 24-hour urine tests for total metanephrines was 812 mg/24 h (normal, 130-520 mg/24 h), for total catecholamines was 53 mg/24 h (normal, 0-135 mg/24 h), and for vanillylmandelic acid was 4.7 mg/24 h (normal, <7 mg/24 h). Thyroid-stimulating hormone was 0.87 (normal, 0.4-4.0 IU/mL). Physical examination revealed normal optic fundi, negative cardiac examination results, and presence of peripheral pulses without bruits. His BP was now 136/74 mm Hg, with a heart rate of 76 beats per minute.

[Thrombolysis in pulmonary embolism - initial experience].

Pulmonary embolism (PE) is a clinical situation difficult to diagnose, at times of great clinical instability, above all when it is massive, which leads to difficulties in the approach and treatment of patients. The treatment has not had any major innovations in recent years, being conventional the use of heparin and more rarely embolectomy. Recently, some clinical trials have defended the use of thrombolytics. The objéctive of this paper is to present our experience, although the series is still small. From April 1996 to November 1997, 11 patients were admitted to our Cardiac Intensive Care Unit with the clinical suspicion of PE, 5 of which with great hemodynamic instability and suspicion of massive PE. The clinical presentation was sudden dyspnea and loss of consciousness in 2 patients, dyspnea and hypotension in 2 patients and shock and respiratory arrest in one case. Gasimetry revealed acute hypoxemia and hypocapnia in all cases, average partial blood pressure in O2 (pO2) of 59 mm Hg and CO2 (pCO2) of 19 mm Hg. ECC and thorax x-ray contributed to the diagnosis in 3 patients, transthoracic echocardiography was decisive for the diagnosis in 5 cases, with visualisation of the thrombus by transesophageal echocardiography in 3 patients. All patients were monitored by Swan-Ganz catheter, the average systolic pulmonary artery pressure (PAP) was 74 mm Hg. Thrombolysis with rTPA (10 mg bolus followed by 90 mg in perfusion in 2 hrs) was administered in 6 episodes in 5 patients. Only in the case of the patient in shock were other complications related to the use of thrombolytics namely high digestive hemorrhage. There was a clear clinical improvement in all cases with great relief of dyspnea reduction of cyanosis and jugular engurgitation. The patient in shock recovered systemic pressures and improved the hemodynamic state. A significant reduction in PAP was observed (average of 32.5 mm Hg). PE recurred in two cases: with one death and therapeutic thrombolytic was repeated in the other patient with good results. After discharge, all patients remained asymptomatic under oral anticoagulation. Despite this small series, the results favour the use of thrombolytics in PE with a clear clinical and hemodynamic improvement.