This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student rotated under Nephrology Division under the supervision and administration of Prof. Jamal Al Wakeel, Head of Nephrology Unit, Department of Medicine and Dr. Abdulkareem Al Suwaida. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

Prepared by: Ramla Al-Mohishy

A 16-yr-old male,high school soccer player was running at the conclusion of an otherwise uneventful practice session, when he developed sudden-onset dyspnea with retrosternal pain. His shortness of breath and chest pain continued unchanged throughout the night. There was no history of trauma, fever, cough, asthma, no use of supplements or illicit drugs

:There is no other family history of coagulopathies, congenital heart disease, cardiomyopathy, rheumatic fever, sudden death, syncope, seizures, or premature atherosclerotic disease.

In examination: HR: 80 bpm, RR 45 b/m, BP:135/79 mm Hg, temp: 36.6°C, SaO 2 of 97%, and a weight of 66 kg. He was in mild to moderate distress, he was ambulatory and talking. CVS: normal S 1 and S 2, regular rate and rhythm without murmur, and normal pulses Resp: the lungs were clear to auscultation. There were no retractions, crackles, wheezes, increased resonance with percussion

Exam: Abdom : was significant for mild subcostal tenderness bilaterally. There was no hepatosplenomegaly, mass, or costovertebral angle tenderness. Normal bowel sounds were present. The abdomen was soft and nondistended. There was no extremity tenderness or swelling. Specifically, there was no calf tenderness

Investigation : CXR and ECG were normal. A helical computed tomography (CT) scan showed bilateral pulmonary emboli (five larger emboli on the right and three to four smaller emboli on the left) with no sign of infarction, consolidation, atelectasis, or pleural effusion.

Pulmonary embolism Pulmonary embolism (PE) is a blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body(commonly deep vain of the leg, through the bloodstream main artery of the lung blood clot,air amniotic fluid,fat tumour

Why it is so important ? ► PE occurs in around 1% of all pt admitted to hospital ► And account for 5% of inhospital death ► Common mood of death in pt with cancer and stroke ► Most common cause of death in pregnancy

Causes the etiology of venous thrombosis and subsequent thromboembolism results from a distortion in Virchow's triad. venostasis, hypercoagul ability, vessel wall inflammation Antithrombin III deficiency Protein C deficiency Protein S deficiency Factor V Leiden Plasminogen abnormality Plasminogen activator abnormality Fibrinogen abnormality Resistance to activated protein C

causes Acquired factors (The most important clinically identifiable risk factors for DVT and PE are: a prior history of DVT or PE recent surgery Pregnancy prolonged immobilization underlying malignancy or chemotherapy

studies of patients who die unexpectedly of pulmonary embolism reveal that they complained of nagging symptoms often for weeks before death related to pulmonary embolism. 40% of these patients had been seen by a physician in the weeks prior to their death

Categorization of PE Acute small/medi PEAcute massive PE Occlusion of segmental pulmon arteries→infarction+effusion Major heamodynamic effects:↓COP, RH failure pathophysiology Pleurtic chest pain, restricted breathing,heamoptysis Faintness or collapse, central chest pain, sever dyspnoea symptoms ↑HR,plural rub,crackle,bloody effusion,low grade fever ↑HR, ↓BP,↑JVP,R ventricular gallop rhythm,split p₂,cyanosis, ↓urine output signs Pleuropulmonary opacities,pleural effusion,linear shadows,raised heamidiaphragm Usually normal,maybe subtle oligaemia CXR Sinus tachycardiaS₁Q₃T₃, RBBBECG Normal or ↑PaCO₂↓PaO₂,and ↓PaCO₂, metabolic acidosis ABG Pneumonia, pnemothorax, Musculoskeletal chest pain MI, pericardial temponad, ODAlternative dx

Diagnosis and investigation PO 2 on arterial blood gases WBC ↑ESR, AST,and LDH without increasing in bili D-dimer

Diagnosis and investigation Imaging Studies CXR Spiral CT V/Q scan ECG

VTE suspected D-dimer +ve Assess clinical risk Measure D-dimer D-dimer(-ve) Risk low D-dimer –ve Risk high U/S leg veins CT pulmonary Angiogram V/Q scan Confirm dx Treat Not DVT/PE

Management

References 1- Kody Moffatt; Phillip J. Silberberg; David J. Gnarra; Medicine and Science in Sports and Exercise. 2007;39(6): ; 2007 American College of Sports Medicine 2-Nicholas A.Boon; et al; Davidson’s principles and practice of medicine;20 edi; p: Sara F Sutherland; pulmonary embolism; May 8, 2009; available online: overview