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, SaO2 of 97% , and a weight of 66 kg .

• He was in mild to moderate distress, he was ambulatory and talking .

•CVS: normal S1 and S2, 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

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 ,

hypercoagulability,

vessel wall inflammation

Antithrombin III deficiencyProtein C deficiencyProtein S deficiency

Factor V Leiden Plasminogen abnormality

Plasminogen activator abnormality

Fibrinogen abnormalityResistance 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 massive PEAcute small/medi PE

pathophysiologyMajor heamodynamic effects:↓COP, RH failure

Occlusion of segmental pulmon arteries→infarction+effusion

symptomsFaintness or collapse, central chest pain, sever dyspnoea

Pleurtic chest pain, restricted breathing,heamoptysis

signs↑HR, ↓BP,↑JVP,R ventricular gallop rhythm,split p₂,cyanosis, ↓urine output

↑HR,plural rub,crackle,bloody effusion,low grade fever

CXRUsually normal,maybe subtle oligaemia

Pleuropulmonary opacities,pleural effusion,linear shadows,raised heamidiaphragm

ECGS₁Q₃T₃, RBBBSinus tachycardia

ABG↓PaO₂,and ↓PaCO₂, metabolic acidosis

Normal or ↑PaCO₂

Alternative dxMI, pericardial temponad, ODPneumonia, pnemothorax, Musculoskeletal chest pain

Diagnosis and investigation

PO2 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 scanECG

•VTE suspected

D-dimer +ve

Assess clinical riskMeasure D-dimer

D-dimer(-ve)Risk low

D-dimer –veRisk high

U/S leg veinsCT 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):899-902; 2007 American College

of Sports Medicine •2-Nicholas A.Boon; et al; Davidson’s principles and

practice of medicine;20 edi; p:725-27•3 -Sara F Sutherland; pulmonary embolism; May 8,

2009; available online: http://emedicine.medscape.com/article/759765-

overview