this lecture was conducted during the nephrology unit grand ground by medical student rotated under...
TRANSCRIPT
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.
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
•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
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