Good Morning and Welcome Applicants! November 11, 2010

Acute Pulmonary Embolism Origin Deep venous system of lower extremities, right heart, pelvic, renal or upper extremity veins Travel to lungs Large thrombi Lodge at bifurcations and can cause hemodynamic compromise Small thrombi Travel distally cause pleuritic chest pain

Acute Pulmonary Embolism - Pathophysiology Impaired gas exchange Mechanical obstruction – V/Q mismatch Inflammatory mediators Surfactant dysfunction, atelectasis and functional intrapulmonary shunting Hypotension Diminished CO Increased PVR leading to decreased RV outflow and decreased LV preload

Acute Pulmonary Embolism More than half of all PE are underdiagnosed Mortality rate 30% without treatment Reduced to 2-8% with anticoagulation RV dysfunction associated with two-fold increase RV thrombus BNP Serum troponins

VTE in Children Central Venous Access Inherited Hypercoagulable State Associated with 2/3 of VTEs in children Inherited Hypercoagulable State Other Conditions Infection, Congenital Heart Disease, Trauma, Nephrotic Syndrome, Lupus Erythematosus or complication from chemotherapy (L-asparaginase and steroids) for ALL

Acute Pulmonary Embolism Clinical Signs Pleuritic chest pain Tachypnea Cough Tachycardia Acute dyspnea Signs of DVT Sudden collapse Most common – nonspecific PE should be considered in the differential diagnosis of cardiorespiratory deterioration in all critically ill children

Diagnosis of Acute Pulmonary Embolism Modified Wells Criteria for PE Clinical symptoms of DVT (3 points) Other diagnosis less likely than PE (3 points) Heart rate >100 (1.5 points) Immobilization or surgery in previous four weeks (1.5 points) Previous DVT/PE (1.5 points) Hemoptysis (1 point) Malignancy (1 point) Traditional clinical probability assessment: High >6 Moderate 2 to 6 Low <2 Simplified clinical probability assessment: PE likely (score >4) PE unlikely (score <=4)

Diagnosis of Acute Pulmonary Embolism CT experienced institutions Angiography is the gold standard though

Vocal Cord Dysfunction AKA – Paradoxical vocal cord motion (PVCM) Paradoxical vocal cord adduction during inspiration

Vocal Cord Dysfunction Signs Wheezing Stridor Dyspnea Cough Chest tightness Exercise intolerance F>M 20-40y 20-40 although it is becoming more common in the pediatric population

Vocal Cord Dysfunction Medical Risk Factors Asthma (50%) GER CF Postnasal drip Cold air Cigarette smoke Brainstem abnormalities Stroke Myasthenia gravis

Vocal Cord Dysfunction Psychological Risk Factors Anxiety over school performance Parent-child conflict Divorce Emotional upset Abuse Psychiatric disturbances Somatization disorder

VCD vs Asthma Inspiratory dyspnea Abnormalities heard on inspiration No response to bronchodilators Normal ABG if hypoxemic Normal A-A gradient Normal CXR PFTs Flattening of inspiratory limb Expiratory dyspnea Abnormalities heard on expiration Respond to bronchodilators Abnormal ABG if hypoxemic VQ mismatch CXR with hyperinflation PFTs Scooped out expiratory limb

VCD Diagnosis Direct visualization

VCD Management Mulitdisciplinary Primary cause if present Acute Panting Short acting benzos Long-term Speech therapy Relaxation techniques Psychological intervention Education Panting with the tongue out increases the glottic aperture resulting in acute relief Psychological intervention if speech therapy and relaxatin techniques do not work