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Author(s): Michele M. Nypaver, MD, 2011

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1 Author(s): Michele M. Nypaver, MD, 2011
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2 Citation Key for more information see: http://open. umich
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3 UMHS PEM Conference Series
Acute Pulmonary Emergencies: Pulmonary Embolism, Pulmonary Edema and Parapneumonic Effusions UMHS PEM Conference Series April 2010 Michele M. Nypaver, MD 3

4 Case Presentation A 13y/o African American female presents to the peds ED with complaints of chest discomfort and SOB, worse with exercise and now even walking. Had URI symptoms several weeks ago (as did others in family), seemed to resolve until day of presentation when CP/SOB became suddenly worse. No fever, occasional dry cough, no V/D, no runny nose, sore throat. No meds/allergies/imm’s UTD

5 More Info? What other questions? Past Medical History
Significant for deep venous thrombus in the right calf in November She received anticoagulation with Lovenox until follow-up Doppler scan demonstrated resolution of the DVT. Currently on no anticoagulation. No bruises, weight loss, No oral contraceptives, no other sx’s on ROS

6 Pediatric Pulmonary Embolism
Review Pathophysiology Suspecting the diagnosis Adult versus pediatric PE Evaluation Treatment 6

7 Please see original image of DVT/Pulmonary Embolism at http://www
Persian Poet Gal, "Blood Clot Diagram (Thrombus)", Wikimedia Commons 7

8 Please see original image of Pulmonary Embolism at http://www
8

9 Please see original image of Pulmonary Embolism at http://www. ncbi
Source Unknown 9

10 PE Pathophysiology Embolic clot size / location determines presentation Cardiac Effects: Clot obstructs RV outflow Sudden increased RV dilatation and pressures RV pressure can affect (reduce) LV fxn If PFO, R to L shunt can occur Vasoconstriction of Pulm Vasculature: Increased Pulm Vasc Resistance Release of neural/humoral mediators which increase pulmonary vasculature resistance DECREASED CO, VQ mismatch Sudden, unpredictable cardiovascular collapse 10

11 Pulmonary Embolus Lung Effects
Clot prevents diffusion of oxygen from alveoli to circulation Overall increases dead space of some portion (or all) of the lung Affected area becomes atalectatic Overall Increase in pulm vascular resistance Decreased alveolar availability for gas exchange 11

12 Adult PE 600,000 cases/yr Traditional risk factors:
Bed rest (> 3 days) Heart dz Malignancy Prior DVT/PE Surgery (in last 3 months) Estrogen RX Pregnancy Hypercoaguable states Recent travel 20-25% Have NO identifiable risk factors on presentation Most incidence data extrapolated from adult studies Best information about children is from Dutch/Canadian literature. Canadian prospective database, Dutch self report from Pediatricians, estimates of incidence were close, but only involved 78 total children with PE. 12

13 Approach to Diagnosis Adult clinical symptoms
Determine pre test probability for the likelihood of PE Direct testing that reflects likelihood of disease while minimize risk to patient and overuse of invasive procedures Caveat: None are 100% sensitive or specific Gold Std: Angiography 13

14 Wells Clinical Prediction Rule for Pulmonary Embolism
Clinical feature Points Clinical symptoms of DVT 3 Other diagnosis less likely than PE 3 Heart rate greater than 100 beats per minute 1.5 Immobilization or surgery within past 4 weeks 1.5 Previous DVT or PE Hemoptysis 1 Malignancy 1 Risk score interpretation (probability of PE): >6 points: high risk (78.4%); 2 to 6 points: moderate risk (27.8%); <2 points: low risk (3.4%) IN a landmark paper done by Wells et al in 1998, a clinical prediction rule was derived that is used largely today. Points are assigned for presence of features with a risk score based probability assigned. There is a lot of debate on the use of the score and the clinical features are in many cases not useful for obvious reasons. Wells PS et al. Ann Intern Med ;129;997 14

15 Clinical Presentation of PE (Adult)
Tachypnea Rales Tachycardia 4th Heart Sound Accentuated S2 Dyspnea Pleuritic chest pain Cough Hemoptysis Girard P. et al. Am J Respir Crit Care Med ;164: Prospective Investigation of Pulmonary Embolism Diagnosis Study (PIOPED). 15

16 Canadian childhood Thrombophilia Registry (N=405)
Incidence of Pulm Embolism 0.07/10,000 Pediatric PE Risk Factors (one or more) Central Venous Catheter 60% Cancer/Bone marrow transplant 25% Cardiac surgery % Surgery (other) % Infection % MVA/trauma/Burn 10% Oral contraception % Obesity % Congenital / acquired pro-thrombotic disorder 2% SLE % What do we know about kids? In contrast to adults, kids tend to have a reason to have a PE and often have multiple reasons. Data are few. And come from thrombophilia registries in Canada and Netherlands and neonatal literature. In contrast to adults, children most often have a specific reason or multiple risk factors for suspicion/dx of PE. In the list, notably, risk in MVA for children/adolescents is less than adults (adult 6/1000 discharges vs 0.7/1000 discharges in kids less than 15 years, Relative risk increased with injury severity scores, catheter placement and major cranial or vascular inj/surgery). Ped Emerg Care 2004: 20 (8) Green et al. Chest 1992:101;1507 16

17 Pediatric PE Neonatal considerations Peri-partum asphyxia Dehydration
Sepsis Most PE’s due to Catheters Aorta, pulmonary, renal Special considerations Renal disease: Nephrotic syndrome (altered levels of antithrombin and increased other coag proteins). Klippel-Trenauay Hemangiomas Anti phospholipid antibodies (Lupus) Non thrombotic emboli: Foreign bodies Tumor emboli Septic emboli Post traumatic fat emboli 17

18 Pediatric PE and DVT Incidence of pediatric PE in children with documented DVT 30% DVT in children may obviate the need to evaluate the chest Pediatric DVT often in upper venous system PE can originate from intracranial venous sinus thrombosis Mortality from DVT/PE in children may be lower than adults (2.2% from Canadian Registry; all deaths were from emboli to upper venous system and were catheter related). 18

19 Clinical Presentations in Pediatric PE
Similar to adults BUT Children have better physiologic reserve Less prominent respiratory rate or heart rate changes compared to adults Other signs/symptoms associated with PE Pleuritic chest pain Hemoptysis Cyanosis RHF Hypoxia Hypercarbia Pulm hypertension Rare cases of paradoxical embolism/stroke (venous to arterial emboli due to cardiac defect or pulm av malformation. 19

20 Case KA Physical Exam: Vitals: Temp 98.0, pulse 120, respiratory rate 36, blood pressure 122/76, pulse ox 95% on room air, weight 60.4 kilograms She has a normal S1 and physiologically split loud S2. She has a 2/6 systolic ejection murmur audible at the right and left upper sternal borders.

21 Case KA Initial Evaluation CBC ABG EKG
Other labs: anticardiolipin antibody, a lipoprotein A level, a homocysteine level, factor V Leiden mutation screening, and prothrombin mutation. Hemodynamic/respiratory monitoring

22 Evaluation of Children with Suspected PE
Toolbox ABG: Low paO2; low paCO2 initially, ominous rise in paCO2 EKG: Sinus tachycardia, RAD, RVH, RBBB Increased a-A gradient D-Dimer: Highly sensitive in adults coupled with clinical evaluation to r/o PE; Few data in children and false positive in presence of infection/malignancy. * No studies documenting sensitivity/specificity of clinical evaluation or imaging tests alone/combination in children Source Unknown A-a gradient = PAO2 − PaO2 Aa Gradient = [FiO2*(Patm-PH2O)-(PaCO2/0.8) ] - PaO2 Aa Gradient = ( /4(PCO2)) - PaO2 22

23 EKG & PE ECG features in PE lack specificity and sensitivity
Value of ECG for the diagnosis of PE is debatable ECG can be normal in pulmonary embolism, and other recognised features of PE include sinus tachycardia (heart rate >100 beats/min), negative T waves in precordial leads, S1 Q3 T3, complete/incomplete right bundle branch block, right axis deviation, inferior S wave notch in lead V1, and subepicardial ischaemic patterns. The mechanism for these ECG changes is acute right heart dilatation, such that the V leads that mostly represent the left ventricle now represent the right ventricle (RV). The presence of inverted T waves on precordial leads suggests massive PE.

24 EKG & PE “S1 Q3 T3” - prominent S wave in lead I, Q and inverted T waves in lead III Right bundle branch block (RBBB), complete or incomplete, often resolving after acute phase Right shift of QRS axis shift of transition zone from V4 to V5-6 ST elevation in VI and aVR generalized low-amplitude QRS sinus tachycardia, atrial fibrillation/flutter, or right- sided PAC/PVC T wave inversion in V1-4, often a late sign.

25 Evaluation of Children with Suspected PE
Source Unknown CXR: infiltrates, atelectasis, unilateral pleural effusion, hypovascularity in lung zone (Westermark’s sign) & pyramid shape infiltrate with peak directed to hilus (Hampton’s hump). Chronic PE can result in findings of RH enlargement, enlarged PA’s. Echo: not helpful for distal clots, better to assess pulm hypertension and massive PE with central position. Source Unknown Source Unknown 25

26 Plain film radiography Chest X-ray
Westermark sign – Dilatation of pulmonary vessels proximal to embolism along with collapse of distal vessels, often with a sharp cut off. Hampton’s hump Source Unknown Source Unknown 26

27 CASE KA from initial presentation
Study: AP chest 12/28/2007. History: Pulmonary embolism. Comparison: None available. Impression: 1. There may be slight prominence of the central pulmonary vasculature otherwise, the lungs are clear. Normal cardiopericardial silhouette. Source Unknown 27

28 Evaluation of PE DVT : Looking for a source
Duplex US: Good for lower extremities Detects echogenic thrombi Absence of flow Non-compressibility of veins Used in series to detect thrombus organization Limitations: Not useful for pelvic DVT, thoracic inlet (vessels beneath the clavicles or within the chest); ok for jugular vein clots versus venography. 28

29 V/Q Scan evaluation for children with suspected PE
V/Q scan primary screening tool for PE in children Safe, sensitive and relatively low radiation Limited to children beyond infancy/toddlers who can cooperate Results: High Probability Intermediate Probability Low Probability Very Low Probability Normal Limitations in interpretation: Poor inter-observer agreement Underlying pulm pathology Use in CHD with R-L shunt Sensitivity/specificity using PIOPED criteria for V/Q studies in children are not clear VQ is the most commonly employed test for pediatric PE Altho has numerous limitations Source Unknown 29

30 Saddle type pulmonary embolus
CT Angio Detects intra-luminal defects Has become the imaging test of choice in adults BUT Limitations sub-segmental arteries, movement or breathing that might occur in peds studies, requires Iodine contrast and radiation. Sensitivity % Specificity % Source Unknown 30

31 Example of pulmonary emboli seen on CT angio cross section.
Source Unknown 31

32 Case KA from initial presentation
Source Unknown

33 MRI evaluation for PE MRI
Recent ability to visualize the pulmonary arteries Limitations Acutely ill patients Long test times Patient monitoring Subsegmental PE’s Sedation requirement in kids Availability of resources Sensit 68-88% Specificity > 95% Source Unknown 33

34 Pulmonary Angiogram Example of pulmonary angiogram: Limitations, invasive, contrast, radiation Source Unknown 34

35 PE Management ABC’s Oxygen Airway support
If intubation required, beware of hypotension IV access RV strain in PE necessitates CAREFUL fluid admin Early vasopressors (norepi) if BP low/unresponsive to judicious fluids Anticoagulation: Heparin Other options: Thrombolytics, Filter, Embolectomy, Surgical embolectomy

36 A sample algorigthm approach to decision making for Pulmonary Embolism is noted here.
Source Unknown 36

37 Pulmonary Embolism: Treatment
IV Heparin vs Low Molecular Weight Heparin (LMWH) IV Un-fractionated (UF) Heparin: Hypotension, massive PE, RF units/kg bolus over 10 minutes Infusion 20 units/kg/h Maintain Prothrombin time (PTT) seconds Oral or LMWH follow up to Heparin LMWH Dosing: For hemodyanamically stable pts Enoxaparin > 2mo/age: 1mg/kg SQ BID < 2mo/age: 1.5 mg/kg SQ daily Reviparin > 5kg: 100 U/kg SQ BID < 5kg: 150 U/Kg SQ BID IV UFH is the only anticoagulant that has been compared to no treatment in a controlled trial and shown to reduce mortality due to PE [1]. Subsequent uncontrolled trials confirmed that anticoagulation is associated with decreased mortality 37

38 Pediatric Pulmonary Edema
Basic definition of pulmonary edema is fluid/flooding of the alveolar space. Pulmonary edema is typically one of two types: Cardiogenic: Hydrostatic or hemodynamic edema Non cardiogenic: Increased permeability edema, acute lung injury, ARDS Clinically the two can be difficult to distinguish but has important implications for treatment Anatomical drawing of Pulmonary Edema removed. Source Unknown 38

39 Pulmonary Edema Pathophysiology 101
Figure 1. Physiology of Microvascular Fluid Exchange in the Lung. In the normal lung (Panel A), fluid moves continuously outward from the vascular to the interstitial space according to the net difference between hydrostatic and protein osmotic pressures, as well as to the permeability of the capillary membrane. The following Starling equation for filtration of fluid across a semipermeable membrane describes the factors that determine the amount of fluid leaving the vascular space: Lp unit permeability (or porosity) of the capillary wall S surface area available for fluid movement Pcap and Pif capillary and interstitial fluid hydraulic pressures cap and if capillary and interstitial fluid oncotic pressures; the interstitial oncotic pressure is derived primarily from filtered plasma proteins and to a lesser degree proteoglycans in the interstitium. s reflection coefficient of proteins across the capillary wall (with values ranging from 0 if completely permeable to 1 if completely impermeable). In normal microvessels, there is ongoing filtration of a small amount of low protein When hydrostatic pressure increases in the microcirculation, the rate of transvascular fluid filtration rises (Panel B). When lung interstitial pressure exceeds pleural pressure, fluid moves across the visceral pleura, creating pleural effusions. Since the permeability of the capillary endothelium remains normal, the filtered edema fluid leaving the circulation has a low protein content. The removal of edema fluid from the air spaces of the lung depends on active transport of sodium and chloride across the alveolar epithelial barrier. The primary sites of sodium and chloride reabsorption are the epithelial ion channels located on the apical membrane of alveolar epithelial type I and II cells and distal airway epithelia. Sodium is actively extruded into the interstitial space by means of the Na+/K+–ATPase located on the basolateral membrane of type II cells. Water follows passively, probably through aquaporins, which are water channels that are found predominantly on alveolar epithelial type I cells.6 Noncardiogenic pulmonary edema (Panel C) occurs when the permeability of the microvascular membrane increases because of direct or indirect lung injury (including the acute respiratory distress syndrome), resulting in a marked increase in the amount of fluid and protein leaving the vascular space. Noncardiogenic pulmonary edema has a high protein content because the more permeable microvascular membrane has a reduced capacity to restrict the outward movement of larger molecules such as plasma proteins. The degree of alveolar flooding depends on the extent of interstitial edema, the presence or absence of injury to the alveolar epithelium, and the capacity of the alveolar epithelium to actively remove alveolar edema fluid. In edema due to acute lung injury, alveolar epithelial injury commonly causes a decrease in the capacity for the removal of alveolar fluid, delaying the resolution of pulmonary edema Figure 1. Physiology of Microvascular Fluid Exchange in the Lung. In the normal lung (Panel A), fluid moves continuously outward from the vascular to the interstitial space according to the net difference between hydrostatic and protein osmotic pressures, as well as to the permeability of the capillary membrane. The following Starling equation for filtration of fluid across a semipermeable membrane describes the factors that determine the amount of fluid leaving the vascular space: Q = K[(Pmv – Ppmv) – ( mv – pmv)], where Q is the net transvascular flow of fluid, K is the membrane permeability, Pmv is the hydrostatic pressure in the microvessels, Ppmv is the hydrostatic pressure in the perimicrovascular interstitium, mv is the plasma protein osmotic pressure in the circulation, and pmv is the protein osmotic pressure in the perimicrovascular interstitium. When hydrostatic pressure increases in the microcirculation, the rate of transvascular fluid filtration rises (Panel B). When lung interstitial pressure exceeds pleural pressure, fluid moves across the visceral pleura, creating pleural effusions. Since the permeability of the capillary endothelium remains normal, the filtered edema fluid leaving the circulation has a low protein content. The removal of edema fluid from the air spaces of the lung depends on active transport of sodium and chloride across the alveolar epithelial barrier. The primary sites of sodium and chloride reabsorption are the epithelial ion channels located on the apical membrane of alveolar epithelial type I and II cells and distal airway epithelia. Sodium is actively extruded into the interstitial space by means of the Na+/K+–ATPase located on the basolateral membrane of type II cells. Water follows passively, probably through aquaporins, which are water channels that are found predominantly on alveolar epithelial type I cells.6 Noncardiogenic pulmonary edema (Panel C) occurs when the permeability of the microvascular membrane increases because of direct or indirect lung injury (including the acute respiratory distress syndrome), resulting in a marked increase in the amount of fluid and protein leaving the vascular space. Noncardiogenic pulmonary edema has a high protein content because the more permeable microvascular membrane has a reduced capacity to restrict the outward movement of larger molecules such as plasma proteins. The degree of alveolar flooding depends on the extent of interstitial edema, the presence or absence of injury to the alveolar epithelium, and the capacity of the alveolar epithelium to actively remove alveolar edema fluid. In edema due to acute lung injury, alveolar epithelial injury commonly causes a decrease in the capacity for the removal of alveolar fluid, delaying the resolution of pulmonary edema Drawing of alveoli in pulmonary edema removed. Net filtration  =  (Lp x S)   x   ( hydraulic pressure   —   oncotic pressure) 39

40 Pulmonary Edema in children
Clinical presentation Poor feeding/poor weight gain Tachypnea/Dyspnea/grunting Tachycardia Cough Evaluation History & Exam: pallor, diaphoresis, Inc RR CXR EKG Other monitors as indicated: Pulmonary Artery Catheterization

41 Pediatric Pulmonary Edema
Negative pressure pulmonary edema Post obstructive pulmonary edema (POPE) Non Cardiogenic pulmonary edema Cardiogenic pulmonary edema 41

42 CXR Findings in pulmonary edema
Increased heart size -- cardiothoracic ratio >0.50. Large hila with indistinct margins Prominence of superior pulmonary veins; cephalization of flow Fluid in interlobar fissures Pleural effusion Kerley B lines Alveolar edema Peribronchial cuffing Limitations: Edema may not be visible until amount of lung water increases by 30% or more Edema produces similar radiographic findings as other materials that may fill the alveoli (pus, blood etc).

43 Source Unknown

44 Source Unknown

45 Example X-Ray of Kerley B Lines
                                                                                                                Kerley B lines are caused by peri-vascular edema, with a base on the pleural surface of the lung and extending horizontally a variable, but usually short, distance toward the center of the chest. Source Unknown

46 Correlation of CXR with Pulmonary Capillary Wedge Pressure
Pulmonary Cap Wedge Pressure and CXR Findings: 5-12 mmHg Normal 12-17 mmHg Cephalization of pulm vessels 17-20 mmHg Kerley lines > 25 mmHg Frank pulmonary edema Changes in pulmonary capillary wedge pressure can be noted on plain film radiography; as pressures increase, findings may occur as noted here. 46

47 Negative Pressure Pulmonary Edema
Etiology Can be associated with any upper airway obstruction Croup, epiglotitis, FB, post op T & A, tumor, hanging, intubation for non airway procedures Clinical Presentation Rapid onset, short lived course Pulmonary edema occurs once obstruction is relieved SOB, cough (frothy pink fluid) Treatment Most require ETI/CPAP/PEEP Diuretics, Inotropic support and invasive hemodynamic monitoring is usually not needed if dx is clear Sx usually resolve in hours

48 A case of negative pressure pulmonary edema A: Acute pulmonary edema
B: Resolving pulmonary edema Large negative intrapleural pressure Increase lymph flow and interstitial edema Pulmonary edema The exact pathogenesis of NPPE remains uncertain, but it seems to be multifactorial. The predominant mechanism is forced inspiration against the closed glottis (Mueller maneuver), inducing a negative gradient of intrapleural and transpulmonary pressure, causing the transudation of fluid from the pulmonary capillaries into the interstitial space.27 The intrapleural pressure may decrease to -50 to -100 cm H2O. In human volunteers, obstructive periods of as little as 10 to 30 seconds have precipitated pulmonary edema.12 The marked increase in the intrapleural negative pressure causes an increase in the venous return to the right ventricle and a decrease in left ventricular output, resulting in an elevation in the pulmonary blood volume and in the microvascular pressure. The final diastolic pressure of the left ventricle increases with the greater negative pleural pressure; this is due to the increased volume of the venous return to the right ventricle, causing a right ventricular distention and a distortion of the interventricular septum, with consequent decrease in the compliance of the left ventricle.28 Another factor involved in the pathogenesis of NPPE is the lack of airflow and alveolar oxygenation during UAO, resulting in hypoxemia, which causes a hyperadrenergic state. The consequent peripheral vasoconstriction shunts the blood centrally, whereas the hypoxia- mediated pulmonary vasoconstriction results in altered Starling forces, favoring formation of pulmonary edema. In addition, the presence of hypoxia and acidosis also cause myocardial depression.28 Pulmonary capillary permeability is increased secondary to physical damage, thus facilitating the formation of pulmonary edema.29,30 This capillary leak of proteinaceous material could account for the classic description of serosanguineous or pink frothy secretions in NPPE. Cardiac Effects: Neg intrapleural pressures also increase venous return to rt heart and pooling of bloood in the pulmonary venous system during inspiration. Increased VR to rt ventricle causes pressure on LV (reduced LV compliance) Source Unknown 48

49 Post obstructive pulmonary edema (POPE)
Type I POPE Postextubation laryngospasm Epiglottitis Croup Choking/foreign body Strangulation Hanging Endotracheal tube obstruction Laryngeal tumor Goiter Mononucleosis Postoperative vocal cord paralysis Migration of Foley catheter balloon used to tamponade epistaxis Near drowningIntraoperative direct suctioning of endotracheal tube adapter Type II POPE Post-tonsillectomy/ adenoidectomy Post-removal of upper airway tumor Choanal stenosis Hypertrophic redundant uvula 49

50 Cardiogenic pulmonary edema
Usually due to congenital heart disease Left to Rt shunt lesions (PDA, VSD) LV filling/emptying defects (Aortic Stenosis) Total Anomalous Pulmonary Veins (TAPV) (obstruct emptying of pulm veins) Arrhythmia Cardiomyopathy Pneumonia/pulmonary infection High output states Iatrogenic

51 Pediatric Cardiogenic Pulmonary Edema: Etiology by presentation time
First week of life Ductal dependant congenital heart lesions, (pre ductal coarctation) and lesions causing pulmonary venous obstruction to vent filling (cor triatriatum) 2-4 weeks of life Left to right shunting lesions (VSD) as pulmonary vascular resistance decreases > 6 months of life Usually specific diagnosis

52 Non Cardiogenic Pulmonary Edema
Definition: Noncardiogenic pulmonary edema is defined as the radiographic evidence of alveolar fluid accumulation without hemodynamic evidence to suggest a cardiogenic etiology (ie, pulmonary wedge pressure 18 mmHg). The accumulation of fluid and protein in the alveolar space leads to decreased diffusing capacity, hypoxemia, and shortness of breath. Most common Cause: ARDS High Altitiude pulmonary edema Neurologic pulmonary edema Reperfusion pulmonary edema Reexpansion pulmonary edema

53 Pulmonary edema and ARDS
Damaged alveolar capillary membrane (permeability pulmonary edema) Allows leakage of fluid and protein from intravascular to interstitial and ultimately into alveolar spaces Presentation: SOB Pulm infiltrates/hypoxemia Etiology: Many DX: pulmonary artery wedge pressure less than 18 mmHg favors acute lung injury (> 18mmHg doesn’t always exclude lung etiology). Other: plasma brain natriuretic peptide (BNP) high in cardiogenic causes. Regardless of etiology, the clinical scenario is similar in most patients once membrane damage has occurred. Sepsis- or ischemia-induced release of cytokines, such as interleukin-1, interleukin-8, and tumor necrosis factor, may play an important role in the increase in pulmonary capillary permeability, at least in part via the recruitment of neutrophils 53

54 Non Cardiogenic Pulm Edema
Treatment No known treatment to correct capillary permeability Supportive measures while lung recovers Airway/ventilatory management Nutrition Fluid: Diuresis/fluid restriction improve lung function and positively affect patient outcome Cardiac management Others: Prostacycline, nitrous oxide, steroids, beta agonists Surfactant Design, Setting, and Patients  A multicenter, randomized, blinded trial of calfactant compared with placebo in 153 infants, children, and adolescents with respiratory failure from ALI conducted from July 2000 to July Twenty-one tertiary care pediatric intensive care units participated. Entry criteria included age 1 week to 21 years, enrollment within 48 hours of endotracheal intubation, radiological evidence of bilateral lung disease, and an oxygenation index higher than 7. Premature infants and children with preexisting lung, cardiac, or central nervous system disease were excluded. Conclusions  Calfactant acutely improved oxygenation and significantly decreased mortality in infants, children, and adolescents with ALI although no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was observed. JAMA. 2005;293: Effect of Exogenous Surfactant (Calfactant) in Pediatric Acute Lung Injury (ALI) 54

55 Neurologic Pulmonary Edema
Exact cause unknown Medulla/nuclei of solitary tract/hypothalamus CNS conditions associated with Neuro pulm edema: Trauma Infection Seizure Cervical spine injuries Clinical: Onset of SOB minutes/hours after neurologic insult DX: Setting, Hemodynamic measurements, including blood pressure, cardiac output, and pulmonary capillary wedge pressure are normal.

56 Neurologic Pulm Edema: Lab theories
Pulmonary venoconstriction can occur with intracranial hypertension or sympathetic stimulation and can elevate capillary hydrostatic pressure and produce pulmonary edema without affecting left atrial, systemic, or pulmonary capillary wedge pressures. Constriction of the pulmonary veins of rats follows head trauma, and can be attenuated with alpha adrenergic antagonists Source Unknown

57 Neurologic Pulm Edema Treatment Airway support Alpha adrenergic drugs
Beta adrenergic antagonists

58 High Altitude Pulmonary Edema (HAPE)
More kids are going places! Rapid ascension to > 12,000 feet Some children are more at risk: Downs Kids who LIVE at altitude…go to lower areas then reascend. Children more predisposed to reascent HAPE Pathophysiology: Accentuated hypoxemia abnormally pronounced degree of hypoxic pulmonary vasoconstriction Release of mediators Leaky endothelium?

59 HAPE Clinical presentation RX: Variable: Hours, days, explosive onset
SOB, cough, sputum (frothy, pink) RX: Oxygen Descent Bedrest Dexamethesone for emergencies Hyperbaric chambers for rescue removals Education: Slow descents Prevention: Nifedipine

60 Emergency Department Therapy of Acute Pulmonary Edema in Children
Assessment Etiology: Likely cardiac vs non cardiac? Oxygen CXR/Exam: Determination of pump status Diuresis Inotropic support? Directed evaluation

61 Parapneumonic Effusions
Pleural effusion associated with lung infection Infection may (rarely) be spread from remote places: retropharyngeal, abd, vertebral, retroperitoneal spaces to pleura Pleural inflammation—leak Proteins Fluid WBC’s Initially sterile—subsequently may become infected=EMPYEMA Presence of grossly purulent fluid in pleural cavity

62 Parapneumonic Effusions
Increasing incidence USA & UK Li et al. Pediatrics 2010 Roxburgh et al. Arch Dis Child 2008 Rise coincident with rise in antibiotic resistance, despite pneumococcal vaccine: serotypes not covered? Mortality highest children < 2y/o Spring/Winter 2X greater than summer/fall Male = Females

63 Changing Etiology Before 1945: Pneumococci/Staph
After PCN/Sulfa: Staph aureus 1980’s: H. influenza/Pneumococci/Staph 1990’s: H. flu disappears! (except adults) 1980’s and up: increase in Bacteroides, Fusobacterium Now: St. pneumonia w resistance patterns (pcn non susceptable) and or pcn susceptable strains in certain communities MRSA Coag (-) St. aureus, Strep viridans, Grp A strep, Alpha hemolytic strep, Actinomyces species. GRP A Strep, TSS and Empyema?

64 Stages of Parapneumonic Effusion
Exudative Normal Glucose Normal ph Low cell count Fibrinopurulent PMN invasion Bacterial/fibrin deposition on pleura Thickened exudate and loculations pH/glucose=decrease LDH = increase Don’t layer out on xray Lasts 7-10 days

65 Stages of Parapneumonic Effusion
Organizational Pleural Peel formation Fibroblasts grow on parietal/visceral pleura Restricts lung reexpansion Impairs function Persistent pleural space Dry tap

66 Complications Infrequent in children Bronchopleural fistula
Lung abcess Empyema necessitatis (perforation thru chest wall)

67 Clinical presentation
Fever Malaise Low appetite Cough Chest pain Dyspnea/Tachypnea: Shallow to minimize pain Splint side Not usually toxic appearing Rarely present as septic shock

68 Clinical Presentation
Source Unknown Mediastinal shift Hypoalbinemia Thromobcytosis Hypoxia Radiology: Plain films Decubitus films Ultrasound Chest CT Source Unknown Source Unknown

69 Effusion Analysis Layering > 1cm: Easier target
Who to tap: Better to find the organism If small and abx already begun, reasonable to wait/see response to abx Thoracentesis w/w/out US guidance Dry tap: Consider sterile 5-10cc fluid/reaspirate Cx Pneumococcal Antigen Latex agglutination and PCR Sensitivity/specificity 90/95% respectively pH, glucose, LDH, cell count & differential Specimens must be on ice and tightly capped Other tests: Blood cx in all pts Misc if indicated: Sputum/tracheal asp, TB, Titers (mycoplasma, ASO, Resp viruses), CBC, CRP, sLDH (to compare to pl sample)

70 ED EVAL ABC’s Assessment for effects on respiratory status
RR, pulse ox, VBG and or ABG CXR (decubitus?) US To tap or not to tap Treatment: Directed at most likely etiology Goals: Sterilize the pleural space, drain as necessary, reexpand the lung

71 Hospitalization & Surgical issues
Most will require hospitalization Surgical intervention is controversial Drain and debride (VATS) Video Assisted Thorocostomy versus Fibrinolytic therapy urokinase, streptokinase, and alteplase (tissue plasminogen activator, tPA). PLUS Chest tube Outcome in children w normal lungs is excellent Early VATS decreases hosp stay and drainage Outcome similar VATS vs Fibrinolytic Rx A systematic review of 67 studies published between 1981 and 2004 regarding the treatment of empyema in children aggregated the data according to the mode of therapy (nonoperative versus primary operative) [16]. The results are summarized in the table (table 1). Treatment with antibiotics and tube thoracostomy was successful in 76 percent of patients. However, avoidance of surgery appears to occur at the expense of increased duration of chest tube (10.6 versus 4.4 days), hospital stay (20 versus 10.8 days), and antibiotic therapy (21.3 versus 12.8 days) and mortality (3.3 versus 0 percent).

72 One approach Drain acutely (no more than 10-20cc/kg) then observe (w Abx) w/o chest tube If reaccumulates---VATS/w chest tube (Texas Childrens) Antibiotics (IV until resolution of fever): Clindamycin alone Clindamycin + Cefotaxime Life Threatening: Vanco + Cefotaxime

73 Who Gets a Chest Tube? Large amounts of free flowing pleural fluid
Evidence of fibrinopurulent effusions (eg, pH <7.0, glucose <40 mg/dL [2.22 mmol/L], LDH >1000 IU [16.67 kat/L], positive gram stain, frank pus) Failure to respond to 48 to 72 hours of antibiotic therapy Compromised pulmonary function (eg, severe hypoxemia, hypercapnia )

74 References Pulmonary Edema Pulmonary Embolism
Pediatr Crit Care Med (3). Sespsis induced pulmonary edema: What do we know? Anesth Clinics North Am (2). General Pediatric Emergencies/Acute Pulmonary Edema. J of Int Care Med (3). Pediatric Acute Hypoxemic Respiratory Failure: Management of Oxygenation. NEJM : Acute Pulmonary Edema Pulmonary Embolism Johnson AS, Bolte R. Pulmonary Embolism in the Pediatric Patient. Ped Emer Care J (8) Hoppe et al. Pediatric Thrombosis. Ped Clin NA 2002;49(6) Monagle P. Antithrombotic therapy in children. Chest ;supp Wells PS et al. Use of a clinical model for safe management of patients with suspected pulmonary embolism. Ann Intern Med 1998;129:997 Monagle P. Outcome of pediatric throboembolic disease: a report from the Canadian childhood thrombophilia registry. Ped Res (6):763 Rathbun SW Sensitivity and specificity of helical computed tomography in the diagnosis of pulmnoary embolism: a systematic review. Ann Intern Med 2000;132:227. Girard P. et al. Am J Respir Crit Care Med ;164:1033 Van Ommen CH et al. Venous throboembolism in childhood: a prospective two year registry in the Netherlands. J Pediatr 2001;139(5):676

75 Source Unknown

76 Additional Source Information
for more information see: Slide 7, Image 1: Persian Poet Gal, "Blood Clot Diagram (Thrombus)", Wikimedia Commons, CC: BY-SA 3.0, Slide 7, Image 2: Please see original image of DVT/Pulmonary Embolism at Slide 8, Image 1: Please see original image of Pulmonary Embolism at Slide 9, Image 1: Please see original image of Pulmonary Embolism at Slide 9, Image 2: Source Unknown Slide 14, Table 1: Wells PS et al. Ann Intern Med ;129;997. Slide 22, Image 1: Source Unknown Slide 25, Image 1: Source Unknown Slide 25, Image 2: Source Unknown Slide 26, Image 1: Source Unknown Slide 26, Image 2: Source Unknown Slide 27, Image 1: Source Unknown Slide 29, Image 1: Source Unknown Slide 30, Image 1: Source Unknown Slide 31, Image 1: Source Unknown Slide 32, Image 1: Source Unknown Slide 33, Image 1: Source Unknown Slide 34, Image 1: Source Unknown Slide 34, Image 2: Source Unknown Slide 36, Image 1: Source Unknown Slide 38, Image 1: Anatomical drawing of Pulmonary Edema removed. Slide 38, Image 2: Source Unknown Slide 39, Image 0: Please see original image of [brief description] at [URL of original, if available]

77 Additional Source Information
for more information see: Slide 43, Table 1: Source Unknown Slide 44, Image 1: Source Unknown Slide 45, Image 1: Source Unknown Slide 48, Image 2: Source Unknown Slide 56, Image 1: Source Unknown Slide 68, Image 1: Source Unknown Slide 68, Image 2: Source Unknown Slide 68, Image 3: Source Unknown Slide 75, Image 1: Source Unknown


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