EDEMA PARU

dr Adyan Donastin, SpP

Kuliah FK UNUSA
 Pendahuluan

Definisi
 Akumulasi cairan di paru

 Menyebabkan gangguan pertukaran gas

Dapat terjadi akut atau gradual

 Gejala dan tanda
Akut
 Sesak nafas atau sulit bernafas berat

 Rasa spt dicekik atau tenggelam

 Suara mengi

 Cemas, restlessness

 Batuk dg dahak pink frothy

 Keringat banyak

 Pucat

 Nyeri dada jika karena penyakit jantung

 Gejala dan tanda lanjutan
Gradual, sering ok gagal jantung
 Sesak nafas bila ada aktivitas fisik

 Bangun wkt malam dg perasaan sesak yg hilang

dg posisi duduk
 BB naik cepat akibat akumulasi cairan dlm tubuh

 Capek

 Loss of appetite
 Penyebab
Kardiogenik:
 Coronary arterial disease

 Kardiomiopati

 Penyakit katub jantung

 Hipertensi
 Penyebab lanjutan
Non kardiogenik
 Infeksi paru : Pneumonia

 Paparan gas toksik : klorin, amoniak

 Penyakit ginjal : gagal ginjal

 Adverse drug reaction : morfin, kokain

 ARDS

 High altitude
 Edem paru akut

 Kardiogenik
 Non kardiogenik
 History and physical examination*
Cardiogenic APE Non-cardiogenic APE
Myocardial ischemia / infarction Pneumonia
Chronic systolic / diastolic failure Sepsis
Mitral / aortic valve dysfunction Aspiration of gastric contents
Volume overload Pancreatitis
S3 gallop Major trauma
Murmur of valvular stenosis / Multiple-blood transfusions
regurgitation Signs of infection / sepsis
Elevated neck veins Abdominal examination
Enlarged liver Warm extremities
Peripheral edema
Cold extremities

* Ware LB et al. The acute respiratory distress syndrome. N Engl J Med 2000; 342: 1334-1349
 Laboratory / Paraclinic testing*
Cardiogenic APE Non-cardiogenic APE
ECG: Toxicology screen
- giant negative T waves Lipase / amylase
- global T waves inversion Elevated troponin (severe sepsis)
- marked QT prolongation Blood gases abnormalities
- left ventricle hypertrophy Sepsis markers
Elevated troponin PCWP < 18 mmHg
Blood gases abnormalities
SIRS markers
PCWP  18 mmHg

* Ware LB et al. Acute pulmonary Edema. N Engl J Med 2005; 353: 2788-2796
Mekanisme
Normal Lung
Sistem pulmonalis
Cardiogenic Pulmonary Edema Non-Cardiogenic Pulmonary Edema
 Diagnosis
 Histori : riwayat penyakit jantung
 Pemeriksaan fisik: ronki basah akhir inspirasi

 Laboratorium:fungsi ginjal,CRP

 Foto toraks:untuk konfirmasi

Peningkatan cairan di dinding alveoli

Upper lobe diversion/vascular redistribution
Patchy alveolar infiltrate
 Terapi
Terapi awal dg mempertahankan oksigenasi
 High-flow oxygen

 Non invasive ventilation

 Mechanical ventilation

Terapi kausal
 ARDS
Acute Respiratory Distress Syndrome
 Permeability Edema
 multiple insults can cause increased pulmonary
vessel permeability resulting in leakage of fluid
and protein
 In its most severe form, the disease is a
combination of vessel permeability and DAD,
leading to the acute respiratory distress
syndrome (ARDS)
DAD (diffuse alveolar damage)
Definitions of the Acute Respiratory Distress Syndrome
Clinical Disorders associated with the ARDS
Normal Alveolus Acute Phase
of Acute Lung Injury or ARDS
Resolution of Acute Lung Injury and ARDS
 ARDS pathology
 Acutely, exudative
edema in the alveoli
causes hyaline
membrane formation
 Type II epithelial
cells then proliferate
and, usually, fibrosis
occurs
ARDS: Radiologic manifestations
 Patchy, diffuse ground glass opacities
 Pattern of opacification does not change with
position change, as the exudates are trapped in
alveoli
 Septal lines, peribronchial cuffing, and thick
fissures are usually ABSENT
 In severe cases, air bronchograms can be seen
 Good rule of thumb: presence of ET tube!
ARDS: Radiologic manifestations

Caution: While a normal sized heart and narrow

vascular pedicle are helpful signs, neither is
specific for injury edema
 ARDS
 Patchy diffuse
ground glass
 Air
bronchograms
 ET tube
 Terapi

 Terapi kausal:sesuai dengan penyakit dasar

 Respiratory support

 General supportive care

 TREATMENT OF
ACUTE LUNG INJURY / ARDS

 Mortality 35-40%  90% (with Sepsis)

 No Measures of Prevention
 Identify and Treat Potentially Reversible
Processes
 Oxygenation to Peripheral Tissues
 Ventilator
 High altitude
pulmonary edema
(HAPE)
 High altitude pulmonary edema
(HAPE)

 Rapid ascension above 3600-3900 m

 Majority of deaths due to high altitude disease
 Mechanism: exaggerated hypoxic pulmonary vasoconstriction (1)
 relative underproduction of nitric oxide
 exaggerated sympathetic activation  release of endothelin
 release of cytokines / mediators
 Genetic susceptibility (2)
1. Swenson ER et al. Pathogenesis of high-altitude pulmonary edema … JANA 2002; 287: 2228
2. Hotta J et al. Polymorphism of Renin-Angio-tensin system genes with HAPE. Chest 2004; 126: 825
 High-altitude pulmonary edema
(HAPE)

 Hypoxia causes non-uniform pulmonary

vasoconstriction, leaving other lung units over-
perfused and predisposed to edema
 Higher pressures can result in some capillary
damage and stress failure
 High-altitude pulmonary edema
 Radiographs show
patchy ground glass with
a central distribution
favoring peribronchial
cuffing and vascular
indistinctness over septal
lines
 HAPE - Treatment

 Oxygen
 Rapid descent
 Absolute bed rest
 Nifedipine – 10 mg s. lingual (1)
 Portable hyperbaric chamber (2)

1. Oelz O et al. Nifedipine for high altitude pulmonary edema. Lancet 1989; 2: 1241
2. Kasic F et al. A self-contained life support system designated for the use with a portable hyperbaric chamber. Biomed Sci Instrum 1989; 25:
79
HAPE – Hyperbaric chamber
 HAPE – Experimental therapies

 Sildenafil
 reduces pulmonary artery pressure
 Increase exercise capacity (1)
 Inhaled nitric oxide (2)

1. Ghofrani HA et al. Sildenafil increases exercise capacity during hypoxia … Ann Intern Med 2004; 141: 169
2. Richalet JP et al. Crit Care Med 2005; 171: 275
 HAPE - Prevention

 Slow ascent – and quick descent if necessary !

 Nifedipine: 20 mg BID prior to ascension  20
TID above 3300 m
 significantly lowered the incidence of HAPE
(1/10 vs 7/11) (1)
 High doses of inhalatory beta-agonists
 Salmeterol 2 x normal dose every 12 hours
 50 percent decrease in the incidence of HAPE
(2)
1. Bartsch P et al. Prevention of high-altitude pulmonary edema by nifedipine. N Engl J Med 1991; 325: 1284
2. Sartori C et al. Salmeterol for the prevention of HAPE. N Engl J Med 2002; 348: 1681
 Neurogenic
pulmonary edema
(NPE)
 Neurogenic pulmonary edema (NPE)

 Minutes to hours from a severe central nervous system

insult1
 Resolution in severeal days2
 Hemodynamic parameters (BP, CO, PCWP) usually
normal

1. Colin GL et al. Neurogenic pulmonary edema. Amm Rev Respir Dis 1984; 130: 941
2. Lagerkranser M et al. Neurogenic pulmonary edema – a review. Acta Med Scand 1982; 212: 267
Neurogenic pulmonary edema -
Etiology
 Neurogenic Edema
 Pathophysiology similar to HAPE– neural
mechanisms result in non-uniform
vasoconstriction
 High protein content of fluid indicates capillary
leakage involved as well
 Neurogenic Edema

 Classically, neurogenic edema has an upper lobe

predominance; however, it can present with any
pattern
 Often clears rapidly, arguing for intact alveoli
 Neurogenic Edema
 54 year-old woman
with intracranial
hemorrhage
 Note upper lobe
predominance
 NPE – Treatment (1)

 Outcome determined by the neurologic insult

 Oxygenation / Ventilation
 care at high PEEP
 influence on ICP
 influence on venous return and hemodynamics / CPP (1)
 possible role of prone position (2)
 Maintenance of low cardiac filling pressures – but care at cerebral
perfusion

1. Cohen NH. Ventilator management in the NICU. In: Critical Care, Kelly B, ed. American Academy of Neurology Course, Annual Meeting,
1996
2. Fletcher SJ et al. Use of prone ventilation in neurogenic pulmonary edema. Br J Anaest 2003; 90: 238
 NPE – Treatment (2)

 Alpha adrenergic antagonists - Phentolamine

 experimental models
 no human trials confirmed
 Beta adrenergic antagonists – experimental data (1):
 increase lymph flow
 reduce pulmonary vascular permeability
 Dobutamine – decrease in pcwp (2)
 Chlorpromazine – alpha blockade and other mechanisms (3)

1. Collin GL et al. Amm Rev Respir Dis 1984; 130: 841

2. Deehan SC et al. Haemodynamic changes in neurogenic pulmonary edema: Effect of dobutamine. Intensive Care Med 1996; 22: 672
3. Wohns RN et al. Chlorpromazine Treatment for neurogenic pulmonary edema. Crit Care Med 1985; 13: 2120
 Reexpansion
pulmonary edema
(REPO)
 Reexpansion pulmonary edema

 Usually unilaterally (1 )
 Post reexpansion after pneumo / hidrotorax (> 1,5 l)
 Minutes – 24 hours after the reexpansion
 Usually self limited; high mortality (up to 20%)
 Suportive treatment

1. Colucci WS. Noncardiogenic pulmonary edema. Uptodate online 2006; www.uptodate.com

 Reexpansion Edema

Right pneumothorax One-hour post chest-tube placement

Others……..
 Opiate overdose pulmonary edema

 Whithin two hours of heroin / methadone overdose (1)

 Complex pathophysiology:
 direct toxicity
 hypoxia
 acidosis
 cerebral edema
 Usually rapid resolution under assisted ventilation

1. Spover KA et al. Heroin - related noncardiogenic pulmonary edema: a case series. Chest 2001; 120: 1628
Salicylate toxicity pulmonary edema*

 In older patients with chronic salicylate intoxication

 Following aspirin overdose
 As a complication of volume resuscitation and sodium bicarbonate
used in the treatment of salicylate intoxication
 Hemodialysis – absolute indication

* Walters JS et al. Salicylate – induced pulmonary edema. Radiology 1983; 146: 289