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Kegawatan Respirasi

(Asma, ARDS, Neardrowning)

Dr. Angga MR, Sp.P

KSM Paru FK Universitas Jember / RSD Dr. Soebandi Jember


2018
Kegawatdaruratan Respirasi
1. Hemoptisis
2. Gagal napas (hipoksemik, hiperkapnik)
3. Pneumotoraks
4. Efusi pleura masif
5. Asma akut
6. PPOK eksaserbasi akut
7. Neardrowning (nyaris tenggelam)
Topik Bahasan
1. Asma akut
2. ARDS ➔ Gagal napas hipoksemik
3. Neardrwoning / tenggelam
ASMA
EKSASERBASI AKUT
PENDAHULUAN

salah satu penyebab utama kasus


kegawatdaruratan dan rawat inap

Pemahaman
EKSASERBASI/ patofisiologi,
terapi
SERANGAN ASMA meningkat

alasan utama pasien untuk


mencari pertolongan Kaplan AG, Balter MS, 2009
DEFINISI

Penyakit inflamasi kronik saluran napas dengan banyak


sel yang berperan terutama sel mast, sel epitel, eosinofil,
limfosit T, makrofag, dan neutrofil. Pada individu
rentan proses tersebut menyebabkan wheezing
berulang, sesak napas, dada terasa penuh (chest
ASMA
tightness), dan batuk terutama malam dan atau
menjelang pagi

EKSASERBASI ASMA
episode peningkatan sesak napas, batuk, mengi, rasa berat di
dada, atau kombinasi gejala-gejala tersebut

STATUS ASMATIKUS
keadaan kegagalan atau tidak respons pada serangan asma
yang telah diterapi secara adekuat baik di unit rawat jalan
maupun di unit gawat darurat
Definisi asma
• Global Initiative for Asthma (GINA) 2018:
“Penyakit heterogen berkarakteristik
gangguan inflamasi kronik saluran napas,
ditandai gejala pernapasan mengi, sesak
napas, rasa berat di dada, & batuk yang
intensitasnya bervariasi dari waktu ke
waktu, disertai keterbatasan aliran udara
ekspirasi yang bervariasi.”
PATOFISIOLOGI
HIPER
RESPONSIF
SAL.NAPAS HIPER
EDEMA
SAL. NAPAS SEKRESI
MUKUS

AIRWAY
BRONKO
REMODEL-
KONSTRIKSI LING
HAMBATAN ALIRAN
UDARA
BAKTERI
VIRUS RESPIRASI/HRV
(M.pneumonie,C.pneumoniae

OBAT, Krisis emosi Alergen,polutan

EKSASERBASI
PDPI,2003: Gilbert TW, Denlinger LC. Role of Infection in The development and Exacerbation of Asthma. NIH Public Acces.Expert Rev
Respir Med. 4. 71-83.2010
What is Asthma?
Patogenesis Asma
Faktor Risiko

• Family History of asthma


• Prematuritas saat bayi
• Rase (African dan Native Americans )
• Sosioekonomik rendah
• Urban settings (polutan)
• Indoor irritants (cigarette smoke, dust mites, pets,
recycled air AC)
• Riwayat Atopi (eczema, alergi dan rhinitis /
sinusitis kronik)
Differential Diagnosis Wheezing
• Asma
• Bronkiolitis (infants), bronchitis,
laryngotracheobronchitis, tracheitis
• Aspirasi benda asing
• Fungsional abnormalitas ( GERD, CF, BPD,
immunodeficiency, dll)
• Struktural abnormalitas ( laryngo-tracheomalacia,
vascular rings, tracheal stenosis / webs, tumors, dll )
Fenotip asma
1. Asma alergi (eosinofilik)
2. Asma non-alergi (neutrofilik)
3. Late-onset asthma
4. Asthma with fixed airflow
limitation
5. Asma obesitas
ASMA AKUT SEDANG
PERBEDAAN KAPASITAS PERTAHANAN ANTIVIRUS SEL EPITEL BRONKIAL NORMAL
DGN SEL EPITEL BRONKIAL ASMATIK
Holgate ST, Robert G. The Role of Airway Epithellium and its interaction with Environmental Factor in Asthma Pathogenesis. Proc Am Thorac Soc
Vol 6 pp 665-659. 2009
KONTROL ASMA YANG JELEK Disfungsi psikologis ( psikosis,
kecemasan, depresi)

Riwayat rawat inap akibat asma Pemakaian bronkodilator dgn dosis


yg makin meningkat

Disfungsi psikologis ( psikosis, Riwayat pemakaian kortikosteroid


kecemasan, depresi) oral sebagai pengontrol

Penyakit Kardiovaskular dan penyakit


Sosio-ekonomi rendah
Paru kronis

Risk factor
Fatal acute asthma
Hodder R, Lougheed D. Management of acute asthma in adults in the emergency department : nonventilatory
management. In Canadian Medical Association Journal, 2010.
MANIFESTASI KLINIS
Tabel 1. Gejala dan tanda umum asma akut/eksaserbasi
(dikutip dari: Hospital Physician,2006)

GEJALA DAN TANDA EKSASERBASI ASMA


Subyektif Obyektif
Dyspneu Takipnea ( berat, > 30x/mnt)
Batuk Takikardi ( berat, > 120x/mnt)
Wheezing Upright positioning
Rasa berat di dada ( chest Pulsus paradoksus ( berat, >
tightness) 12mmhg)
Diaphoresis Retraksi sternokleidomastoid
Produksi sputum Perubahan derajat kesadaran
Payah ( exhaustion) Telegraphic speech

(dikutip dari: Hospital Physician,2006)


MANIFESTASI KLINIS
Suatu penelitian pernah menyebutkan bahwa 10% penderita 1
asma akut tidak merasakan sesak napas, tetapi hanya
merasakan batuk dan didapatkan wheezing.

Penderita biasanya menyadari timbulnya serangan asma ini 1


apabila FEV1 sudah mencapai 50% atau lebih dari nilai normal
atau saat residual volume mencapai hingga 200% normal

1
Suatu fakta dalam penelitian, didapatkan hasil, 90 % penderita
yang merasa dirinya asimtomatik, ternyata 40% dari mereka
didapatkan wheezing.

2
Obstruksi berat Wheezing
1.Young DJ, Salzman GA. Status Asmaticus in adult Patients.Clinical Review Article in Hospital Physician. 2006
2.Kotaru C,McFadden ER. Acute exacerbations of asthma. In Asthma and Chronic Obstructive Pulmonary diseases. Basic
Mechanism and Clinical Management. Edited by Peter Barnes, Jefrfrey Dazen.2008
PENILAIAN DAN EVALUASI

TATALAKSANA EKSASERBASI ASMA DIMULAI DGN PENILAIAN


DERAJAT BERAT SERANGAN DAN EVALUASI YG MELIPUTI RISK
FACTOR FATAL ASTHMA*

OKSIGENASI & BRONKODILATOR


KECUALI SERANGAN BERAT DAHULUKAN*
DIAGNOSIS BANDING EKSASERBASI ASMA**
1. Obstruksi jalan napas atas
2. Aspirasi benda asing
3. Sindroma disfungsi korda vokalis
4. Edema paru
5. PPOK eksaserbasi akut
6. Reaksi Konversi hysterik

*Jain DG, Singal SK, Clark RK. Understanding and managing Acute Severe and Difficult Asthma. In Clinical Medicine. Journal Indian Academy of
Clinical Medicine. Vol.7.2006

**Hodder R, Lougheed D. Management of acute asthma in adults in the emergency department : nonventilatory management. In Canadian
Medical Association Journal, 2010.
EVALUASI SAAT
EKSASERBASI
ana • Onset, penyebab potensial, keparahan gejala, respon terhadap pengobatan
mne sebelum masuk IGD, riwayat penyakit dan hospitalisasi asma, serta penyakit
penyerta.
sis
• Menilai tingkat keparahan eksaserbasi dan status pasien secara keseluruhan,
Pem. termasuk kesadaran, status cairan, sianosis, distres napas dan mengi
fisik • Identifikasi kemungkinan komplikasi yang timbul, seperti pneumonia,
pneumotoraks, dan pneumomediastinum

• Pengukuran serial fungsi paru yang dilakukan saat datang, dan diulangi 30 dan 60 menit
Fx setelah terapi awal, sangat penting dalam penilaian tingkat keparahan eksaserbasi.
• Pada asma eksaserbasi berat dan mengancam jiwa, tes fungsi paru di triase tidak
paru dianjurkan.

• Umumnya pasien dengan eksaserbasi asma tidak memerlukan pemeriksaan laboratoium


Lab • Diindikasikan untuk mendeteksi gagal napas, toksisitas teofilin, atau konsisi yang
mempersulit pengobatan asma (penyakit kardiovaskuler, pneumonia, atau diabetes)

24
Camargo CA, Rachelefsky G. Managing Asthma Exacerbations in the Emergency Departement. Summary of the National
Asthma Education and Prevention Program Expert Panel. Proc Am Thorac Soc. Vol.6.357-366. 2009
WASPADAI HENTI NAPAS

• Kesadaran menurun, gerak napas torakoabominal,


tidak terdengar suara napas mengi (wheezing)
dan bradikardia
• Tidak didapatkan pulsus paradoksus oleh karena
keletihan otot pernapasan

A silent chest is a medical emergency (so severe


obstruction that there is no airflow to cause
wheezes)
25
Severe asthma attack

• Eksaserbasi akut dari asma yang tidak respon


dengan pengobatan standar
• Gejala mencakup sesak dada, sesak napas yang
progresif, batuk kering, penggunaan otot
aksesori
• Episode mengancam jiwa, darurat medis
• Dapat menyebabkan gagal napas

STATUS
26
ASMATIKUS
GAMBARAN KLINIS SEVERE ASTHMA
Feature Severe attack Life theatening
Breathless At rest Cyanosed at rest

Speech Words or phrases Too breathless to


speak
Alertness Agitated Drowsy,confused

Resp rate > 25 x Tends to slowdown

Pulse >110x May progressively


slow with shock
Wheeze Loud Silent chest

PEF/FEV1 < 33%,respons thd b < 20%, sedikit/tak


dilator jelek respons thd b dilator
Paco2 < 40 mm Hg > 40 mm Hg
27
PEMERIKSAAN PENUNJANG
FOTO TORAKS
• A chest x-ray should be obtained on any patient with
severe status asthmaticus
• In order to define the extent of the associated
parenchymal disease, any evidence of extra-alveolar air
(pneumothoraces, pneumomediastinum), and to
differentiate other disease entities.
• Patients who have less severe disease may not require
• CXR depending on presence or absence of other
indications (ie, fever).
TANPA MENUNDA
TERAPI
28
BLOOD GASES (BGA)

• Not always indicated during as asthma exacerbation.


• A blood gas is indicated if:
a. You cannot determine the severity of the exacerbation
b. You believe the patient is worsening substantially and
you want to quantify the degree of worsening
c. Serial blood gases may be necessary to evaluate
progression of disease if you feel the patient is difficult to
evaluate clinically.

TANPA MENUNDA
TERAPI
29
MEDIKASI
Pra-rumah sakit
Inhalasi β2 agonis kerja singkat 2-4 puff tiap 20 mnt pd 1 jam
pertama. Setelah satu jam pertama, dosis β2 agonist tergantung
pada derajat berat eksaserbasi. Pada eksaserbasi ringan
dilanjutkan 2-4 puff tiap 3 hingga 4 jam. Eksaserbasi sedang
memerlukan 6-10 puff dalam 1 sampai 2 jam. Glukokortikoid oral
sebaiknya diberikan

OKSIGENASI Penanganan di RS
Saturasi dipertahankan minimal 92%

Β2 AGONIS KERJA SINGKAT


Obat utama, per inhalasi sangat dianjurkan,kontinyu pd 1 jam pertama
Pemberian dg antikolinergik, memberikan perbaikan fungsi paru dan
menurunkan angka rawat inap
GINA 2013
KORTIKOSTEROID SISTEMIK
• HARUS DIBERIKAN PADA SEMUA DERAJAT EKSASERBASI,KECUALI DERAJAT
RINGAN
• DERAJAT RINGAN DIBERI KORTIKOSTEROID SISTEMIK BILA: TDK RESPONS
β2 agonist DAN ATAU RIWAYAT KORTIKOSTEROID ORAL
SEBELUMNYA

TERAPI LAIN
• Direkomendasikan pd serangan berat yg
tdk respons pd β2 agonist dan
MgSO4 Kortikosteroid sistemik
• Pertimbangan efiksasi, aman, murah

• Dipertimbangkan bila curiga


Antibiotik ada infeksi bakterial
Short Acting β2 Agonis (saba)
• Inhalasi SABA : drug of choice
• Acute attack: perlu dosis yang lebih besar dan
beberapa kali pemberian
• Nebulizer salbutamol 2,5 mg/ 20 menit → 3 x
• Dilanjutkan tiap jam dlm bbrp jam pertama
• SABA subcutan: bila px tidak respon dgn tx
inhalasi yg adekuat
• SABA IV : tidak rutin diberikan. per individu( tak
respons dg inhal/sc dan gagal napas )
KORTIKOSTEROID
• Meta analisis 700 artikel:
Me↓ angka MRS
Me ↓ relaps dlm 7-10 hari yg akan datang
• Dosis dan cara pemberian: masih kontroversi
• Dosis rendah: manfaat kurang
tinggi : manfaat tambahan ?
• Rekomendasi
• Prednison: 30 mg/6-8 jam
• Metil pred : 40-120 mg/6-8 jam dlm 48 jam
diturunkan menjadi :60-80 mg/hari
OKSIGEN
• Oxygen is a drug. It has benefits and
complications associated with its use.
• Asthmatics are hypoxic due to ventilation-
perfusion mismatch (V/Q mismatch).
• If the V/Q mismatch is severe, and full
saturation is not neccessary. Oxygen is directly
toxic to the lung in high concentrations (>50-
60% for >24 hours),
• Low-flow O2 ( 1-3 L/mt nasal ): safe practice
• O2 1-3 L/mt → Sat < 90 % : BGA
34
ANTIKOLINERGIK
• Anticholinergic agents. Ipatroprium bromide
(Atrovent) (0.25-0.5mg q4-8h).
• Anticholinergic agents are believed to work by
blocking the irritant receptors and inhibiting
cGMP metabolism, which results in
bronchodilation
• Bukan sebagai first-line agent
• Efek bronkodilatiasi < Saba pd peak effect
• Ipratropium br : optimal dose? 0,25 mg-0,5 mg
utk nebulizer
TEOFILIN
• Inferior dibandingkan SABA sebagai monoterapi di
UGD
• Perbaikan FEV1 & durasi terapi sebelum KRS (Terapi
UGD) < SABA
• Loading dose: 5-6 mg/Kg BB IV dlm 15-20 mt
• Maintenance: 0,5 – 0,9 mg/Kg BB/jam
• Serum level : 8-12 ug/ml
TERAPI LAIN

Hidrasi agresif tidak dianjurkan untuk orang dewasa,


namun mungkin cocok untuk bayi dan anak-anak
yang mengalami dehidrasi akibat dari laju napas yang
meningkat dan penurunan asupan oral.**

SEDATIF = LARANGAN*
Mukolitik? Chest fisioterapi?
PERHATIAN
Gagal napas→ intubasi

* GINA,2013
**Camargo CA, Rachelefsky G. Managing Asthma Exacerbations in the Emergency Departement.
Summary of the National Asthma Education and Prevention Program Expert Panel. Proc Am Thorac Soc.
Vol.6.357-366. 2009
INTUBASI
• indikasi: pasien dengan presentasi apnea atau koma,
hiperkapnia persisten atau meningkat, kelelahan, depresi
status mental.
• Konsultasi dan kerja sama dengan anestesi dalam
manajemen ventilator
• Pada saat intubasi, volume intravaskular harus
dipertahankan atau diganti karena hipotensi umumnya
menyertai inisiasi ventilasi tekanan positif.
• Ventilator tekanan tinggi harus dihindari, karena resiko
barotrauma.

-Camargo CA, Rachelefsky G. Managing Asthma Exacerbations in the Emergency Departement. Summary of the National
Asthma Education and Prevention Program Expert Panel. Proc Am Thorac Soc. Vol.6.357-366. 2009
Penanganan Asma Eksaserbasi di
Rumah Sakit
Penilaian Awal
Anamnesis, PF (auskultasi, penggunaan otot bantu napas, denyut jantung, frekuensi
napas),
APE atau VEP1 , saturasi oksigen, dan tes lain yang diperlukan

Terapi Awal
• Inhalasi β2-agonis kerja cepat secara terus menerus selama 1 jam.
• Oksigen sampai tercapai saturasi O2 > 90% (95% pada anak-anak)
• Steroid sistemik jika tidak ada respons segera, atau jika pasien sebelumnya
sudah menggunakan steroid oral atau jika derajat keparahan sudah berat
• Sedasi merupakan kontra-indikasi terapi asma eksaserbasi.

Penilaian Ulang setelah 1 jam


APE, saturasi Q2, tes lain yang diperlukan

GINA Updated
2013
lanjutan ….
Penilaian Ulang stlh 1 jam

Derajat Sedang Derajat Berat


• APE 60-80% dari yang diperkirakan • APE < 60% dari yang diperkirakan
• Pem. Fisik : gejala sedang, penggunaan • PF: gejala berat saat istirahat, retraksi dada
otot bantu pernapasan • Riwayat faktor resiko mendekati asma yang
fatal
• Tidak ada perbaikan setelah terapi awal
• Oksigen
• Inhalasi β2-agonis dan anti-kolinergik • Inhalasi β2 -agonis dan anti-kolinergik
setiap 60 menit • Oksigen
• Glukokortikosteroid oral • Glukokortikosteroid sistemik
• Teruskan terapi 1-3 jam jika ada perbaikan • Magnesium IV

Penilaian Ulang stlh 1-2 jam

Respons tidak baik Respons buruk


Respons baik
selama 1-2 jam selama 1-2 jam
Ref. GINA
Updated 2013
Respons Baik Respons tidak lengkap Respons jelek
• Bertahan 60 menit setelah selama 1-2 jam selama 1 jam
terapi terakhir • Pasien resiko tinggi
• Pasien resiko tinggi • PF: gejala berat, kesadaran
• PF : normal
• PF: gejala ringan-sedang menurun, kebingungan
• APE > 70%
• APE < 70% • APE < 30%
• Tidak stres
• Saturasi O2 tidak membaik • PCO2 > 45mm Hg
• Saturasi O2 > 90%
(95% pada anak-anak) • PO2 < 60mm Hg

Pulangkan ke Rumah
Rawat Rumah Sakit Rawat di ICU
• Lanjutkan β2-agonis inhalasi
(acute care setting) • Inh β2-agonis + anti-kolinergik
• Pertimbangkan steroid oral • Steroid IV
• Pertimbangkan inhaler • Inh β2-agonis ± anti-kolinergik
• Pertimbangkan β2 -agonis IV
kombinasi • Steroid sistemik • Oksigen
• Edukasi pasien: • Oksigen
• Pertimbangkan teofilin IV
Cara pakai obat yang benar • Magnesium IV
• Intubasi dan ventilasi mekanik
Buat rencana aksi • Monitor APE, saturasi O2 , nadi
jika perlu
Follow-up teratur

Perbaikan Tidak
Kriteria bisa dipulangkan membaik Rawat di ICU
• jika APE > 60% dari yang Jika tidak ada perbaikan
setelah 6-12 jam
diperkirakan
• Kondisi tetap pada saat
terapi oral / inhalasi
PENILAIAN ULANG & PEMULANGAN

RESPON •sebaiknya diobservasi selama 30-60 menit


S BAIK untuk memastikan stabilitas respons

PEMULAN •Bila APE (PEFR) minimal 70% Prediksi atau nilai


GAN terbaik

• Diberikan sistemik(oral) antara 3-10 hari pasca


KORTIK pemulangan.
OSTER • Kepatuhan rendah → depo intramuskuler lebih baik
OID

- GINA,2010
-Camargo CA, Rachelefsky G. Managing Asthma Exacerbations in the Emergency Departement. Summary of the National
Asthma Education and Prevention Program Expert Panel. Proc Am Thorac Soc. Vol.6.357-366. 2009
EDUKASI

Edukasi umum: untuk membantu pasien


mengenali dan merespon gejala asma.

• Tinjauan terhadap teknik penggunaan inhaler

• Rujukan untuk tindak lanjut

• Rencana terapi saat pemulangan

Camargo CA, Rachelefsky G. Managing Asthma Exacerbations in the Emergency Departement. Summary of the
National Asthma Education and Prevention Program Expert Panel. Proc Am Thorac Soc. Vol.6.357-366. 2009
ICU Management
• Continuous Salbutamol
• Kortikosteroid iv
• Magnesium Sulfate (IV)
• IV Terbutaline or Epinephrine
• Ketamine
• Intubation for respiratory failure
TERAPI ASMA STABIL
• CONTROLLER
Inhalasi Glukokortikoid

• GINA 2013
• Leukotrien modifier
• Long acting inhaled / oral β2 agonis
• Sustained release theophylin
• Anti Ig E (omalizumab)

RELIEVER
• Rapid Acting inhaled β2 agonis
• Theopyline
• Antikolinergik
Derajat kontrol asma
Tatalaksana asma (stabil)
ARDS
(Acute Respiratory Distress Syndrome)
ARDS
(Acute Respiratory Distress Syndrome)
• Definisi
• Patogenesis
• Penyebab
• Diagnosis ARDS
• Tatalaksana ARDS
Definisi (The Berlin Definition)
• “acute diffuse, inflammatory lung injury,
leading to increased pulmonary vascular
permeability, increased lung weight, and
loss of aerated lung tissue…[with]
hypoxemia and bilateral radiographic
opacities, associated with increased venous
admixture, increased physiological dead
space, and decreased lung compliance.”
ARDS Patogensis
PENYEBAB ARDS
▪ Sepsis • Aspiration
▪ Severe trauma • Pneumonia
▪ Surface burns • Pulmonary
▪ Multiple blood contusion
transfusions • Pulmonary
▪ Drug overdose embolism
▪ Following bone • Inhalational injury
marrow • Near drowning
transplantation
▪ Multiple fractures
Diagnosis ARDS (The Berlin Definition)
ARDS
Clinical Presentation

▪ Dyspnea, Tachypnea
▪ Persistent hypoxemia, despite the
administration of high concentrations of
inspired oxygen
▪ Increase in the shunt fraction
▪ Decrease in pulmonary compliance
▪ Increase in the dead space ventilation
Basic Management Strategies for Patients
with ALI/ARDS

▪ Identify and treat underlying causes


▪ Ventilatory support
▪ Lung protective ventilatory support strategy
▪ Application of PEEP
▪ Restore and maintain hemodynamic function
▪ Conservative fluid replacement strategy
▪ Vasopressors and inotropics support
▪ Prevent complications of critical illness
▪ Ensure adequate nutrition
▪ Avoid oversedation
▪ Using weaning protocol with spontaneous breathing trials
▪ Continous use of steroids for fibroproliferative phase ?
questionable
Prone Positioning

▪ Relieves the cardiac and abdominal


compression exerted on the lower lobes
▪ Makes regional Ventilation/Perfusion ratios
and chest elastance more uniform
▪ Facilitates drainage of secretions
▪ Potentiates the beneficial effect of
recruitment maneuvers
Near Drowning
Near drowning

• Definisi
• Patogenesis
• Penyebab
• Diagnosis ARDS
• Tatalaksana ARDS
Definisi
• 2002, World Congress on Drowning,
Amsterdam: “respiratory embarrassment
from submersion / immersion in a liquid
medium”

“near drowning”
“dry or wet drowning”
“secondary drowning”
“delayed onset respiratory distress”
Vocabulary
• Drowning – death within 24 hours

• Near-drowning – survival past 24 hours


Pathophysiology of Drowning
• Submersion
• Panic and Flailing (if conscious)
• Inhalation and aspiration or laryngospasm
• Hypoxia
• Cardiopulonary arrest
Who?
• Usually young, healthy individuals
2006 Drowning
• U.S.A. – 5000 died
• Worldwide – over 100,000 died
Tiga korban terbanyak
• Toddlers

• Adolescents

• Elderly
Toddlers drown..where???
• Toilets

• Bathtubs

• Buckets
Coastal Areas
• Swimming pools more likely
Adolescents
• Stupidity
Young Adults
• Alcohol
– 40% adult drownings
– 75% boat drownings
Elderly
• Lack of instability
• Reduce vision
Drowning Pathophysiology: Pulmonary
• Aspirate small amounts (22ml/kg)
➢Fluid shifts
➢Aspiration of debris
➢Infection (rare)
➢Surfactant depletion
• Pulmonary oedema, pneumonia (25-50%),
ARDS < 10%
←Neurogenic
←Altered capillary permeability
←Forced inspiration against a closed glottis
←Surfactant dysfunction
Near Drowning Pathophysiology
• Hypoxic episode interrupted with ROSC
• End organ damage with
– ARDS (often delayed)
– Hypoxic encephalophy
– Renal failure (ATN)
– Pancreatic necrosis
– DIC
– Cardiac dysrrhythmias
Fresh Water Inhalation (90%)
• Hypotonic load to alveoli
• Water absorbed into circulation
• Surfactant washout
• Alveolar cell damage
• Chemical pneumonitis, pulmonary edema
• Hypervolemia
• Hyponatremia
• Hemodilution
• Hemolysis
Salt Water Inhalation (10%)
• Hypertonic load to alveoli
• Protein rich effusion into alveoli
• Surfactant damage, alveolar basement
membrane damage
• Alveolar cell damage
• Chemical pneumonitis, pulmonary edema
• Hypovolemia
• Hypernatremia
• Hemoconcentration
Salt versus Fresh Water
• Modell, series of 91 near drowning victims
• No significant electrolyte abnormalities
• No difference in treatment, but be vigil
• Differences in bacteria, chemical
composition (chlorine), and temperature of
the aspirated water more significant
• Conn: Animal model
Hypothermia
• Water conduction of heat
• Pulmonary heat exchange
• Cold water absorption
• Temperature of water a factor in fresh water
near drowning
• Symptoms vary with degree of hypothermia
• Is hypothermia destructive or protective?
Prognostic Factors
• Submersion Time?
• Level of hypothermia?
• CPR?
• Mental Status?
• Combinations?
Prognosis
• No CPR
– May develop ARDS
• Bystander CPR
– Steady recovery
– Steady decline
• Late ED CPR
– Very poor prognosis
Complicating Factors
• Spinal cord injury
• Hypothermia
• Panicking
• Syncope
• Seizures
Dry-drowning
• 10-20% of submersions
• Laryngospasm
• Hypoxia
• Loss of consciousness
Wet-drowning
• Aspiration of water
• Dilution of surfactant
• Diminished gas transfer
• Atelectasis
• Ventilation perfusion mismatch
Pulmonary Injury
• Contaminated foreign material
• Particulate matter
• Bacteria
• Vomitus
• Chemical irritants
Two extremes
• Fair cardiovascular and neurological
function
– Minimal disability
• Unstable cardiovascular function and coma
– Poorly
– Hypoxic CNS injury
End Organ Damage
• Renal injury
– Hypoxia
– Myoglobinuria
– Hemoglobinuria
• Hematologic
– Hemolysis
– DIC
Treatment
Prehospital Care
• Resuscitation
– Time optimizes outcome
• Removal from water
– C-spine protection
• CPR As Soon As Possible
Airway
• Breathing
– High flow oxygen by facemask
• Not Breathing
– Bag valve mask
– Endotracheal tube
• Unconscious
• Protect from aspiration
Who to transport?
• Amnesia
• Loss or depressed consciousness
• Period of apnea
• Period of artificial respirations
• Even if asymptomatic
Don’t Forget
• Warm patient
– Hypothermia
• Monitor
– Vital sign, saturation O2
• IV access
– Warm isotonic fluids
Terapi IGD
• Continue care
– Airway
– Oxygen
– Ventilation
– Warmed fluids
– Warming adjunts
– Treat associated injuries
GCS > 12
• Oxygen to keep sat > 95%
• Observe 4-6 hours
• Pulmonary exam normal
• Saturation normal
• Discharge home
• No xray or labs needed
GCS < 13
• High flow oxygen
• Intubation for low PaO2
• CXR, Labs
• Continuous cardiac monitoring
• Frequent reassessments
Seizure
• Dilutional hyponatremia
• Control seizures
• Correct electrolytes
• Residual disorder uncommon
Emergency Department Arrest
• Warm water drowning
• Recovery doubtful
• Consider early discontinuation of efforts
• Risk profound neurological handicaps
Hospital Management
• Supportive
• Avoid ARDS
• Pneumonia rare
• Dopamine, epinephrine drips
• 48 hour window
No benefit
• Mannitol
• Loop diuretics
• Hypertonic saline
• Fluid restriction
• Hyperventilation
• Controlled hypothermia
• Barbiturate coma
Prevention
• Infants
– Parental vigilance
• Toddler
– Pool fencing
• Adolescent/Young Adult
– Control Alcohol/Drug Use
– Swimming lessons
• Elderly
– Same as infant/toddler
Predictors of Death or Severe Neur Impairment After Submersion

At site of submersion
• Immersion duration > 10’
• Delay in commencement of CPR
In the ED
• Asystole on arrival or CPR duration > 25’
• Fixed and dilated pupils and GCS < 5
• Fixed and dilated pupils and arterial pH < 7
In the ICU
• No spontaneous purposeful movements and abnormal
brainstem function 24h after immersion
• Abnormal CT scan within 36h of submersion

Oh’s Intensive Care Manual, 6th Ed 2009


Drowning: PICU Management
• Ventilation: normocapnia, optimise oxygenation,
minimise VILI
• Circulation: fluids, inotropes, monitoring to optimise
haemodynamics, perfusion
• Prophylactic anticonvulsants? No evidence
• Continuous EEG monitoring of unconscious pt
• Glucocorticoids? No evidence (Foex, ADC, 2002) ?
↑infection, ?? role later if ARDS
• Prophylactic antibiotics? No evidence (Wood, ADC, 2010)
even with CXR changes…selects resistant bugs
• Therapeutic Hypotherrmia “Cooling” ?
Conclusions
• Neardrowning is a common cause of
accidental death
• Remember:
– Initiate ventilation early
– Don’t forget trauma as a cause
– Aggressive treatment of complications:
• Head, Lung, and Temperature

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