The document discusses the Department of Internal Medicine at Hasanuddin University in Makassar, Indonesia. It outlines the department's vision to become an excellent, independent, and maritime-focused center for training specialists in internal medicine by 2026. It aims to provide evidence-based, research-oriented education and high quality healthcare while increasing the quantity and quality of internal medicine research at the national and international levels. The department also aims to implement a digitalized and transparent system for managing its internal medicine program.

1. DEPARTMENT OF INTERNAL MEDICINE
HASANUDDIN UNIVERSITY
Mahadhir Md Jangnga
DEPARTEMENT OF INTERNAL MEDICINE
FACULTY OF MEDICINE
HASANUDDIN UNIVERSITY MAKASSAR
2022

2. Menjadi pusat Pendidikan yang unggul, mandiri, berwawasan
benua maritim untuk menghasilkan Dokter Spesialis Penyakit
Dalam yang humanis dan mampu bersaing secara regional,
nasional maupun global pada tahun 2026 dengan didukung
oleh Sumber Daya Manusia yang professional dan
bertanggung jawab
VISI

3. 1. Menyelenggarakan Pendidikan di bidang Ilmu Penyakit Dalam
berbasis evidence-based medicine, riset dan berwawaran
benua maritim
2. Memberikan pelayanan Kesehatan di bidang Ilmu Penyakit
Dalam yang humanis, paripurna dan bermutu
3. Meningkatkan kuantitas dan kualitas penelitian dasar dan
aplikatif Ilmu Penyakit Dalam yang bertaraf nasional dan
internasional
4. Menerapkan system digitalisasi pada proses Pendidikan dan
manajemen Program Studi Ilmu Penyakit Dalam yang
transparan, akuntabel, responsible, independent, terintegrasi
dan berkeadilan
MISI

7. Diagnostic criteria fro ALI and ARDS
ALI ARDS
Onset Acute Acute
Oxygenation (PaO3/FiO2) ratio
in mmHg,
<300 <200
Chest Radiologi appearance Bilaeral Pulmonary infiltration
which may or may not be
symetrical
Bilaeral Pulmonary infiltration
which may or may not be
symetrical

10. Patogenesis
• The initial (early) phase of ALI/ARDS is characterized by increased
permeability of the endothelial and epithelial barriers of the lung
• accumulation of protein-rich and highly cellular edema fluid in the
interstitium and alveoli.
• The inflammatory cells, lung epithelial cells, and fibroblasts produce
cytokines that amplify the inflammatory response.
• Procoagulant pathways are up-regulated and fibrinolysis is depressed,
leading to extravascular and intravascular fibrin deposition
• Intravascular fibrin deposition and thrombin formation lead to vascular
obstruction and alterations in the microvasculature

11. • Acute fase
• Resolusi fase
• Fibrotic fase

15. Management ALI & ARDS
• A. Non Pharmacologic
1. Mechanical Ventilation
- Lower Tidal Volume <10 mL/kg.
- Positive End-Expiratory Pressure (PEEP)
2. Hemodynamic Management
- A lower vascular filling pressure/volume status prioritizes the lungs
(reduced pulmonary edema, improved compliance, better gas
exchange) -> Fluid balance negative, The recommendation to use
lower tidal volume (less than or equal to 6 mL/kg predicted body
weight) ventilation with a plateau pressure less than or equal to 30
cmH2O
- A higher vascular filling pressure/volume status prioritizes cardiac
output, organ perfusion (improved kidney function, etc), and oxygen
delivery.

16. • B. Pulmonary Targeted Pharmacologic
1. Surfactant Therapy, not be effective in improving survival rate,
because patients with ALI/ARDS usually die of sepsis and multiple
organ failure.
2. Inhaled Vasodilators, vasodilate pulmonary vasculature in the
ventilated regions of the lungs result in a decrease in pulmonary
artery pressure, a decrease in right-to-left shunting, and an increase
in PaO2/FiO2.
- Nitric oxide (NO), has no impact on important clinical outcomes and
should not be recommended as standard therapy of ARDS. Because NO does
transiently improve oxygenation.
- Inhaled Prostacyclins, derivatives of arachidonic acid cause vasodilation,
inhibit platelet aggregation, and have anti-inflammatory. there is no evidence
that inhaled prostacyclins improve survival in patients.

17. • C. Systemic Pharmacologic Therapy
1. Vasodilator: Intravenous prostaglandins cannot be recommended for
treatment of patients with ALI/ARDS
2. Anti-inflammatory Agents:Glucocorticoid, anti-inflammatory and
antifibrotic properties, Ketoconazole, Lisofylline and Pentoxifylline
3. Antioxidant Therapy: N-acetylcysteine, Procystein, and albumin
4. Anticoagulant Therapies:
5. Agen vasoactive: β2-Adrenergic Agonist
6. Keratinocyte Growth Factor

18. . Glucocorticoid
- Therapy of Early ARDS:
double-blind placebo controlled trial of early corticosteroid therapy for ARDS is a study by
Bernard et al. Metylprednisolon(30 mg/kg intravenously every 6 hours) The mortality rate
at 45 days was 30/50 (60%) in the MPSS group and 31/49 (63%) in the placebo group (P =
0. 74).
- Late-Phase ARDS :
Based on a presentation of the results of the Late Steroid Rescue Study at the American
Thoracic Society meeting in May 2005 in San Diego, was not different between the placebo
and the methylprednisolone-treated groups.
- Conclusion
current evidence suggests that glucocorticoids should not be used in prevention (evidence
level I, grade B) or therapy of either early (evidence level II, grade D) or late (evidence level
I, grade B) phases of ALI/ARDS

20. • Anticoagulant Therapies:
• 1. Heparin, anticoagulant not only has an effect in the process of
coagulation and fibrin deposition, moreover heparin is able to
modulate the inflammatory process in ARDS binding to
proinflammatory cytokines, chemokines and complement factors in a
nonspecific manner.
• 2. Aspirin, Aspirin is a nonselective inhibitor of the cyclooxygenase
pathway and could reduce the formation of fibrin pathological
process due to reduce in platelet recruitment and in inflammation

21. • Agen vasoactive :
• β2-Adrenergic Agonist,
• Experimental data suggest a positive effect of beta adrenergic
agonists (β2 agonist) in the alveolar fluid clearance and a decrease in
the endothelial permeability. One of the most used beta adrenergic
agonists are salbutamol (intravenous) or albuterol (nebulized)
• All these data do not support the use of beta 2 adrenergic agonists
and suggest that beta adrenergic agonists may have injurious cardiac
effect and may worsen outcome in those patients

22. • The process for guideline creation adhered to that of the National
Institute for Health and Care Excellence (NICE).
• Ten topics were chosen based on existing guideline recommendations
and the experience of committee members. These included: ►
Corticosteroids. ► ECMO. ► ECCO2 R. ► Fluid strategy. ► High-
frequency oscillation ventilation (HFOV). ► Inhaled vasodilators
(iVasoD). ► Lung protective ventilation: tidal volume (Vt). ►
Neuromuscular blocking agents (NMBA). ► PEEP. ► Prone
positioning