Adriani Pemicu 4 KGD

Pemicu 4 KGD
Adriani Hartanto
405150101
ACUTE RESPIRATORY DISTRESS
SYNDROME
• a clinical syndrome of severe dyspnea of rapid
onset, hypoxemia, and diffuse pulmonary
infiltrates leading to respiratory failure
ARDS
ARDS
• Exudative phase
– alveolar capillary endothelial cells and type I
pneumocytes (alveolar epithelial cells) are injured
 loss of the alveolar barrier  edema interstisial
& alveolar spaces
– Encompasses the first 7 days of illness after
exposure to a prcipitating ARDS risk factor, with
the patient experiencing the onser of respiratory
symptoms
• Proliferative phase
– Lasts from day 7 – day 21
– organization of alveolar exudates
– type II pneumocytes proliferate along
alveolar basement membranes 
synthesize new pulmonary surfactant
and differentiate into type I
pneumocytes
• Fibrotic phase
– extensive alveolar-duct and interstitial
fibrosis
ARDS
• Clinical presentation
– occurring most often within 12 to 72 hours of the
predisposing event
– Anxious, agitated and dyspneic
– Inflammatory changes in the lung  lung
compliance ↓
– Hypoxemia that is resistant to oxygen therapy
ARDS
• Chest Radiograph
– Diffuse, bilateral alveolar infiltrate
• ABG analysis
Prognosis
• The development of
progressive pulmonary
hypertension is
associated with a poor
prognosis.
• The acute phase of
ARDS usually resolves
completely.
• Less commonly,
residual pulmonary
fibrosis occurs, in
which the alveolar
spaces are filled with
mesenchymal cells and
new blood vessels
sars
SARS
• Symptoms of SARS
• Severe acute • Incubation period of 2-
respiratory syndrome 10 days
(SARS) is a viral • In general,begins with
a high fever
respiratory illness (temperature greater
caused by a than 100.4°F
[>38.0°C]).
coronavirus, called • headache, an overall
SARS-associated feeling of discomfort,
and body aches.
coronavirus (SARS- • also have mild
CoV). respiratory symptoms
at the outset.
• SARS was first • About 10 percent to 20
reported in Asia in percent of patients
have diarrhea.
February 2003 • After 2 to 7 days, SARS
• Since 2004, there patients may develop a
dry cough.
have not been any • Most patients develop
known cases of SARS pneumonia and
Lymphopenia
reported anywhere in
the world.
http://www.cdc.gov/sars/about/fs-sars.html http://www.cdc.gov/sars/surveillance/ab
• How SARS spreads:
– by close person-to-person contact.
– most readily by respiratory droplets (droplet spread)
produced when an infected person coughs or sneezes
in short distance (generally up to 3 feet)
– through the air and deposited on the mucous
membranes of the mouth, nose, or eyes of persons
who are nearby.
– also can spread when a person touches a surface or
object contaminated with infectious droplets and then
touches his or her mouth, nose, or eye(s).
– It is possible that the SARS virus might spread more
broadly through the air (airborne spread) or by other
ways that are not now known.
http://www.cdc.gov/sars/surveillanc
http://www.cdc.gov/sars/about/fs-sars.html e/absence.html
Case Detection
• Severe respiratory illness in the context of a documented
exposure risk is the key to diagnosing SARS-CoV disease.
Providers should therefore consider SARS-CoV disease in
patients requiring hospitalization for:
• Radiographically confirmed pneumonia or acute respiratory
distress syndrome of unknown etiology, AND
• One of the following risk factors in the 10 days before illness
onset:
– Travel to mainland China, Hong Kong, or Taiwan, or close contact with
an ill person with a history of recent travel to one of these areas, OR
– Employment in an occupation associated with a risk for SARS-CoV
exposure (e.g., healthcare worker with direct patient contact; worker
in a laboratory that contains live SARS-CoV), OR
– Part of a cluster of cases of atypical pneumonia without an alternative
diagnosis
• Infection control practitioners and other healthcare personnel
should be alert for clusters of pneumonia among two or more
healthcare workers who work in the same facility.
http://www.cdc.gov/sars/about/fs-s
http://www.cdc.gov/sars/surveillance/abs
Infection Control and Clinical
Evaluation
• Healthcare facilities should re-emphasize the importance of
basic infection control measures for respiratory infections and
consider adopting a "respiratory hygiene/cough etiquette"
strategy.
• All patients admitted to the hospital with radiographically
confirmed pneumonia should be:
– Placed on droplet precautions
– Screened for risk factors for possible exposure to SARS-CoV
– Evaluated with a chest radiograph, pulse oximetry, complete blood
count, and etiologic workup as indicated.
• If there is a high index of suspicion for SARS-CoV disease (by
clinicians and health department), the patient should
immediately be placed on SARS isolation precautions, and all
contacts of the ill patient should be identified, evaluated, and
monitored. Prompt SARS-CoV laboratory diagnostics should
be arranged through the health department.http://www.cdc.gov/sars/about/fs-s
Lab Testing
• Antibody testing using an enzyme immunoassay (EIA)
• reverse transcription polymerase chain reaction (RT-PCR)
tests;
– During the first week of illness: Nasophyaryngeal (NP) swab plus
oropharygeal (OP) swab and a serum or plasma specimen
– After the first week of illness: NP swab plus OP swab and a stool
specimen
• Perform laboratory testing judiciously and in consultation
with the local or state health department.
• Providers should report all positive test results
immediately to the local or state health department.
• Arrange for confirmatory testing at an appropriate test
site through the local or state healthhttp://www.cdc.gov/sars/about/fs-s
department.
SARS
• febrile severe lower respiratory illness that
is caused by infection with a novel
coronavirus, SARS-associated coronavirus
(SARS-CoV)
• The vast majority of patients with SARS-
CoV disease
1) have a clear history of exposure either to
a SARS patient(s) or to a setting in which
SARS-CoV transmission is occurring, and
2) develop pneumonia
• Laboratory tests are can be helpful but do
not reliably detect infection early in the
illness
https://www.cdc.gov/sars/clinical/guidance.html
• absence of person-to-person transmission of SARS-CoV
anywhere in the world, the diagnosis of SARS-CoV
disease should be considered only in patients who
require hospitalization for radiographically confirmed
pneumonia and who have an epidemiologic history that
raises the suspicion of SARS-CoV disease.
• The suspicion for SARS-CoV disease is raised if, within 10
days of symptom onset, the patient:
– Has a history of recent travel to mainland China, Hong
Kong, or Taiwan (see Figure 1, footnote 3) or close contact1
with ill persons with a history of recent travel to such
areas, or
– Is employed in an occupation at particular risk for SARS-
CoV exposure, including a healthcare worker with direct
patient contact or a worker in a laboratory that contains
live SARS-CoV, or
– Is part of a cluster of cases of atypical pneumonia without
an alternative diagnosis
https://www.cdc.gov/sars/clinical/fig1.ht
• Once person-to-person transmission of SARS-CoV has
been documented in the world, the diagnosis should still
be considered in patients who require hospitalization for
pneumonia and who have the epidemiologic history
described above.
• In addition, all patients with fever or lower respiratory
symptoms (e.g., cough, shortness of breath, difficulty
breathing) should be questioned about whether within
10 days of symptom onset they have had
– Close contact with someone suspected of having SARS-CoV
disease, OR
– A history of foreign travel (or close contact with an ill
person with a history of travel) to a location with
documented or suspected SARS-CoV, OR
– Exposure to a domestic location with documented or
suspected SARS-CoV (including a laboratory that contains
live SARS-CoV), or close contact with an ill person with such
an exposure history.
https://www.cdc.gov/sars/clinical/fig2.html
ACUTE RESPIRATORY FAILURE
Respiratory Failure
• Is a condition in which the respiratory system
fails in one or both of its gas-exchanging
functions
Sumber: Fishman’s Pulmonary Diseases and Disorders 4th Ed Volume 2 – Section Lung Failure (Chap 143)
Respiratory Systems & Controllers
Respiratory
Peripheral
CNS Efferents Muscles,
Nerves
Chest Wall
Airways Alveoli
Ventilatory Demand vs Supply
Ventilatory Ventilatory Ventilatory

supply supply supply
Ventilatory Ventilatory Ventilatory

demand demand demand
Ventilatory supply exceeds demand Ventilatory supply equals demand Ventilatory demand
exceeds supply
Factors that Increase Ventilatory
Demand
• Increased VD/VT  Acute asthma, emphysema,
late phase of acute respiratory distress syndrome,
pulmonary emboli
• Increased VO2  Fever, sepsis, trauma, shivering,
increased work of breathing, massive obesity
• Increased RQ  Excessive carbohydrate feeding
• Decreased PaCO2  Hypoxemia, metabolic
acidosis, anxiety, sepsis, renal failure, hepatic
failure
Factors that Diminish Ventilatory Supply
Factor Examples
Decreased respiratory muscle
strength
Muscle fatigue Recovery from acute respiratory failure, high RR,
increased inspiratory time
Disuse atrophy Prolonged mechanical ventilation, following phrenic
nerve injury
Malnutrition Protein – calorie starvation
Electrolyte abnormalities Low serum phosphate or potassium concentrations
Arterial blood gas Low pH, low PaO2, high PaCO2
abnormalities
Fatty infiltration of diaphragm Obesity
Unfavorable alteration in Flattened domes of diaphragm caused by hyperinflation

diaphragm length - tension
relationship
Categories of Respiratory Failure
CNS Abnormalities PNS or Chest Wall Abnormalities
• Pharmacologic • Neuromuscular causes

• Narcotic/sedative drugs overdose (most striking • Gullain-Barre syndrome
feature  acute overdose, long-standing use of • Myasthenia gravis
some (methadone)  chronic hypercapnia) • Polyomyositis
• Structural • Muscular dystrophies & metabolic muscle
• Meningoencephalitis disorders
• Localized tumors • Pharmacologic causes
• Vascular abN of medulla • Use of depolarizing & non-depolarizing
• Strokes affecting medullary control centers paralyzing agents (esp in conjunction with
• Metabolic systemic corticosteroirds)
• Severe myxedema • Cholinergic crisis (during myasthenia gravis
• Hepatic failure therapy)
• Advanced uremia • Administration of aminoglycosides to
myasthenia patients
• Metabolic alkalosis due to diuretic use
• Primary disorder of chest wall
• Obesity-hypoventilation syndrome
• Severe kyphoscoliosis
• Flail chest
• Extensive thoracoplasty
• Morbid obesity
• Massive abdominal distention (ascites /
distended bowel loopsl)
Categories of Respiratory Failure
Airway Abnormalities Alveoli Abnormalities
• Upper airway obstruction • Mostly hypoxemic resp. failure

• Acute epiglottitis • Hypercapnia may complicate the
• Aspirated foreign body picture
• Tracheal tumor • Cardiogenic & non-cardiogenic
• Narrowing of trachea / glottis pulmonary edema
by fibrotic tissue • Diffuse pneumonia
• Lower airway obstruction • Extensive pulmonary
• COPD hemorrhage
• Asthma • Aspiration of stomach contents
• Advanced cystic fibrosis • Near-drowning
Approach to The Patient
• Diagnosis begins with clinical suspicion of its presence.

• Confirmation of diagnosis  through arterial blood gas
analysis.
• Evaluation for underlying cause must be initiated early,
frequently in the presence of concurrent treatment for acute
respiratory failure.
• Diagnosis of chronic respiratory failure is usually easily
established with clinical findings or chronic hypoxemia, but
acute respiratory failure requires more careful analysis.
• ABG analysis should be done once respiratory failure is
suspected on clinical grounds, to assist in 1) distinction
between acute and chronic forms, 2) assess magnitude and
metabolic impact, 3) help guide management.
Approach to The Patient
• Signs and symptoms of acute RF reflects the underlying disease
process & associated hypoxemia or acidemia due to hypercapnia.
• Apparent  localized pulmonary findings (pneumonia, pulmonary
edema, asthma, or COPD).
• Predominant findings may be systemic (hypotension due to sepsis).
• Principal manifestation may be remote from thorax (abdominal pain
in acute pancreatitis, or leg pain due to long bone fracture)  each
associated with acute (adult) respiratory distress syndrome (ARDS).
• Frequently, neurological / CV SS predominate.
• Neurology : restlessness, anxiety, confusion, seizures, coma, asterixis (in
severe hypercapnia).
• CV : tachycardia, variety of arrhythmias.
• There may be few/no findings other than complaints of dyspnea (esp
patients with hypoxemia due to pulmonary embolism).
Changes in Arterial Blood Gases in Acute Respiratory
Failure
Failed Respiratory System Component pH PaCO2 PaO2 PaO2- VE VA
PaCO2
Central nervous system    NL or   
Peripheral nervous system or chest bellows    NL or   
Airways
In acute asthma
Early phase (before respiratory failure)   NL   
“Crossover point” NL NL NL or    NL
With development of respiratory muscle      
fatigue
In COPD
Non-CO2 retainer  NL or     
CO2 retainer
Baseline NL to     NL or  
Flare     NL,  or 

Alveoli
Before respiratory muscle fatigue develops      
After respiratory muscle fatigue develops      
Principles of Management
• Triage decisions  acuity of resp failure, degree of
hypoxemia hypercapnia and acidemia, presence of co-
morbid conditions (cardiac disease, renal insufficiency),
clinical direction that patient takes over the first few
minutes/hours of obervation
• Airway management  is key! Intubation (in chronic resp.
insufficiency) depends on critical ABG values & patient’s
early acute course. If in first dew minutes/hours progressive
hypoxemia/hypercapnia is observed  intubation +
mechanical ventilation.
• Correction of hypoxemia and hypercapnia  PaO2 60 mmHg
or higher (in coronary/cerebrovascular patient). Use nasal
prongs / face mask / controlled-flow oxygen via Venturi
mask. While correcting hypoxemia, coexisting hypercapnia
and respiratory acidosis must also be addressed
• Search for underlying cause
Monitoring Patients with Acute Respiratory
Failure
• Repeated assessment!
• Most  RR, tidal volume, use of accessory muscles, presence of
paradoxical breathing movements indicate worsening resp. failure
that requires mechanical ventilation
• Rapid, shallow breathing and paradoxical thoracoabdominal
breathing movements  in worsening asthma and COPD
• Placed on mechanical ventilation  monitor carefully for
ventilator-associated complications
• Also with risk of complications  indwelling arterial & venous
catheters, patient immobilization, use of broad range of
pharmacologic agents
• Particular monitoring techniques  pulse oxymetri (in critical
care), hypotention due to intrinsic positive end-expiratory pressure
(PEEP) (in status asthmaticus requiring mechanical ventilation)
Prognosis
• Morbidity and mortality in acute hypoxemic
respiratory failure  depends on underlying
cause.
– Younger patients have better survival rates than
older patients.
– Patients with preexisting lung disease, higher FIO2,
or PEEP requirements, or lower PaO2, may not
necessarily have poorer chance of survival.
• Morbidity and mortality in acute hypercapnic
respiratory failure
Avian Flu
Avian Flu: Overview
• Is a zoonotic human infection

with an influenza strain that
primarily affects birds.
• Influenza virus is an
orthomyxovirus—an
enveloped, segmented,
negative-sense RNA virus (-
ssRNA)
• Influenza virus has 3 strains—
A, B, and C. Avian influenza is
caused by influenza A virus,
which has 8 RNA segments.
• Avian influenza is a potential
and unpredictable threat to
humans because of the
segmented nature of the
genome.
Sumber: http://emedicine.medscape.com/article/2500029-overview,
Avian Flu: Serovars
• The serotypes of influenza A virus are identified based
on the hemagglutinin (H) and neuraminidase (N)
proteins; 16 H serotypes and 9 N serotypes have been
identified.
• For example, one currently circulating strain is
designated as H3N2.
• The strain previously considered the greatest threat
was H5N1, mostly because of the high associated
mortality rate (up to 60%) in infected humans. H5N1
infections have decreased substantially in recent years,
and the most recent avian influenza of note is H7N9,
first described in China in 2013.
Sumber: http://emedicine.medscape.com/article/2500029-overview
Avian Flu: Antigenic Drift
• The immune response to these antigens is
responsible for most host protection.
• The viral RNA polymerase lacks error-checking
mechanisms and, as such, the antigenic drift
from year to year is sufficient to ensure a
significant susceptible host population.
• However, the segmented genome also has the
potential to allow re-assortment of genome
segments from different strains of influenza in a
co-infected host.
Avian Flu: Epidemiology
• Race  appears to be a factor only to the

extent that geographic differences in the
rate of HPAI among birds and the degree
of bird-to-human contact are significant.
• Sex In Egypt, 90% of fatalities due to
avian influenza have involved women, a
pattern that has not been readily
apparent elsewhere. Most cases of H7N9
have been reported in men.
• Age  highest case-fatality rate among
persons aged 10-39 years. Unlike seasonal
influenza (which disproportionately
affects very young and very old
individuals), young adults make up a large
proportion of the avian influenza cases.
Avian Flu: Pathogenesis
• Avian influenza is still primarily a respiratory infection but

involves more of the lower airways than human influenza
typically does  likely due to differences in the
hemagglutinin protein and the types of sialic acid residues
to which the protein binds.
• Avian viruses tend to prefer sialic acid alpha(2-3) galactose
(in humans, is found in the terminal bronchi and alveoli).
Conversely, human viruses prefer sialic acid alpha(2-6)
galactose, which is found on epithelial cells in the upper
respiratory tract. One group has reported that ex vivo
cultures of human tonsillar, adenoidal, and
nasopharyngeal tissues can support replication of H5N1
avian influenza.
Avian Flu: Clinical Features
• The key history component  exposure to sick, dead, or dying

poultry or humans with avian influenza. Many cases involve close
contact, such as plucking or gutting of dead birds, removing
infected carcasses, or ingesting incompletely cooked bird meat or
blood.
• Some cases have had no link to prior exposure to sick birds,
suggesting that spread from asymptomatic birds is possible or that
the virus can be transmitted environmentally on fomites.
• The time from exposure to disease is slightly longer than in human
influenza, although this interval can be as short as 2 days. Intervals
of up to 17 days have been reported, although most cases occur
within one week of exposure.
• !!! Respiratory symptoms are the most common presentation.
More severe respiratory distress occurs around 5 days from the
initial symptoms. The sputum is sometimes bloody.
Avian Flu: Clinical Features & Suspicion
• Other symptoms  Risk factors or features that should

raise the index of suspicion include the
include the following: following:
– Fever (temperature  Travel to (within the last 2 wk) or location
in a country with known avian influenza
>38°C) cases in animals or humans
 Unusual comorbidities 
– Diarrhea (watery, non- encephalopathy or diarrhea
bloody) (possibly a poor  History of exposure to birds, especially
living in close proximity to birds, contact
prognostic sign) with sick or dying birds, or consumption
– Vomiting of incompletely cooked bird meat
 History of exposure to individuals with
– Chest and/or abdominal known avian influenza, especially family,
or to sick people in a country with known
pain human cases of avian influenza
– Encephalitis
Avian Flu: Diagnosis
• Physical exam:  Lab tests:

• Tachypnea and crackles are
common.  Nasal wash specimens for
• Wheeze is occasionally apparent. detection of virus and viral
• Conjunctival suffusion/conjunctivitis
is not uncommon. subtyping  crucial.
• Case reports have described other  Leukopenia
occasional signs (eg, bleeding gums,
always in the presence of viral  Relative lymphopenia
pneumonia)
• Radiography study:  Thrombocytopenia (common).
• Chest radiography  most common  Elevated levels of liver enzymes
finding is multifocal consolidation;
effusions a& lymphadenopathy are (SGOT/SGPT)
also observed, as well as cystic
changes.  Disseminated intravascular
coagulation (DIC) (rare).
Avian Flu: Differential Diagnosis
• Community-Acquired • Pneumococcal Infections
Pneumonia (CAP) • Severe Acute Respiratory
• H1N1 Influenza (Swine Flu) Syndrome (SARS)
• Hantavirus Pulmonary
Syndrome
• Influenza
• Middle East Respiratory
Syndrome (MERS)
• Pediatric Pneumococcal
Infections
Avian Flu: Management
• Mainstay of treatment   Antivirals  Neuraminidase

administration of antiviral
medications activity inhibitor:
• Supportive care  oxygen therapy,  Amantadine
intravenous fluids and parenteral
nutrition  Rimantadine (Flumadine)
• Severe cases  ventilatory support
with intubation & low-volume  Oseltamivir (Tamiflu)
(high-frequency) ventilation.
• Antiviral therapy  tailored to the  Zanamivir (Relenza)
patient's age and the antiviral
resistance profile of the virus from
the area of exposure. Therapy  Uricosuric Agents  Inhibitor
should be initiated even when the of tubular secretion of active
presentation is late.
• Antibiotics  treat bacterial metabolite of drug 
pneumonia, but are not empirically adjunctive therapy.
necessary.
 Probenicid
Avian Flu: Prognosis
• The prognosis of confirmed human cases of
avian influenza is related to the degree and
duration of hypoxemia.
• he cases to date have exhibited a 60%
mortality rate.
• The risk of mortality depends on the degree of
respiratory disease rather than the bacterial
complications (pneumonia).
Avian influenza
• infection with avian (bird) influenza
(flu) Type A viruses
• occur naturally among wild aquatic
birds worldwide and can infect
domestic poultry and other bird
and animal species
• do not normally infect humans.
However, sporadic human
infections with avian flu viruses
have occurred
https://www.cdc.gov/flu/avianflu/avian-in-humans.htm
Influenza A virus :
• divided into subtypes on the basis of two proteins on the surface of the
virus: hemagglutinin (HA) and neuraminidase (NA)
• All known subtypes of influenza A viruses can infect birds, except
subtypes H17N10 and H18N11, which have only been found in bats.
• Only two influenza A virus subtypes (i.e., H1N1, and H3N2) are
currently in general circulation among people.
• H7N7 and H3N8 virus infections can cause illness in horses, and H3N8
virus infection cause illness in horses and dogs
• Sporadic H5 virus infection of humans has occurred, such as with Asian
lineage HPAI H5N1 viruses currently circulating among poultry in Asia
and the Middle East
• The most frequently identified H7 viruses associated with human
infection are Asian lineage avian influenza A(H7N9) viruses, which were
first detected in China in 2013
• H7N2, H7N3, H7N7 virus infections have been reported. These viruses
have primarily caused mild to moderate illness in people, with
symptoms that include conjunctivitis and/or upper respiratory tract
symptoms.
• Rare, sporadic H9N2 virus infections in people have been reported to
generally cause mild upper respiratory tract illness; one infection has
https://www.cdc.gov/flu/avianflu/influenza-a-virus-subtypes.htm
Avian Influenza A Virus Infections in Humans
• Infected birds shed avian influenza virus in
their saliva, mucous and feces
• Human infections with bird flu viruses can
happen when enough virus gets into a
person’s eyes, nose or mouth, or is inhaled
• happen when virus is in the air (in droplets or
possibly dust) and a person breathes it in, or
when a person touches something that has
virus on it then touches their mouth, eyes or
nose
• occurred most often after unprotected
contact with infected birds or surfaces
contaminated with avian influenza viruses
S/S
• Mild – severe
• Conjunctivitis
• Influenza like illness (fever, cough, sore throat,
muscle aches)
• Accompanied by nausea, abdominal pain, diarrhea,
vomiting
• Severe respi illness (shortness of breath, difficulty
breathing, pneumonia, ARD, viral pneumonia, respi
failure)
• Neurologic changes (altered mental status, seizures)
• Involve other organ systems
• Asian lineage H7N9 & HPAI asian lineage H5N1 
most serious illness & highest mortality in humans
Diagnosis
• collecting a swab from the upper respiratory
tract (nose or throat) of the sick person (more
accurate when the swab is collected during
the first few days of illness)  lab : molecular
test, by trying to grow the virus, or both
• possible to diagnose avian influenza A virus
infection by looking for evidence of
antibodies the body has produced in
response to the virus (requires two blood
specimens (one taken during the first week of
illness and another taken 3-4 weeks later) 
take several weeks to verify the results, and
testing must be performed in a special
laboratory, such as at CDC
Treatment
• neuraminidase inhibitor
• most viruses are susceptible to
oseltamivir, peramivir, and
zanamivir, some evidence of
antiviral resistance has been
reported in Asian H5N1 and Asian
H7N9 viruses isolated from some
human cases
Prevention
• avoid sources of exposure
• had contact with infected birds may
be given influenza antiviral drugs
preventatively
• Seasonal influenza vaccination will
not prevent infection with avian
influenza A viruses, but can reduce
the risk of co-infection with human
and avian influenza A viruses
https://www.gov.uk/gove
rnment/uploads/system/u
ploads/attachment_data/
file/358673/Investigation_
and_management_of_pos
sible_human_cases_of_av
ian_influenza_A_H7N9__f
low_diagram_July_new.p
https://www.gov.uk/government/u
ploads/system/uploads/attachment
_data/file/358675/Case_manageme
nt_of_suspected_human_case.pdf
2 Phase 3 Management of asymptomatic contacts of
confirmed human case(s) of avian influenza A/H5N1
1 January 2009. Please check for updates at:
http://www.hpa.org.uk/webw/HPAweb&HPAwebStandard/HPAweb_C/1195733851442?p=1160495617107
The clinician attending a confirmed human case of avian influenza should notify the local Health Protecti on Unit (HPU) as soon
as possible. The local HPU will advise, in liasion with HPA Centre for Infections (CfI), on the assessment of contacts, clinical
management and use of oseltamivir prophylaxis.
- Start oseltamivir prophylaxis4 as soon as possible

unless more than 7 days have elapsed since last
exposure. Current licensed indication for post-
exposure prophylaxis is a 10-day course of therapy.
- If exposure is ongoing (e.g. caring for the patient)

then prophylaxis to be continued for 10 days after last
Close contacts1 of a symptomatic case or
1 healthcare workers2 caring for a symptomatic case
Yes exposure.
- HPU to provide information leaflets5 and coordinate

active follow up: daily assessments for up to 7 days
after last exposure to the symptomatic case and
passive follow up until the course of oseltamivir is
completed.
- The extent of serological investigation will be agreed

No
by the Incident Management team in discussion with
CfI. However as a minimum, a 10ml clotted blood
specimen should be taken 28 days after last exposure
to the case and sent to CfI for serology.
Casual contact of a symptomatic case - Prophylaxis not indicated.
2 in transit (air/train/ferry/coach/car) Yes

- Provide information and advise on passive follow up
Refer to Port Health algorithm for advice3 for 7 days after last contact with case. HPU to
coordinate.6
No
3 Casual contact of an asymptomatic case Yes No action required however information leaflets may
be helpful.
If a contact becomes unwell, the local HPU should liaise with the Pandemic Influenza Office in the first instance. If
unavailable, contact appropriate consultant in the Respiratory & Systemic Infections Department or the Virus
Reference Laboratory at CfI to discuss next steps.
Footnotes:
1 A close contact is defined as an individual sharing a household or remaining unprotected whilst within speaking distance (<1 metre) while caring for a patient
with confirmed or strongly suspected H5N1 infection. (adapted from WHO Rapid Advice Guidelines on pharmacological management of humans infected with
avian influenza A(H5N1) virus, May 2006 www.who.int/csr/disease/avian_influenza/guidelines/pharmamanagement/en/index.html)
2 Health care worker or anyone else engaged in direct clinical care or examination of symptomatic patient. Ideally, the number of people involved should be
kept to a minimum.
3 Port Health algorithm for information on travel exposures. (to follow)
4 Refer to dosing schedule for oseltamivir prophalyxis. (http://www.bnf.org/bnf/bnf/current/119743.htm)
5 Refer to information leaflets on active follow up. (link to information leaflets to follow)
6 Passive follow up: provision of information to individual (or responsible carer) and request that any febrile respiratory or other unexplained illness within 7
days of last contact be reported (24 hour reporting).
https://www.gov.uk/government/
In case of uncertainty, discuss with local Health Protection Unit.
uploads/system/uploads/attachm
Health Protection Agency www.hpa.org,uk
ent_data/file/358676/2phase3con
tactsofconfirmedcasealgorithm20
090101b.pdf
Acute Severe Asthma
Status Asthmaticus
Status asthmaticus
• extreme form of an asthma exacerbation that can
result in hypoxemia, hypercarbia, and secondary
respiratory failure
• acute exacerbation of asthma that remains
unresponsive to initial treatment with
bronchodilators
• vary from a mild form to a severe form with
bronchospasm, airway inflammation, and mucus
plugging that can cause difficulty breathing, carbon
dioxide retention, hypoxemia, and respiratory
failure
RF
• Viral infections
• Air pollutants - Such as dust, cigarette
smoke, and industrial pollutants
• Medications - Including beta-blockers,
aspirin, and nonsteroidal anti-
inflammatory drugs (NSAIDs)
• Cold temperature
• Exercise
Clinical review: Severe asthma,
Primary survey
• As for all patients, the initial evaluation should center
around the “ABCs.” History taking and a more detailed
examination can occur after you assure adequate airway,
breathing, and circulation. This need only takes a few
seconds to minutes, but is essential.
– Airway: Can the patient maintain
his/her airway? Is the mental status
adequate to protect the airway?
– Breathing: What is the degree of air
exchange? Is the patient cyanotic?
– Circulation: How is the perfusion? The
pulses?
History
• Previous history of wheezing?
• If known asthmatic, what are maintenance
meds? Compliance? Time of last
• aerosol?
• Previous office/clinic/ED visits?
• Previous hospitalizations, intubations, last
steroid course?
• When did this exacerbation begin?
• Precipitating factors?
• General medical history, including any
medications.
Vital signs
• Temperature: fever may indicate URI, pneumonia,
other source of infection
• Pulse: Usually tachycardic, even before treatment
• Respiratory rate: Usually tachypneic.
• Blood pressure: Pulsus paradoxus over 10-15
correlates well with moderate to severe disease, as
it indicates the effect that air trapping is having on
the cardiac output. It is best measured with a
sphygmomanometer and a stethoscope, and is the
difference in systolic BP between the pressure at
which an observer first hears faint pulse sounds and
the pressure at which all sounds are heard.
Breath sounds / chest exam
• There must be air movement in order to appreciate wheezing, lack or wheezing does NOT
necessarily mean everything is fine!
• I:E ratio is usually 5:2, may be up to 1:4 with a severe attack
• Symmetry of breath sounds
– Some asymmetry may be heard with asthma alone due to mucous plugging and atelectasis.
– Increased wheezing unilaterally may indicate presence of a foreign body
– Significantly decreased breath sounds unilaterally may indicate pneumonia
– or pneumothorax.
• The use of accessory respiratory muscles(abdominal paradoxic breathing,
• sternocleidomastoid use, nasal flaring, intercostal retractions) correlates with the severity
of airway obstruction. Wheezing is a less sensitive indicator of the degree of obstruction
present.
• Feel for the presence of crepitus in the neck or chest wall, signifying air leak and significant
obstruction
Cardiac exam
• Attention should be paid to rate and blood
pressure, including the presence of pulsus
paradoxus. In addition, are the heart tones
normal, is there a murmur (any evidence of
pre-existing heart disease)
Mental status
• Confusion or obtundation suggest significant
hypercapnia or hypoxemia, and necessitate
immediate action!!!
• Clinical asthma score
Prognosis
• In general, unless a complicating
illness such as congestive heart failure
or chronic obstructive pulmonary
disease is present, status asthmaticus
has a good prognosis if appropriate
therapy is administered
• Delays can result from poor access to
health care on the part of the patient
or even delays in using corticosteroids
• with acute asthma should use
corticosteroids early and aggressively
Complications
• Cardiac arrest
• Respiratory failure or arrest
• Hypoxemia with hypoxic ischemic
central nervous system (CNS) injury
• Pneumothorax or
pneumomediastinum
• Toxicity from medications
Treatment*
• High concentration of oxygen (by face mask)  achieve
oxygen saturation of >90%
• High doses of short-acting inhaled β2-agonists (nebulizer or
via a metered dose inhaler with a spacer)
• Not satisfactory response β2-agonists  add : inhaled anti-
cholinergic
• Refractory to inhaled therapies  slow infusion of
aminophylline
– MONITOR BLOOD LEVELS! Especially in oral theophylline
• IV or nebulizer Magnesium sulfate + inhaled β2-agonists :
• Severely ill patients w/ impending respiratory failure : IV β2-
effective,
agonists +well tolerated,intubation
prophylactic but not routinely recommended
• Patients with respiratory failure :
– Intubate + institute ventilation
– Conventional bronchodilator
– Not respond  Anesthetic : halothane
– NO Sedatives : may depress ventilation
– Antibiotics : not routinely unless there are signs of pneumonia.
Harrison’s Principle of
Inhaled β2-agonists
• Safe, effective (obstruction)
• Salbutamol (albuterol: most frequently used
agent : its potency, duration of action (four to
six hours) and β2-selectivity.
– 2.5 mg of salbutamol (0.5 ml) in 2.5 ml NS for each
nebulisation

Anticholinergics and methylxanthines
• Anticholinergics (ipratropium bromide) :
controversy on their ability to offer additional
bronchodilation
• Methylxanthines (theophylline) : not generally
recommended, some warrant its use in ED :
– enough data : benefits patients after 24 hours.
– non bronchodilating  action on the diaphragm
and anti-inflammatory effects,

Corticosteroid treatment
• speed the resolution, reduce relapse, reduce
mortality
• Recommended for most patients, especially who
don’t respond to β2-agonists
• Long-term treatment inhaled corticosteroids
– Reduce hospitalization rates in younger patients with
asthma
– Reduce the risk of rehospitalization and all-cause
mortality in elderly asthmatics

Subcutaneous epinephrine and terbutaline
• Considered to :
– who are not responding adequately to continuous
nebulised salbutamol
– who are unable to cooperate (depression of
mental status, apnea, coma)

PULMO TB
Tuberculosis
Etiology: Mycobacterium tuberculosis
Clinical Features:
1) Primary Tuberculosis
Fever, malaise, weight loss and chest pain
2) Reactivation Tuberculosis
Fever, night sweats, malaise, fatigue and weight loss.
Produtive cough, hemoptysis, dyspnea and
pleuritic chest pain
Diagnosis
1) Skin test (Mantoux test)
2) Chest Radiography
3) Cultures (Ziehl-Neelsen)
Limmer D, O'Keefe MF. Emergency Care. 11th ed. Chapter 16.
Treatment
• Daily four-drug (INH, RIF, PZA, EMB) therapy for 8
weeks, followed by either INH/RIF or
INH/rifapentine for 18 weeks
• Daily four-drug therapy for 2 weeks, followed by
two times per week for 6 weeks, with subsequent
INH/RIF or INH/rifapentine for 18 weeks
• Three times weekly four-drug therapy for 8
weeks, followed by INH/ RIF three times weekly
for 18 weeks
• Daily three-drug therapy (INH, RIF, EMB) for 8
weeks followed by INH/RIF for 31 weeks
PE
Harrison’s Principle of Medicine, 18th ed

Large bilateral pulmonary emboli (intravascular
filling defects in contrast scan identified by red
arrows).
Pleural Effusion
excess quantity of fluid in the pleural

space
Terminology
• Pleuritis (also referred to as pleurisy) = inflammation of the pleura.
Can occur w/ or w/o exudation
• Parapneumonic effusion = A pleural effusion associated with bacterial
pneumonia, bronchiectasis, or lung abscess
• Complicated parapneumonic effusion = parapneumonic effusions that
require tube thoracostomy for their resolution.
• Empyema (or pus in the pleural space) requires the presence of bacteria
on Gram’s staining of the pleural fluid.
• Loculated effusion = Fluid anatomically confined and not freely flowing in

the pleural space
– occur when there are adhesions between the visceral and the parietal
pleurae.
Rosen's, 7th ed.

Etiology
Most common
• Western countries : congestive heart failure,
followed by malignancy, bacterial pneumonia,
and pulmonary embolism.
• In other countries : tuberculosis
Rosen's, 7th ed.

Pathogenesis
• Pleural fluid formation (influx) > pleural fluid
absorption (efflux)
• Normal :
– Fluid enters - parietal pleura ( systemic
capillaries)
or - interstitial spaces of the lung ( visceral
pleura)
or - peritoneal cavity (small holes in the
diaphragm)
– Fluid removed - lymphatics (in parietal pleura) &
• Rosen’s : pulmonary capillaries (inHarrison’s
visceralPrinciple
pleura)of
• Movement of fluid : Starling’s law.
• Direction of pleural fluid flow : difference in hydrostatic
pressure between the systemic and the pulmonary
circulations
• Dynamic equilibrium : influx = efflux, with ±1 L of fluid
traversing the pleural space in 24 hours.
• Amount of fluid that remains in the pleural space is small
(∼0.1–0.2 mL/kg body weight)
• Clinically or radiographically undetectable
Rosen's, 7th ed.

Transudative effusion
• Transudates = ultrafiltrates of plasma,

containing very little protein.
• Develops when : hydrostatic pressure ↑or
oncotic pressure ↓ within pleural
microvessels.
• Causes :
– CHF (90%) hydrostatic pressure ↑
– Cirrhosis, nephrotic syndrome, malnutrition 
hipoalbuminemia  effusion
Rosen's, 7th ed.

Exudative effusion
• Exudates = high Etiology :
amounts of protein • 1st common form :
• Reflecting an parapneumonic effusion
abnormality of the  infection of the
pleura itself. adjacent lung
• 2nd most common form :
malignant effusion
Pathogenesis :
• May also response to
• Increased membrane
inflammatory abdominal
permeability or
processes : pancreatitis or
defective lymphatic
subphrenic abscess
drainage.
Outcome :
• Inflammation in
pulmonary or pleura • Reabsorbed; organize into
can result in an fibrous tissue  pleural
exudative effusion. adhesions. Rosen's, 7th ed.
Rosen's, 7th ed.
Clinical Features
• Symptoms : Due to the underlying disease
• Small pleural effusion : asymptomatic
• New PLEf : localized pain or referred to
shoulder
• PF volume >= 500 mL dyspnea on exertion
or at rest (compromised pulmonary function)
Rosen's, 7th ed.

Diagnostic Approach
• Determine whether the effusion is a transudate or an
exudate.
– Transudate : alteration of systemic factors
Causes : LV failure and cirrhosis.
– Exudate : alteration of local factors
Causes : bacterial pneumonia, malignancy, viral infection, and
pulmonary embolism.
• Some pleural effusions may have characteristics of both
Exudative pleural effusions : >= 1 of the
criteria
1. Pleural fluid protein : serum protein >0.5
2. Pleural fluid LDH : serum LDH >0.6
3. Pleural fluid LDH > 2/3 normal upper limit for serum
• If >=1 exudative criteria are met AND the patient is clinically

thought to have a condition producing a transudative
effusion  measure the protein levels in the serum – in the
pleural fluid
– If this gradient> 31 g/L (3.1 g/dL)  almost all such
patients have a transudative pleural effusion.
• If exudative pleural effusion, obtain the following tests :

description of the fluid, glucose level, differential cell count,
microbiologic studies, and cytology.
• Pleural fluid analyses
– pH <7.3 - parapneumonic effusions, malignancies,
rheumatoid effusions, tuberculosis, and systemic
acidosis.
– pH < 7.0 – empyema (or esophageal rupture).
– pH < 7.0 & glucose <50 mg/dL indications for
tube thoracostomy.
Rosen's, 7th ed.

• Approach to the diagnosis
of pleural effusions.
PF = pleural fluid;
CHF = congestive heart failure;
CT = computed tomography;
LDH = lactate dehydrogenase;
PE = pulmonary embolism;
TB = tuberculosis
Medicine, 18th ed
• History :
– Viral : prodrome symptoms (low-grade fever, sore throat,
etc)  no?  may be : pulmonary embolism
• Classic physical signs :
– Diminished breath sounds
– Dullness to percussion
– Decreased tactile fremitus
– Occasionally a localized pleural friction rub*
– Massive effusions : signs of mediastinal shift
Rosen's, 7th ed.

• Chest radiography :
– Blunting of the costophrenic angle on the upright chest radiograph
– <250 mL visible in posterior costophrenic gutter on a lateral projection
– 250-500 mL : frontal (AP or PA) projection
– >500 mL :
• hemidiaphragm is obscured*
• upwardly concave meniscus may be seen because pleural fluid
has a tendency to layer higher laterally than centrally
• Pleural fluid can extend up a major fissure and appear as a
homogeneous density in the lower 2/3 of the lung field.
– Massive pleural effusion : totally opacified hemithorax.
Rosen's, 7th ed.

Figure 75-5. Radiographs of pleural effusion along major
and minor fissures.
Rosen's, 7th ed.
• Ultrasound and CT : localizing effusions and
characterizing underlying lung processes.
Ultrasound
• It can be used to guide thoracentesis and
decrease the risk of complications, particularly in
the case of small or loculated effusions.
• Pleural effusion : hypoechoic fluid located above
the diaphragm w/ loss of the usual mirror-image
artifact.
• Pleural effusions < 500 mL, however, can be

missed with bedside radiography.
Rosen's, 7th ed.

Diagnosis
• The presence of free pleural fluid - demonstrated with
– Lateral decubitus radiograph
– Computed Tomography (CT) of the chest, or
– Ultrasound
• If the free fluid separates the lung from the chest wall by >10
mm  therapeutic thoracentesis
Management
Factors indicating the likely need for a procedure more invasive than a
thoracentesis (in increasing order of importance) include:
1. loculated pleural fluid
2. pleural fluid pH < 7.20
3. pleural fluid glucose < 3.3 mmol/L (<60 mg/dL)
4. positive Gram stain or culture of the pleural fluid
5. the presence of gross pus in the pleural space
• If the fluid recurs after the initial therapeutic thoracentesis &

presentation of the above characteristics  repeat thoracentesis
• If the fluid cannot be completely removed with the therapeutic
thoracentesis :
– Insert a chest tube and instilling a fibrinolytic (e.g.,
streptokinase, 250,000 units)
– or performing thoracoscopy with the breakdown of adhesions.
– Decortication : when the above are ineffective.
ASPIRATION PNEUMONIA
Aspiration pneumonia
• results from inhalation of stomach
contents or secretions of the oropharynx,
leading to lower respiratory tract infection
• aspiration may cause:
– Chemical pneumonitis
– Obstruction
– Bacterial infection
• The usual site for an aspiration pneumonia
is the apical and posterior segments of the
lower lobe of the right lung
• If the patient is supine then the aspirated
material may also enter the posterior
segment of the upper lobe
http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
Epid
• It is common. One study of elderly
patients implicated aspiration
pneumonia in 10% or cases of
community-acquired pneumonia
• Aspiration pneumonia is relatively
common in hospital and usually
involves infection with multiple
bacteria, including anaerobes.
• It is more common in men, young
children and the elderly
Pathogens
• Pathogens of community-acquired aspiration pneumonia are
often the normal flora of the oropharynx, including:
– Streptococcus pneumoniae
– Staphylococcus aureus
– Haemophilus influenzae
– Anaerobes - eg, Peptostreptococcus, Fusobacterium and Prevotella
spp. 'Streptococcus milleri' group
– Klebsiella pneumoniae - increasingly seen in those with a history of
alcohol misuse.
• Pathogens of nosocomial aspiration pneumonia include[2]:
– Oral anaerobes - as above
– Gram-positive cocci - eg, Peptostreptococcus spp., Peptococcus spp
– Gram-negative bacilli - eg, enterobacteria (Klebsiella pneumoniae,
Escherichia coli, Enterobacter spp.), Pseudomonas aeruginosa
– Meticillin-resistant S. aureus (MRSA).
RF
• Impaired consciousness: drug or alcohol misuse,
general anaesthesia, seizures, sedation, acute
stroke, central nervous system lesions, head injury
• Poor mobility, nil by mouth status, increasing age,
chronic obstructive pulmonary disease (COPD),
male gender and increasing number of medications
• Swallowing disorders: oesophageal stricture,
dysphagia, stroke, bulbar palsy, pharyngeal disease
(eg, malignancy), neuromuscular disorders (eg,
multiple sclerosis).
• Other: tracheo-oesophageal fistula, ventilator-
associated pneumonia, periodontal disease, gastro-
oesophageal reflux, post-gastrectomy,
tracheostomy.
S/S
• Nonspecific symptoms - eg, fever, headache,
nausea, vomiting, anorexia, myalgia, weight
loss.
• Cough.
• Dyspnoea.
• Pleuritic chest pain.
• Purulent sputum.
• Signs may include tachycardia, tachypnoea,
decreased breath sounds and dullness to
percussion over areas of consolidation,
pleural friction rub.
• Severe infection may lead to hypoxia and
septic shock
DD
• Other causes of respiratory
distress, including:
– Other causes of pneumonia
– Bronchiolitis.
– Croup.
– Epiglottitis.
– Foreign body in respiratory tract
– Asthma.
– Cardiovascular disease.
Investigations
• Blood count: neutrophil leukocytosis.
• Electrolytes and renal function: dehydration, electrolyte
• imbalance.
• Blood culture.
• Blood gases.
• Culture of sputum: n patients with bacterial aspiration
pneumonia, this may show organisms normally resident in the
pharynx.
• CXR:
– Right, middle and lower lung lobes are the most common sites.
– Aspiration when upright may cause bilateral lower lung infiltrates.
– Right upper lobe often shows consolidation in those with a history of
alcohol misuse who aspirate in the prone position.
• Lung CT is only very occasionally required.
• Specimens obtained from bronchoscopy may help to guide
choice of antibiotic treatment
Management
• Mechanical obstruction: removal of the object, normally by
bronchoscopy.
• Tracheal suction if seen early.
• Intubation with positive pressure ventilation may be required.
• Bacterial infection of lower airways (the choice of antibiotics
will be influenced by any recent previous antibiotic treatment,
microbiology culture results and the patient's condition):
– Initial empirical antibiotic therapy while awaiting culture results.
– Antimicrobial therapy should be based on the patient's characteristics,
the setting in which aspiration occurred, the severity of pneumonia,
and available information regarding local pathogens and resistance
patterns
– Community-acquired aspiration pneumonia is often initially treated
with co-amoxiclav. Metronidazole may need to be added if there is
evidence of complications - eg, lung abscess
– Hospital-acquired aspiration pneumonia: a suitable combination in
patients who have already recently been treated with antibiotics is
piperacillin with tazobactam.
• The role of steroids is uncertain and
not of proven benefit.
• Supportive therapy with fluid
management, bronchodilators and
physiotherapy may help.
• Referral to speech and language
therapists.
Complication
• Lung abscess / bronchiectasis
• ARD
Prognosis
• This depends on the underlying cause, general well-
being of the patient, presence of complications,
speed of diagnosis and effective treatment.
Prevention
• Keep the head of the bed at a 30° angle: this
reduces the risk or aspiration pneumonia in those at
risk
• Nasogastric feeding for at-risk patients - eg, poor
gag reflex, dysphagia.
ACUTE COPD EXACERBATION
Edema paru
Edema paru
• Definisi ekstravasasi cairan • Etiologi dan patofisiologi
yang berasal dari vaskular paru 1. Edema paru kardiak akibat gagal
masuk ke dlm interstitium dan jantung kiri shg tekanan end-
alveoli paru diastolic ventrikel meningkat. Sbg
akibatnya, tek. Hidrostatik vena
pulmonalis dan kapiler paru juga
akan meningkat dan terjadi
ekstravasasi cairan ke jaringan
2. Edema paru non-kardiak bukan
akibat peningkatan tek.vena
pulmonalis. Penyebabnya ialah
peningkatan permeabilitas kapiler,
penurunan tek.onkotik plasma,
peningkatan tek limfatik maupun
penyebab neurogenik. Contohnya:
tenggelam, aspirasi benda asing,
cedera inhalasi, overload cairan,
ARDS, SAH, hipoalbuminemia dsb.
Edema paru
• Diagnosis • 2. pemeriksaan fisis
1. Anamnesis – Ronki basah halus sbg
- Sesak napas yg akibat dr cairan yg
bertambah hebat dlm terakumulasi di dlm
waktu singkat (jam/hari), alveolus
disertai ortopnea
– Wheezing, bila terjadi
- Kadang dpt ditemui
gejala batuk dg sputum edema pd saluran napas
berbusa kemerahan – Pd edema paru kardiak,
- Pd pasien edema paru ditemukan tanda2
kardiak, dpt ditemukan peningkatan intrakardiak
adanya riwayat seperti gallop S3,
penyakit/keluhan jantung peningkatan JVP, edema
sebelumnya (infark
jantung, aritmia, kelainan perifer, hepatomegali &
katup) hipertensi
Harrison’s principles of intenal medicine

Edema paru
• Diagnosis – Pada edema paru yg berat, tampak
gambaran opasitas alveolar dg batas
3. Pemeriksaan penunjang tdk tegas
Sangat disarankan utk melakukan – Bisa disertai dg efusi pleura
pemeriksaan rontgen thorax pd
pasien dg kecurigaan edem paru. – Pd edema paru kardiak, ditemukan
Tanda2 edema paru pd rontgen juga pembesaran ruang jantung
toraks :
- penebalan peribronkial
- peningkatan corakan vaskuler
hingga ke zona atas paru (gambaran
kranialisasi). Gamabaran tersebut
disebbakan oleh pelebaran vena
paru bag. Atas krn jumlah cairan yg
berlebihan
- adanaya Kerley B SIGN
menandakan adanya interstitial
edema

Pulmonary Edema
• Cardiogenic Edema • Non Cardiogenic
Edema
Edema paru
Goldman Cecil 24th edition
Edema paru- tatalaksana
• Pastikan jalan napas pasien bebas • Pasang akses vena segera dan monitor
• Posisikan setengah duduk tekanan darah, monitor EKG atau
• Berikan O2 sampai 8L/menit dg nasal oksimetri
kanul atau sungkup. Pertimbangkan utk • Pd kongesti paru dg tek sistolik baik,
intubasi endotrakeal dan dukungan berikan vasodilator atau diuretik
ventilator apabila : – nitrogliserin: ISDN dosis 0,4-0,6 mg
– Klinis sesak bertambah, takipnea, ronkhi sublingual, dpt diulang setiap 5-10 menit;
meningkat atau ISDN IV dosis 3-5 ug/kgbb apabila tek.
Darah sistolik 95 mmHg. Apabila belum ada
– PaO2 tdk bs dipertahankan >= 60 mmHg dg perbaikan, dpt diberikan nitropusida IV,
O2 konsentrasi dan aliran tinggi dimulai dr dosis 0.1 ug/kgbb/menit. Dosis
– Tdk mampu mengurangi edema secara dianikkan sampai klinis membaik atau tek.
adekuat Darah 85-90 mmHg pd pasien yg tadinya
normotensi, atau selama perfusi ke perifer
msh dpt dipertahankan
– Utk edema paru berat/ tdk membaik dg
nitrat, berikan diuretik furosemid 40-80mg IV
bolus, dpt diulang atau dosis ditingkatkan tiap
4 jam, atau dilanjutkan drip kontinu sampai
tercapai produksi urin 1ml/kgbb/jam.
– Bila perlu, berikan morfin sulfat IV (3-5 mg)
dpt diulang tiap 25 menit sampai dosis total
15 mg
Edema paru-tatalaksana
• Apabila tekanan darah • Penanganan lanjut pd
menurun atau terdapat pasien dg edema paru
tanda2 hipoperfusi, pikirkan kardiak :
kemungkinan gagal jantung – Diagnostik: pulmonary artery
akut. Pertimbangkan catheter (PAC), EKG,
pemberian : angiografi utk infark miokard
– Dopamin 5-15 ug/kgbb/menit – Terapi : intra-aortic ballon
IV atau NE 0,5-30 ug/menit IV pump (IABP),
bila tekanan sistolik < 100 reperfusi/revaskularisasi
mmHg atau
– Dobutamin 2-20
ug/kgbb/menit IV bila tek
sistolik 70-100 mmHg. Dosis
dpt dinaikkan sesuai respon
klinis

https://www.ncbi.nlm.nih.gov/pmc/articles/P
MC5408000/
• Algoritma ringkas penanganan
Edema paru edema paru (kardiak & non-
kardiak)
Kongesti paru & Vasodilator, diuretik bila

Ya
tek sistolik >90 ada overload cairan
mmHg ?
Tidak
Tek pengisian Tidak

jantung masih Fluid challenge test
adekuat?
Ya
tidak Inotropik, vasodilator, alat
bantu mekanik
-asidosis dg pengembalian CO2
msh adekuat?
Ya Periksa kembali (reasses)
-Saturasi O2>65%
-Perfusi perifer adekuat? secepatnya
Parrisis JT, Nikolau M, Mebazaa A, Ikonomidis I, Delgado J, Vilas-Boas F, dkk.
Acute pulmonary oedem: clinical characteristics, prognostic factors and in
Hospital management
https://www.ncbi.nlm.nih.gov/pmc
/articles/PMC5408000/figure/f1/
Pneumothorax
• Keadaan terdapatnya Udara/ Gas dalam Rongga
Pleura.
• Pada keadaan normal, Rongga Pleura Tidak
terdapat udara.
etiology
• Blunt trauma
• Penetrating trauma
• Spontaneous occurrence
• Iatrogenic
Classification
PSPrimer
P. Spontan
PSsekunder
Pneumo-
thorax
P. traumatic iatrogenic
Non-
iatrogenic
Pneumothorax Spontan Primer
• occurs without known lung disease
rupture of a subpleural bleb
multiple
↑ wall tension
Distention & eventual

rupture
Pneumothorax Spontan Sekunder
• underlying lung disease : • Patof :
– COPD
break in the pleura
– cystic fibrosis
– pulmonary infections
– interstitial lung disease air travels down a
pressure gradient
– Neoplasms into the intrapleural
– drug
dyspnea
useand hypoxemia space until pressure
equilibrium occurs
with partial or total
decreased vital lung collapse.
capacity
Pneumothorax Traumatic Iatrogenic
• Komplikasi tindakan medis
• Terbagi menjadi 2:
– Pneumothorax Traumatic Iatrogenic Accidental  tindakan
parasentesis dada, biopsi pleura, biopsi transbronkial,
barotrauma
– Pneumothorax Traumatic Iatrogenic artifisial  biasa
untuk terapi
Pneumothorax Traumatic non-Iatrogenic
• Jejas kecelakaan :
– Jejas terbuka
– Jejas tertutup
– barotrauma
Klasifikasi Lain
Berdasarkan jenis fistula :
1. Pneumothorax Terbuka  saat inspirasi
mediastinum tergeser ke arahyang terluka
(sucking wound)
2. Pneumothorax Tertutup  tekanan udara di
ruang pleura lebih tinggi dari sisi hemithorax
kontralateral, tp masih lebih < atmosfer
3. Tension Pneumothorax = penumothorax
ventil
Patofisiologi
Akibat peningkatan tekanan
Intrabronkial ( batuk/ bersin )
↓
Tekanan diteruskan s/d alveoli
( locus minoris / Bullae - fibrotik pada
alveoli )
↓
Alveoli robek sehingga
merobek pleura di sekitarnya
↓
Udara masuk intrapleura
↓
Pneumotoraks
Tension Pneumothorax
• Tekanan meningkat  penekanan dinding dada  mediastinum terdesak 
jantung terdesak  venous return turun  bocor dari paru  sesak makin hari
makin cepat  penurunan kesadaran  TD turun  oksigenasi turun  gawat
darurat  dekompresi segera agar udara dpt keluar
• Tatalaksana: oksigenasi, pasang selang (tusuk)
Clinical Features
• Dyspnea  80%
• Decreased breath sounds
• Tachypnea (24 breaths/min)
• Tachycardia (120 beats/min)
• Hyperresonance
• Tracheal deviation
• Hemodinamik compromise
Diagnosis
• Needle decompression
• expeditious chest tube thoracostomy
• 6-foot upright posteroanterior chest
radiograph (radiolucent area) GOLD
STANDARD
• CT
• USG  traumatic pneumothorax
Hasil pemeriksaan Endoskopi:
• Derajat 1 : pneumotoraks dengan gambaran
paru yang mendekati normal
• Derajat 2 : pneumotoraks dengan
perlengketan diserati hemotoraks
• Derajat 3 : pneumotoraks dengan diameter
bleb atau bulla
• Derajat 4 : pneumotoraks dengan banyak bulla
yg besar, diameter > 2 cm
Treatment
• Goals : Observation
– elimination of oxygen 3-4L/min
intrapleural air primary
catheter
– optimization of spontaneous
aspiration pneumothorax
pleural healing
– prevention of tube + WSD
recurrences thoracostomy
• Transthoracic pleurodesis
needle biopsy & video-assisted
thoracentesis  thorascopy
iatrogenic (VAT)
thoracotomy
Komplikasi
• Gagal nafas akut
• Pio-Pneumothoraks
• Hidro-Pneumothoraks/ Hemo-Pneumothoraks
• Henti jantung paru
• Kematian
• Pneumomediastinum dan emfisema subkutan 
komplikasi pneumothoraks spontan  sering karena
pecahnya esophagus atau bronkus.
prognosis
• Hampir separuhnya  kekambuhan
• Kekambuhan jarang terjadi pada pasien yang diakukan
torakkotomi terbuka
Analysis Blood Gas
ABG Analysis
• pH: 7.35-7.45
• PaCO2: 35-45mmHg
• HCO3: 22-26 mEq/L
• PaO2: > 80mmHg
• Oxygen Saturation >95%
Henry’s clinical diagnosis and management by

laborathory methods. 22 ed. China: Saunders
Elsevier:2006.
Analysis
• pH =Alkalosis
• pH =Acidosis
Normal values 7.35-7.45

Elsevier:2006.
Analysis
• PaCO2 = Respiratory
• PaCO2 = Respiratory
Normal value 35-45mmHg

Elsevier:2006.
Comparison Chart
pH PaCO2 HCO3
Resp Acid.
Resp Alk.
Metab Acid
Metab Alk

Elsevier:2006.
Respiratory Acidosis
Any disease process which decreases the
ability of the lungs to exchange CO2 for
oxygen.
Increased K+
Pneumonia
Asthma
CHF

Elsevier:2006.
Respiratory Acidosis
pH PaCO2

Elsevier:2006.
Respiratory Alkalosis
Anything which greatly increases
respiratory rate.
Fever
Pain
Anxiety
Overvenitilation with a mechanical venitalator
Decreased K+
Elsevier:2006.
Respiratory Alkalosis
pH PaCO2

Elsevier:2006.
Metabolic Acidosis
Anything which increases the
accumulation of acids or decreases the
amount of bicarbonate in the body.
Renal failure
Loss of bases from diarrhea
Increased K+
Diuretic therapy which causes HCO3 loss
Elsevier:2006.
Metabolic Acidosis
pH HCO3

Elsevier:2006.
Metabolic Alkalosis
Anything which decreases H ions in
The body or increases bicarbonate.
Prolonged vomiting

Elsevier:2006.
Metabolic Alkalosis
pH HCO3

Elsevier:2006.
Determining ABG’s
• First, Look at the pH.
• It can be high >7.45 (alkalosis)
• It can be low <7.35 (acidosis)
• It can be normal 7.35- 7.45 (normal)

Elsevier:2006.
Determining ABG’s
• A normal pH may indicate perfectly normal
blood gases, or it may be an indication of a
compensated imbalance.
• A compensated imbalance is one in which
the body has been able to correct the pH by
either respiratory or metabolic changes
(depending on the primary problem)

Elsevier:2006.
Example of compensation
• Pt. With primary metabolic acidosis starts out
with a low bicarbonate level but a normal
carbon dioxide level. Soon afterward, the
lungs try to compensate for the imbalance by
exhaling large amounts of carbon dioxide.
(hyperventilation)

Elsevier:2006.
Determine Primary Cause of
Disturbance
• Evaluate the PaCo2 & HCO3 in relation to the

pH.
• PaCo2 – 35-45mmHg
• HCO3 – 22-26 mEq/L

Elsevier:2006.
Interpreting ABG’s
• pH > 7.45 (alkalosis) and the PaCO2 is,
< 35 mmHg, the primary disturbance is respiratory
alkalosis. This occurs when a pt. hyperventilates and
“blows off” too much carbon dioxide.
• pH > 7.45 (alkalosis) and the HCO2 is > 26 mEq/L, the

primary disturbance is metabolic alkalosis. This
situation occurs when the body gains too much
bicarbonate, an alkaline substance.

Elsevier:2006.
• pH <7.35 (acidosis) and the PaCO2 is >
40mmHg, the primary disturbance is
respiratory acidosis. This situation occurs
when a patient hypoventilates and thus
retains too much carbon dioxide, an acidic
substance.

Elsevier:2006.
• pH < 7.35 (acidosis) and the HCO3 is
< 22mEq/L, the primary disturbance is
metabolic acidosis. This situation occurs when
the body’s bicarbonate level drops , either
because of direct bicarbonate loss or because
of gains of acids such as lactic acid or ketones.

Elsevier:2006.

Adriani Pemicu 4 KGD

Hochgeladen von

Dokumentinformationen

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

Adriani Pemicu 4 KGD

Hochgeladen von

Copyright:

Verfügbare Formate

Pemicu 4 KGD

Ventilatory Ventilatory Ventilatory

Ventilatory Ventilatory Ventilatory

Unfavorable alteration in Flattened domes of diaphragm caused by hyperinflation

• Pharmacologic • Neuromuscular causes

Airway Abnormalities Alveoli Abnormalities

• Upper airway obstruction • Mostly hypoxemic resp. failure

• Diagnosis begins with clinical suspicion of its presence.

• Is a zoonotic human infection

• Race  appears to be a factor only to the

• Avian influenza is still primarily a respiratory infection but

• The key history component  exposure to sick, dead, or dying

• Other symptoms  Risk factors or features that should

• Physical exam:  Lab tests:

• Mainstay of treatment   Antivirals  Neuraminidase

- Start oseltamivir prophylaxis4 as soon as possible

- If exposure is ongoing (e.g. caring for the patient)

- HPU to provide information leaflets5 and coordinate

- The extent of serological investigation will be agreed

Casual contact of a symptomatic case - Prophylaxis not indicated.

2 in transit (air/train/ferry/coach/car) Yes

4 Refer to dosing schedule for oseltamivir prophalyxis. (http://www.bnf.org/bnf/bnf/current/119743.htm)

Clinical review: Severe asthma,

Clinical review: Severe asthma,

Clinical review: Severe asthma,

Clinical review: Severe asthma,

Harrison’s Principle of Medicine, 18th ed

excess quantity of fluid in the pleural

• Loculated effusion = Fluid anatomically confined and not freely flowing in

Rosen's, 7th ed.

Rosen's, 7th ed.

Rosen's, 7th ed.

• Transudates = ultrafiltrates of plasma,

Rosen's, 7th ed.

Rosen's, 7th ed.

• Some pleural effusions may have characteristics of both

• If >=1 exudative criteria are met AND the patient is clinically

• If exudative pleural effusion, obtain the following tests :

Rosen's, 7th ed.

Rosen's, 7th ed.

Rosen's, 7th ed.

• Pleural effusions < 500 mL, however, can be

Rosen's, 7th ed.

• If the fluid recurs after the initial therapeutic thoracentesis &

Harrison’s principles of intenal medicine

Harrison’s principles of intenal medicine

Harrison’s principles of intenal medicine

Kongesti paru & Vasodilator, diuretik bila

Tek pengisian Tidak

Distention & eventual

Henry’s clinical diagnosis and management by

Normal values 7.35-7.45

Henry’s clinical diagnosis and management by

Normal value 35-45mmHg

Henry’s clinical diagnosis and management by

Henry’s clinical diagnosis and management by

Henry’s clinical diagnosis and management by

Henry’s clinical diagnosis and management by

Henry’s clinical diagnosis and management by

Henry’s clinical diagnosis and management by

Henry’s clinical diagnosis and management by

Henry’s clinical diagnosis and management by

Henry’s clinical diagnosis and management by

Henry’s clinical diagnosis and management by