KULIAH-Blok18-2012

63
Pemeriksaan Laboratorium Pada Kelainan Sistem Respirasi Dr. Sanarko Lukman Halim, SpPK Bagian Patologi Klinik F.K. UKRIDA

Transcript of KULIAH-Blok18-2012

Page 1: KULIAH-Blok18-2012

Pemeriksaan Laboratorium Pada

Kelainan Sistem Respirasi

Dr. Sanarko Lukman Halim, SpPKBagian Patologi Klinik

F.K. UKRIDA

Page 2: KULIAH-Blok18-2012

Tujuan PembelajaranSetelah mempelajari topik ini, mahasiswa memahamitentang berbagai pemeriksaan laboratorium yangdiperlukan pada berbagai kelainan/penyakit saluranpernafasan serta interpretasi hasil pemeriksaan1. Respiratory Acidosis dan Respiratory Alkalosis

akibat penyumbatan saluran pernafasan atau pada kelainan paru,rongga torak.

2. Kelainan paru yang disebabkan infeksi, alergi, trauma, kelainan koagulasi, cystic Fibrosis atau penyakit sistemik

Page 3: KULIAH-Blok18-2012

Fungsi Sistem Respiratorik• Oxygen transport• Respiration• Ventilation

– Air Pressure Variances– Airway Resistance– Compliance

• Lung Volumes and Capacities• Diffusion• Perfusion• Ventilation and Perfusion Balance and

ImbalanceThe act of moving air into and out of the lungs is called breathing.

Page 4: KULIAH-Blok18-2012

Respiratory Structures and Organs

Page 5: KULIAH-Blok18-2012

Transpor Gas• Oxygen is carried in

the blood in two forms: dissolved and attached to hemoglobin

• PaO2 represents the level of dissolved oxygen in plasma (about 3%)

• Rest is carried on hemoglobin - oxyhemoglobin

Page 6: KULIAH-Blok18-2012

Human Respiration• Works together with the circulatory system• Exchange of gases between atmosphere, blood,

and cells• If respiratory system and/or circulatory system

fails, death will occur• Cells need O2 for work; release CO2 as a waste

product• Accumulation of excess CO2 is toxic to cells and

MUST be removed

Page 7: KULIAH-Blok18-2012

Respiratory System• Intakes oxygen• Releases carbon

dioxide waste

Circulatory system• Transports gases

in blood between lungs and cells

Page 8: KULIAH-Blok18-2012

Kelainan Paru dan Saluran Pernafasan pCO2 ↑, pO2 ↓ → Respiratory Acidosis

• Airway obstruction • Asthma• Bronchitis, bronchiectasi, pneumonia,

Aspiration pneumonia, Hospital acquired pneumonia, Pneumonia in Immuno-supressed pneumonia.

• TBC• Chronic Obstructive Pulmonary Disease

(COPD)• Pulmonary Embolism

Page 9: KULIAH-Blok18-2012

Kelainan Paru dan Saluran Pernafasan pCO2 ↑, pO2 ↓ → Respiratory Acidosis

• Environment Lung DiseasesAsbestosis, Building-related Diseases

• Atelectasis• Abcess in the Lungs• Lung Cancer• Hyalin Membrane Disease

Page 10: KULIAH-Blok18-2012

FAKTOR-FAKTOR yang MENGURANGI FUNGSI RESPIRASI

• Positioning• Environment• Air pollution• Pollens and allergens• Smoking• Drugs and alcohol• Nutrition• Restricted lung movement• Airway obstruction

Page 11: KULIAH-Blok18-2012

Gagal PernafasanRespiratory FailurePaO2<60mmHg respiratory failure

Notice: sea level, quiet, inspire air rule off other causes ( heart disease)

PaCO2: The carbon dioxide partial pressure of

arterial bloodNormal: 35-45mmHg (4.7-6.0kPa) mean: 40mmHgSaO2: Saturation of arterial blood oxygenNormal: 0.95-0.98Significance: a parameter to evaluate hypoxia,but not sensitive

Page 12: KULIAH-Blok18-2012

Penyebab2 Asidosis RespiratorikRespiratory pathophysiology

respiratory arrestairway obstructionsevere pneumoniachest traumapneumothorax

Acute drug intoxicationespecially narcotics, sedatives

Residual neuromuscular blockadeHead trauma

Page 13: KULIAH-Blok18-2012

Penyebab2 Asidosis Respiratorik menahun

Chronic lung disease Neuromuscular diseaseExtreme obesity Chest wall deformity

Page 14: KULIAH-Blok18-2012

Penyebab2 Alkalosis RespiratorikPainAnxietyHyperventilationHypoxemiaRestrictive lung

diseaseSevere

congestive heart failure

Pulmonary emboli

DrugsSepsisFeverThyrotoxicosisPregnancyOveraggressive

mechanical ventilation

Hepatic failure

Page 15: KULIAH-Blok18-2012

Four primary conditions are possible 1. Respiratory acidosis

+ acute blood response+ chronic renal response

2. Respiratory alkalosis + acute blood response + chronic renal response

3. Metabolic acidosis+ respiratory response

4. Metabolic alkalosis+ respiratory response

Page 16: KULIAH-Blok18-2012

Blood Gas Alterations 1/2• Respiratory Acidosis

– Lower pH due to CO2 accumulation or retention in the blood greater than the high normal value

– Controlled by the lungs– Compensation attempts

• Kidneys attempt to excrete nonvolatile acids and retain HCO3

-Caused by inefficient respiration and/or hypoventilation-Can be acute or chronic–Tachycardia and cardiac arrythmias seen in acute respiratory acidosis

Page 17: KULIAH-Blok18-2012

Blood Gas Alterations 2/2• Respiratory Alkalosis

–pH is high due to low CO2–Increased respiratory rate blows

off CO2–Blood contains too little carbonic

acid (carbonic acid deficits)–Compensation

• Kidneys will excrete bicarbonate

Page 18: KULIAH-Blok18-2012

Management of Alterations Respiratory Acidosis

–Determine underlying cause of hypoventilation and treat the cause

• Respiratory Alkalosis –Determine underlying cause of

hyperventilation and treat the cause

Page 19: KULIAH-Blok18-2012

Sampel utk Analisa Gas Darah

clean procedure (gloves, alco wipe)Have gauze for application of pressure post

arterial puncture4 mins of pressure is idealEspecially in patients who are

anticoagulated23G needle easier, but use what you preferROTATION and INVERSION of the tube for 20

seconds to dissolve and mix the heparin Ice only necessary if there will be a delay from

sampling to testing.

Page 20: KULIAH-Blok18-2012

Hasil tes AGDpH - measures acidity/alkalinitypCO2 (partial pressure of CO2)

measures respiratory component[HCO3-] – (bicarbonate concentration)

measures metabolic componentderived value (H-H equation)

pO2 (partial pressure of O2)BE (base excess)O2 saturationSometimes AG (anion gap)Sometimes electrolytes and glucose

Page 21: KULIAH-Blok18-2012

Nilai Rujukan Gas Darah

Blood Gas Parameter Parameter Reported and Symbol Used

Normal Value

Carbon dioxide tension*

PCO2 35 – 45 mm Hg (average, 40)

Oxygen tension* PO2 80 – 100 mm Hg

Oxygen percent saturation

SO2 97

Hydrogen ion concentration (–Log CH+)*

pH 7.35 – 7.45

Bicarbonate HCO3- 22 – 26 mmol/L

Analisa Gas Darah/Arterial Blood Gases (ABG)

* Indicates measured parameter Normal values may differ slightly in exams

Page 22: KULIAH-Blok18-2012

 High pH Low pH

 Alkalosis Acidosis

 HighPaCO2

LowPaCO2

HighPaCO2

LowPaCO2

 Metabolic Respiratory Respiratory Metabolic

Page 23: KULIAH-Blok18-2012

Perlu di Tanya? Is the patient acidotic or alkalotic?

If pH < 7.35, the patient is acidoticIf pH > 7.45, the patient is alkalotic? Is the primary cause respiratory or

metabolic?? Is there compensation?? Is the patient hypoxic?

? (oxygen status, A-a)? What is going on?

Page 24: KULIAH-Blok18-2012

Oxygen status• Hypoxaemia

• decreased oxygen content of blood • pO2 less than 60 mmHg and

saturation is less than 90%

• Hypoxia• Levels of pO2 sufficiently low to

have an adverse effect on tissue function

Page 25: KULIAH-Blok18-2012

Jenis-jenis Hipokia Hypoxic hypoxia

due to low blood pO2e.g. due to lung disease processes

Anaemic hypoxiainadequate O2 delivery to tissues

e.g. in anaemia or CO poisoning Circulatory hypoxia

inadequate blood flow to tissuese.g. shock

Histotoxic hypoxiainability of tissue to use the oxygen

classically, in cyanide poisoning

Page 26: KULIAH-Blok18-2012

• CO2 and PCO2

– Pulmonary function & CO2 homeostasis– CO2 elimination

• Hyperventilation– Lowering PCO2

– Alveolar hyperventilation– Causes of alveolar hyperventilation

• Hypoventilation– Raising PCO2

– Alveolar hypoventilation– Causes of alveolar hypoventilation

Page 27: KULIAH-Blok18-2012

EquivalencesDisorder Cause Mechanism

Respiratory acidosis

Hypercapnia Alveolar hypoventilation

pH PCO2 CO2 retention

Respiratory alkalosis

Hypocapnia Alveolar hyperventilation

pH PCO2 blow off CO2

Page 28: KULIAH-Blok18-2012

Respiratory Compensation for Preventing Change in pH

AcidosisCO2 H+

AcidaemiapH , PCO2

CO2 removalVia respiration

Normal pH

Normal or CO2 removal

Slow or CO2 removal

Cells/Tissue Blood

Lungs

Blood

Hypoventilate

Hyperventilate

Acidosis may be accompanied by acidaemia.The change in pH may be prevented by respiratory removal of CO2.

Page 29: KULIAH-Blok18-2012

Respiratory Compensation for Preventing Change in pH

AlkalosisCO2

HCO3-

AlkalaemiapH , PCO2 , HCO3

-

CO2 retentionVia respiration

Normal pH

Normal or CO2 retention

Slow or CO2 retention

Cells/Tissue Blood

Lungs

BloodHypoventilate

Hyperventilate

Alkalosis will not be accompanied by alkalaemia if enough CO2 has been retained to prevent the change in pH.

Page 30: KULIAH-Blok18-2012

Terms used for describing compensation• Compensated

– The compensatory mechanisms have come into play in a normal manner; does not necessarily imply that the plasma pH is within the normal range

• Uncompensated– Compensation cannot occur due to some

abnormality; patient may show no sign of compensation

• Partially compensated– Intermediate state where compensation is

occurring but is not yet as complete as it should be

Page 31: KULIAH-Blok18-2012

Metabolic and Respiratory Acid-Base Changes in Blood

pH pCO2 HCO3-

Acidosis1. Acute metabolic N 2. Compensated metabolic N 3. Acute respiratory N4. Compensated respiratory N

Alkalosis1. Acute metabolic N 2. Chronic metabolic 3. Acute respiratory N4. Compensated respiratory N

=decreased; =increased; N=normal

Page 32: KULIAH-Blok18-2012

Sputum (bukan Ludah) Collection• Proper patient instruction

– Food should not have been ingested for 1-2 h prior to expectoration

– The mouth should be rinsed with saline or water

– Patient should breathe and cough deeply– Patient should expectorate into a

sterile container• Transport container immediately to lab• Perform Gram stain and plant specimen as

soon as possible

Page 33: KULIAH-Blok18-2012

Sputum collection

• Sputum of less than 2ml should not be processed unless obviously purulent

• Only 1 sputum per 24hr .submitted • Some scoring system should be used to

reject specimen that re oral contamination.

Page 34: KULIAH-Blok18-2012

Sputum collection

• Transportation in <2 hr is recommended with refrigeration if delays anticipated.

• Handle all samples using universal precautions.

• Perform Gram stain and plant specimen as soon as possible

Page 35: KULIAH-Blok18-2012

Induced sputumPatients who are unable to produce sputum maybe assisted by respiratory therapy technician.Aerosol induced specimen are collected byallowing the patient to breath aerosolized dropletsof a solution of 15% sodium chloride and 10%glycerin for approximately 10 minute . Obtainingsuch specimen may avoid the need for a moreinvasive procedures ,such as bronchoscopy orneedle aspiration, in many cases.

Page 36: KULIAH-Blok18-2012

Sputum Gram Stain and CultureProponents• Demonstration of

predominant morphotype on Gram stain guides therapy

• Accuracy is good when strict criteria are used

• Cheap, so why not?

Antagonists• Poor specimen

collection• Intralaboratory

variability (Gram stain interpretation)

• Low sensitivity and specificity

• Empiric treatment guidelines

• Not cost effective

Page 37: KULIAH-Blok18-2012

Gastric aspirationThe gastric aspiration is used exclusively forisolation of acid-fast bacilli and may be collectedfrom patients who are unable to produce sputum,particularly young children. The relative resistanceof mycobacteria allows them to remain viable for ashort period. Gastric lavage must be delivered tothe lab immediately so that the acidity can beneutralized. Specimen can be first neutralized andthen transported if immediate delivery is notpossible.

Page 38: KULIAH-Blok18-2012

Definition Pleural Effusions• Increased amount of fluid within the

pleural cavity– Stedman’s Medical Dictionary

• Accumulation of fluid between the layers of the membrane that lines the lungs and the chest cavity– Medline Plus

Urgent pleural disorders• Pleural emergencies: haemorrhage - haemothorax

elevated pleural pressure- tension pneumothorax

- massive pleural effusion

Page 39: KULIAH-Blok18-2012

Haemothorax pleural fluid with Ht > 50% blood Ht

CAUSES:• chest trauma: penetrating / non – penetrating

(lung blood vessels, chest wall, diaphragm, pleural adhesions, mediastinum, large vessels, abdomen)

• iatrogenic(pleural biopsy, subclavian or jugular CVC placement, thoracentesis, transthoracic or transbronchial NA, esophageal variceal TH,...)

• nonthraumatic(pleural malignancy, anticoagulant TH, spontaneous rupture of vessel (AO aneurism), bleeding disorder, thoracic endometriosis)

Page 40: KULIAH-Blok18-2012

Tipe• Hydrothorax• Hemothorax• Chylothorax• Pyothorax / Empyema

Efusi PleuraKlasifikasi a. Transudate

– Ultrafiltrate of plasma

– Small group of etiologies

b. Exudate– Produced by host

of inflammatory conditions

– Large group of etiologies

Page 41: KULIAH-Blok18-2012

DISORDERS• Obstruction of Upper

Airway• Atelectasis• Tracheobronchitis• Pneumonia

– Bacterial– Viral– Fungal– Aspiration– Hypostatic– Chemical

• Tuberculosis• Abscess

• Pleural disorders• Pulmonary edema• Chest Trauma• Pulmonary Emboli

(PE)• Chronic obstructive

pulmonary disease (chronic airflow limitation)– Bronchitis– Emphysema– Asthma– Bronchiectasis

Page 42: KULIAH-Blok18-2012

Diagnostic Tests• CBC• Chest x-ray/ CT• MRI/Fluoroscopic studies• Sputum culture and

sensitivity• ABG’s• Pulse oximetry

• Bronchoscopy• Mantoux• Pulmonary

angiography• Pulmonary Function

Test• VQ Scan• Thoracentesis

Page 43: KULIAH-Blok18-2012

The Tuberculosis (TB) PandemicTB is spread from an

infectiousperson to a vulnerable personthrough the air

TB usually affects the lungsbut can affect any part of an infected person

Page 44: KULIAH-Blok18-2012

HIV/AIDS and TB: A Deadly Combination

• HIV suppresses the human immune system• TB suppresses the human immune system• Each makes the other worse synergistically

Page 45: KULIAH-Blok18-2012

Definition of Asthma• Chronic inflammatory disorder of the

airways in which many cells and cellular elements play a role. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are associated with widespread but variable airflow obstruction that is reversible either spontaneously, or with treatment.

Page 46: KULIAH-Blok18-2012

Bronchial Asthma

Page 47: KULIAH-Blok18-2012

Risk Factors for COPDHost factors

• Alpha-1-antitrypsin deficiency

• Asthma and airway hyperresponsiveness

• Disordered lung development

Environmental factors• Tobacco smoke• Occupational

dusts/chemicals• Air pollution• Childhood

infections• Lower

socioeconomic status

Page 48: KULIAH-Blok18-2012

Chronic Bronchitis• Persistent cough with sputum production

for at least 3 months in ≥ consecutive years

• Simple / Chronic asthmatic / Obstructive• Most frequent in middle-aged men• Higher incidence in urban dwellers• May coexist with emphysema• Presents with exertional dyspnoea and

frequent respiratory tract infections

Page 49: KULIAH-Blok18-2012

Komplikasi Bronkhitis Menahun• ↓PaO2 ↑PaCO2 ….Respiratory failure• Respiratory tract infections (H. influenzae,

Strep. Pneumoniae)• Pulmonary hypertension → Cor

pulmonale• Atypical metaplasia / dysplasia of

respiratory epithelium….Bronchogenic carcinoma

Page 50: KULIAH-Blok18-2012

Emphysema• Abnormal permanent enlargement of the

airspaces distal to the terminal bronchiole, accompanied by destruction of their walls

• Types: (1) centrilobular(2) panlobular(3) paraseptal(4) irregular

• Associated with heavy cigarette smoking

Page 51: KULIAH-Blok18-2012

Patogenesis Emfisema

Page 52: KULIAH-Blok18-2012

Bronchiectasis• A chronic necrotising infection of the

bronchi and bronchioles associated with abnormal permanent dilation of these airways

• Presents with cough, productive of large amounts of foul-smelling, purulent sputum, hamoptysis and digital clubbing

• Pooled secretions in lower lobes → respiratory tract infections

Page 53: KULIAH-Blok18-2012

Bronchiectasis Aetiology • Bronchial obstruction

Tumour, foreign bodies, mucous impactionAsthma / Chronic bronchitis

• InfectionTuberculosis, Staphylococcus aureus, Measles, Pertussis

• CongenitalCongenital bronchiectasis, Cystic fibrosis, Intralobar sequestration, Immunodeficiency, Kartagener’s syndrome, Yellow nail syndrome

Page 54: KULIAH-Blok18-2012

Cystic Fibrosis Genetic defect

Page 55: KULIAH-Blok18-2012
Page 56: KULIAH-Blok18-2012

Lung Abscess

Figure 16-1. Lung abscess. A, Cross-sectional view of lung Figure 16-1. Lung abscess. A, Cross-sectional view of lung abscess. abscess. AFC,AFC, Air-fluid cavity; Air-fluid cavity;

RB,RB, ruptured bronchus (and drainage of the liquified contents ruptured bronchus (and drainage of the liquified contents of the cavity); of the cavity); EDA,EDA, early development of abscess; early development of abscess; PM,PM, pyogenic membrane. Consolidation (B) and excessive pyogenic membrane. Consolidation (B) and excessive

bronchial secretions (C) are common secondary anatomic bronchial secretions (C) are common secondary anatomic alterations of the lungs.alterations of the lungs.

A

AFC

RB

EDAPM

B

C

Page 57: KULIAH-Blok18-2012

Atelectasis Assessment and Diagnostic Findings

• SpO2 < 90%• PaO2 < 80• PaCO2 > 45• HCO3- to

compensate

Page 58: KULIAH-Blok18-2012

Evaluasi Laboratorium• Deteksi berkurangnya fungsi saluran

pernafasan dan alveoli → Analisa Gas Darah.• Deteksi adanya infeksi dengan memperhatikan

1. Petanda hematologi adanya infeksi/inflamasi:* Jumlah Leukosit, Gambaran Darah Tepi,

LED, CRP, IgE. 2. Deteksi kuman: pembiakan, preparat,secara

imunologis• Periksa adanya cystic fibrosis sebagai

penyebab sputum kental→ infeksi, sesak nafas (DD/ Asma)

Page 59: KULIAH-Blok18-2012

Retensi CO2 PCO2

• Meningkatnya CO2 → H+ → AsidosisAnalisa gas darah Respiratory Acidosis

Reaction shifts right

Retention of CO2 by the lungs CO2, PCO2

CO2 + H2O H2CO3 H+ + HCO3-

Reaction shifts right [H+], pH, acidosis

Page 60: KULIAH-Blok18-2012

Mikrobiologi• The culture of lower respiratory specimens may

result in more unnecessary microbiologic effort than any other type of specimen.”

• Overtreatment has lead to resistance – Multidrug resistant Streptococcus

pneumoniae– Resistance among hospital acquired

pathogens such as Acinetobacter, Pseudomonas aeruginosa E.coli K.pneumonia (ESBLs) MRSA and others

Page 61: KULIAH-Blok18-2012

Categories of Lower Respiratory Tract Infections

• Acute bronchitis• Community acquired pneumonia• Hospital acquired pneumonia• Pneumonia in the

immunocompromised host

Page 62: KULIAH-Blok18-2012

Community Acquired Pneumonia Diagnosis Available Test Methodologies

• Sputum Gram stain and culture• Blood cultures• Serologic studies• Antigen detection tests• Nucleic acid amplification tests

Page 63: KULIAH-Blok18-2012

McPherson RA., Pincus MR., Editors Henry’s Clinical Diagnosis and Management by Laboratory Methods 21st edition, ISBN-13:978-1-4260-0287-1 Saunders Elsevier 2007

Daftar Kepustakaan

1. Gaw A, Clinical Biochemistry, ISBN 0-443-04481-3 Churchill Living Stone New York, 1995, 92-93 Churchill Living Stone New York ISBN 0-443-04481-3. 1995

2. Abraham P. editor, Physiology, ISBN-13: 978-1-905704-64-4, Amber Books London , 2007 6

3. Johnston SL, Holgate ST, Asthma: Critical Debate, ISBN 0-632-05721-1 Oxford,England, Blackwell Science,2002.