Interpretasi Trigger

http://www.emedicinehealth.com/pediatric_vital_signs/article_em.htm
Quick Overview
Blood pressure, body temperature, pulse rate, and respiratory rate are the routine vital signs
measured in medicine. These vital signs remain relatively constant throughout our adult life.

As infants and children grow and age, their normal values for vital signs change. Body
temperature does not change with age, and normal body temperature is considered
98.6 F (37 C).
Two tables of normal vital signs for the pediatric population are presented below. Heart
rates may be slightly slower when asleep.

Age (year)

Respiratory Rate
(breaths/min)

Heart Rate (beats/min)

<1

30-60

100-160

1-2

24-40

90-150

2-5

22-34

80-140

6-12

18-30

70-120

>12

12-16

60-100

Lower limits of systolic pressure

0-28 days: 60 mm Hg
1-12 months: 70 mm Hg
1-10 years: 70 mm Hg + (2 times age in years)

Vital Signs at Various Ages

Age

Prematur

Heart Rate
(beats/min)
120-170 *

Blood Pressure
(mm Hg)
55-75/35-45

Respiratory Rate
(breaths/min)
40-70

e
0-3 mo

100-150 *

65-85/45-55

35-55

3-6 mo

90-120

70-90/50-65

30-45

6-12 mo

80-120

80-100/55-65

25-40

1-3 yr

70-110

90-105/55-70

20-30

3-6 yr

65-110

95-110/60-75

20-25

6-12 yr

60-95

100-120/60/75

14/22

12 > yr

55-85

110-135/65/85

12-18

* From Dieckmann R, Brownstein D, Gausche-Hill M (eds): Pediatric Education for

Prehospital Professionals. Sudbury, Mass, Jones & Bartlett, American Academy of
Pediatrics, 2000, pp 43-45. Continue Reading
REFERENCES:
Kleigman, R.M., et al. Nelson Textbook of Pediatrics, 19th ed. Philadelphia: Saunders,
2011.
Marx, J., et al. Rosen's Emergency Medicine: Concepts and Clinical Practice. 8th ed.
Philadelphia: Saunders, 2013.
http://www.webmd.com/children/normal-breathing-rates-for-children

Normal Breathing Rates for Children

Babies and children normally breathe faster than older children and adults. A child who
has a fever or who feels anxious breathes faster than normal. The table below shows
the normal rate of breathing for children.
Normal breathing rates for children
Age

Newborn to 6 months

Breaths per minute

30-60

Normal breathing rates for children

Age

Breaths per minute

6 to 12 months

24-30

1 to 5 years

20-30

6 to 12 years

12-20

ByHealthwise Staff
Primary Medical ReviewerWilliam H. Blahd, Jr., MD, FACEP - Emergency Medicine
Specialist Medical ReviewerDavid Messenger, MD
Current as ofJune 4, 2014

Normal Vital Signs

In most medical settings, the four standard primary vital signs are as follows: [1]

Heart rate (pulse)

Respiratory rate
Blood pressure
Body temperature
Normal values for each of these vital signs vary by age and, in some cases, by sex.

Heart rate
Table 1. Normal Heart Rate by Age (Open Table in a new window)

Approximate Age Range

Heart Rate

Newborn

100-160

0-5 months

90-150

6-12 months

80-140

1-3 years

80-130

3-5 years

80-120

6-10 years

70-110

11-14 years

60-105

15-20 years

60-100

Adults

50-80

Respiratory rate
Table 2. Normal Respiratory Rate by Age (Open Table in a new window)

Approximate Age Range

Respiratory Rate

Newborn

30-50

0-5 months

25-40

6-12 months

20-30

1-3 years

20-30

3-5 years

20-30

6-10 years

15-30

11-14 years

12-20

15-20 years

12-30

Adults

16-20

Blood pressure
The normal blood pressure in adults is 120 (systolic)/80 (diastolic). Normal blood pressure in children and
adolescents varies by age.
Table 3. Normal Blood Pressure by Age in Children and Adolescents (Open Table in a new window)

Approximate Age Range

Systolic Range

Diastolic Range

1-12 months

75-100

50-70

1-4 years

80-110

50-80

3-5 years

80-110

50-80

6-13 years

85-120

55-80

13-18 years

95-140

60-90

Temperature
The average normal core temperature is generally considered to be between 98.0F (36.6C) and
98.6F (37C) when measured orally and about 1F higher when measured rectally.[2]

Retraksi interkosta
- retraksi interkostal (meningkatnya pemakaian otot-otot leher dan dada sebagai usaha untuk bernafas).

Bronkiolitis
GEJALA
Gejalanya berupa:
- batuk
- wheezing (bunyi nafas mengi)
- sesak nafas atau gangguan pernafasan
- sianosis (warna kulit kebiruan karena kekurangan oksigen)
- takipneu (pernafasan yang cepat)
- retraksi interkostal (otot di sela iga tertarik ke dalam karena bayi berusaha keras untuk bernafas)
- pernafasan cuping hidung (cuping hidung kembang kempis)
- demam (pada bayi yang lebih muda, demam lebih jarang terjadi).

Krup (Laringotrakeobronkitis)
Gejala lainnya yang mungkin ditemukan:
- stridor (bunyi pernafasan yang bernada tinggi)
- sianosis (warna kulit menjadi kebiruan karena kekurangan oksigen)
- retraksi interkostal (meningkatnya pemakaian otot-otot leher dan dada sebagai usaha untuk bernafas).
DIAGNOSA
Diagnosis ditegakkan berdasarkan gejala dan hasil pemeriksaan fisik yang menunjukkan adanya retraksi
interkostal pada saat anak menghirup nafas.
Pemeriksaan dengan stetoskop menunjukkan adanya wheezing (bunyi nafas mengi), fase inspirasi
(penghirupan udara) dan ekspirasi (penghembusan udara) yang memanjang dan berkurangnya suara
pernafasan.
Rontgen leher bisa menunjukkan adanya penyempitan trakea.

7. Retraksi intercostal terlihat pada saat penarikan intercosta secara paksa sehingga costa
tertarik keatas.
Diagnosis etiologik berdasarkan pemeriksaan mikrobiologis dan/atau serologis
merupakan dasar terapi yang optimal. Akan tetapi, penemuan bakteri penyebab tidak selalu mudah karena
memerlukan laboratorium penunjang yang memadai. Tidak ada gejala distress pernafasan, takipneu, batuk, ronki,
dan peningkatan suara pernafasan dapat menyingkirkan dugaan pneumonia. Terdapatnya retraksi epigastrik,
interkostal, dan suprasternal merupakan indikasi tingkat keparahan.

Pneumonia
3. TANDA dan GEJALA
Sesak Nafas
Batuk nonproduktif
Ingus (nasal discharge)
Suara napas lemah
Retraksi intercosta
Penggunaan otot bantu nafas
Demam
Ronchii
Cyanosis
Leukositosis
Thorax photo menunjukkan infiltrasi melebar

1.

Retraksi interkosta : kemungkinan retraksi pada obstruksi jalan nafas

2. Retraksi Intercostal pada saat inspirasi

Menunjukkan adanya obstruksi jalan nafas atau menurunnya complence paru-paru

yang menyebabkan paru-paru kolaps.
VOCAL FREMITUS
Palpasi thorax
Tactil fremitus : kedua telapak tangan pemeriksa menempel pada dinding thorax : seperti
pada bagian posterior atau punggung, kemudian pasien disuruh berucap kata-kata
seperti 77
dengan nada yang sedang kemudian secara simetris, dibandingkan getaran yang
timbul pada
dinding thorax yang dirasakan pada kedua telapak tangan pemeriksa.

- Fremitus meningkat bisa pada :

- Infiltrat paru
- Compressive atelektasis
- Cavitas paru
Fremitus taktil memberikan informasi yang berguna mengenai kepadatan jaringan paru-paru
dan rongga dada dibawahnya.
Fremitus meningkat pada keadaan dengan infiltrat paru, compressive atelektasis, cavitas paru.
Keadaan seperti ini kepadatan paru-paru meningkat seperti konsolidasi, sehingga
meningkatkan penghantaran fremitus taktil.
Fremitus menurun atau melemah pada keadaan penebalan pleura, efusi pleura, pneumotoraks,
emfisema paru dan obstruksi dari bronkus. Keadaan klinis yang mengurangi penghantaran
gelombang suara ini akan mengurangi fremitus taktil. Jika ada jaringan lemak yang berlebihan
di dada, udara atau cairan di dalam rongga dada, atau paru-paru yang mengembang secara
berlebihan, fremitus taktil akan melemah.

Fremitus vokal menurun pada saluran udara bagian atas dapat menunjukkan
Para obstruksi bronkus utama dari
Pneumo-, hidro-, haemothorax
Emfisema paru-paru
adipositas juga dapat menjadi penyebab penurunan fremitus vokal.
Suara fremitus meningkat
Pada pneumonia
Dalam Abses
Dalam ateletasis
Dalam gua
Tidak adanya fremitus biasanya menunjukkan obstruksi bronkus besar dari, yang mungkin terjadi sebagai hasil dari
aspirasi benda asing. Penurunan atau fremitus absen adalah selalu dicatat dan dilaporkan untuk penyelidikan lebih
lanjut. Selama palpasi getaran lain yang menunjukkan kondisi patologis dicatat. Salah satunya adalah friction rub
pleura, yang memiliki sensasi okulasi. Hal ini sinkron dengan gerakan pernapasan dan merupakan hasil menentang
permukaan lapisan pleura yang meradang bergesekan satu sama lain.
Kertak dirasakan sebagai sensasi, kasar retak sebagai menekan menyerahkan daerah yang terkena. Ini adalah hasil
dari keluarnya udara dari paru-paru ke dalam jaringan subkutan dari cedera atau intervensi bedah. Kedua
menggosok gesekan pleura dan kertak biasanya dapat didengar serta dirasakan.

PALPASI

1. Menurunnya atau hilangnya Vocal Fremitus

Vokal fremitus terjadi karena transmisi getaran melalui bronchotracheal melalui septum
paru dan pleura. Gangguan transmisi karena misalnya destroyed lung, penebalan
pleura, atau efusi akan menurunkan vocal fremitus. Sumbatan jalan nafas atas akan
menghilangkan vocal fremitus.
2. Meningkatnya vocal fremitus
Peningkatan tekanan di septum paru akan meningkatkan transmisi getaran. Terjadi
pada pneumonia.
PERKUSI
1.

PERKUSI
Suara perkusi

Paru normal : sonor/resonan

Pneumothoraks : hipersonor

Jaringan padat (jantung, hati) : pekak/datar

Daerah yang berongga : tympani

Batas organ
Sisi dada kiri : dari atas ke bawah ditemukan sonor/resonan-

tympani : ICS 7/8 (Paru-lambung)

Sisi dada kanan : ICS 4/5 (paru-Hati)
Dinding posterior :-Supraskapularis (3-4jari di pundak) batas

atas paru

-Setinggi vertebratorakal 10 garis skapula batas bawah

paru

RONKI BASAH HALUS

1.

Ronki basah. Ronki basah sering juga disebut dengan suara

krekels (crackles) atau rales. Ronki basah merupakan suara berisik dan
terputus akibat aliran udara yang melewati cairan. Ronki basah halus,
sedang atau kasar tergantung pada besarnya bronkus yang terkena dan
umumnya terdengar pada inspirasi. Ronki basah halus biasanya terdapat
pada bronkiale, sedangkan yang lebih halus lagi berasal dari alveolus yang
sering disebut krepitasi, akibat terbukanya alveoli pada akhir inspirasi. Sifat
ronki basah ini dapat nyaring (infiltrat)atau tidak nyaring (pada edema paru).
Krekel dapat dihilangkan dengan batuk, tapi mungkin juga tidak. Krekels
mencerminkan inflamasi atau kongesti yang mendasarinya dan sering timbul

pada kondisi seperti pneumonia,bronkitis, gagal jantung kongesti,

bronkiektasis, dan fibrosis pulmonal serta khas pada pneumonia dan
interstitial atau fibrosis.Timing (waktu) ronkhi ini sangat penting. Ronki
inspirasi awal menunjukan kemungkinan penyakit pada jalan napas kecil,
dan khas untuk hambatan jalan napas kronis. Ronki lainnya terdengar pada
inspirasi awal dan bersifat kasar sedang. Ronki berbeda dengan yang
terdengar pada gagal ventrikel kiri yang terjadi di akhir siklus pernapasan.
Ronki pada inspirasi akhir atau paninspirasi menunjukan kemungkinan penyakit yang mengenai
alveoli dan dapat bersifat halus, sedang, atau kasar. Ronki halus dideskripsikan sebagai bunyi rambut
yang digosok-gosok dengan jari-jari tangan. Bunyi ini secara khas disebabkan oleh fibrosis paru.
Ronki sedang biasanya akibat gagal ventrikel kiri, bila ada cairan alveoli merusak fungsi dari
surfaktan yang disekresi dalam keadaan normal. Ronki kasar khas untuk pengumpulan sekret yang
tertahan dan memiliki kualitas seperti mendeguk yang tidak mengenakan. Bunyi ini cenderung
berubah dengan batuk yang juga memiliki kualitas yang sama. Bronkiektasis paling sering
menyebabkan terjadinya ronki, tetapi setiap penyakit yang menimbulkan retensi sekret dapat
menyebabkan gangguan ini.
Ronki mungkin disebabkan oleh hilangnya stabilitas jalan napas perifer yang kolaps pada saat
ekspirasi. Tekanan inspirasi yang tinggi menyebabkan terjadinya pemasukan udara cepat ke dalam
unit-unit udara distal. Hal ini menyebabkan pembukaan yang cepat dari alveoli dan bronkus kecil
atau bronkus sedang yang mengandung sekret pada bagian-bagian paru yang berdeflasi sampai
volume residu.
3

Ronki basah (
crackles
atau rales)merupakan suara napas yang terputus-putus, bersifat nonmusical, biasanya terdengar
saat inspirasi akibat udara yang melewati cairan dalam salurannapas. Ronki basah dibagi ronki
basah halus dan kasar tergantung besarnya bronkus yangterkena. Ronki basah halus terjadi
karena adanya cairan alveoli pada bronkiolus, sedangkan padaronki basah yang lebih halus
berasal dari alveoli (krepitasi)akibat terbukanya alveoli pada akhirinspirasi terjadi terutama pada
fibrosis paru. Sifat ronki basah ini dapat bersifat nyaring (bila adainfiltrasi misal pneumonia)
atau tidak nyaring (edema paru). (Rumende, 2007)AdapunPatomekanisme ronchi basah
yaitu : Jika tekanan hidrostatik anyaman kapiler paru-paru meningkat melebihi tekanan
onkotik pembuluh darah maka akan terjadi transudasi cairan ke dalam interstisial. Apabila
kecepatannyamelebihi kecepatan drainase limfatik maka akan timbul edema interstisial. Bila
terjadi peningkatan tekanan lebih lanjut, cairan akan merembes ke alveoli sehingga menimbulkan
edema paru.
Seperti klarifikasi ronchi basah yaitu bunyi yang terdengar bila terdapat cairan di dalam
bronkus atau alveoli. Ronchi terdengar di basal medial paru karena cairan terakumulasi di
bagian bawah paru karena pengaruh gaya gravitasi
KREPITASi
Krepitasi

Krepitasi (ronki) adalah bunyi singkat, tidak kontinue, tidak musikal, banyak didengar
selama inspirasi. Bunyi krepitasi seperti bunyi yang dibuat dengan menggosokkan rambut di
dekat telinga atau bunyi ketika memasukkan garam ke dalam api. Krepitasi ditemukan pada
edema paru-paru, gagal jantung kongestif dan fibrosis paru.

Ronchi basah (krepitasi) : bunyi tambahan yang terdengar tidak kontinyu pada waktu
inspirasi seperti bunyi ranting kering yang terbakar, disebabkan oleh secret di dalam
alveoli atau bronkiolus. Ronki basah dapat halus, sedang, dan kasar. Ronki halus dan
sedang dapat disebabkan cairan di alveoli misalnya pada pneumonia dan edema paru,
sedangkan ronki kasar misalnya pada bronkiekstatis.

normal values: RBC, Hgb, Hct, and Indices

Male

Age

RBC
(106/mm3)

HGB
(g/dL)

HCT (%) MCV (fL) MCH

(pg)

MCHC
(%)

Birth

4.1 - 6.7

15.0 24.0

44 - 70

102 - 115 33 - 39

32 - 36

1 Month

3.8 - 5.4

10.5 14.0

44 - 56

72 - 88

24 - 30

32 - 36

3 Months 3.8 - 5.4

10.5 14.0

32 - 42

72 - 88

24 - 30

32 - 36

6 Months 3.8 - 5.4

10.5 14.0

32 - 42

72 - 88

24 - 30

32 - 36

9 Months 3.8 - 5.4

10.5 14.0

32 - 42

72 - 88

24 - 30

32 - 36

1 Year

3.8 - 5.4

10.0 14.0

32 - 42

72 - 88

24 - 30

32 - 36

2 Years

4.0 - 5.3

11.5 14.5

32 - 42

72 - 88

25 - 31

32 - 36

4 Years

4.0 - 5.3

11.5 -

32 - 42

76 - 90

25 - 31

32 - 36

14.5
8 years

4.0 5.1

11.5 14.5

33 - 43

76 - 90

25 - 31

32 - 36

14 Years

4.1 5.3

12.5 16.1

35 - 45

78 - 95

26 - 32

32 - 36

Adult

4.3 5.9

13.5 18.0

42 - 52

78 - 100

27 - 31

32 - 36

Female
Age

RBC
(106/mm3)

HGB
(g/dL)

HCT (%) MCV (fL) MCH

(pg)

MCHC
(%)

Birth

4.1 - 6.7

15.0 24.0

44 - 70

102 - 115 33 - 39

32 - 36

1 Month

3.5 - 5.4

10.5 14.0

44 - 56

72 - 88

24 - 30

32 - 36

3 Months 3.5 - 5.4

10.5 14.0

32 - 42

72 - 88

24 - 30

32 - 36

6 Months 3.5 - 5.4

10.5 14.0

32 - 42

72 - 88

24 - 30

32 - 36

9 Months 3.5 - 5.4

10.5 14.0

32 - 42

72 - 88

24 - 30

32 - 36

1 Year

3.5 - 5.4

10.5 14.5

32 - 42

72 - 88

24 - 30

32 - 36

2 Years

4.0 5.3

11.5 14.5

32 - 42

72 - 88

25 - 31

32 - 36

4 Years

4.0 5.3

11.5 14.5

32 - 42

76 - 90

25 - 31

32 - 36

8 years

4.0 5.3

11.5 -

33 - 43

76 - 90

25 - 31

32 - 36

14.5
14 Years

4.1 5.3

12.0 15.0

35 - 45

78 - 95

26 - 32

32 - 36

Adult

4.2 5.4

12.5 16.0

37 - 47

78 - 100

27 - 31

32 - 36

Table HE-2. Normal Values: WBC and Differential Count

Age

WBCCel Segment Band

Eosinop Basophi Lymphocy Monocy
ls x
ed
Neutrop hils (%) ls (%)
tes (%)
tes (%)
3
10 /mm Neutrop hils (%)
3
hils (%)

Birth

9.1 34.0

32 - 62

10 - 18

0-2

0-1

26 - 36

0-6

24 Hours

9.4 34.0

32 - 62

10 - 18

0-2

0-1

26 - 36

0-6

1 Week

5.0 21.0

19 - 49

8 - 16

0-4

36 - 46

0-9

2 Weeks

5.0 20.0

14 - 34

7 - 15

0-3

0-1

43 - 53

0-9

4 Weeks

6.0
14.0

15 - 35

7 - 13

0-3

0-1

41 - 71

0-7

2 Months

6.0
14.0

15 - 35

5 - 11

0-3

0-1

42 - 72

0-6

4 Months

6.0
14.0

14 - 34

6 - 12

0-3

44 - 74

0-5

6 Months

6.0
14.0

13 - 33

6 - 12

0-3

46 - 76

0-5

8 Months

6.0
14.0

12 - 32

5 - 11

0-3

47 - 77

0-5

1 Year

6.0
14.0

13 - 33

5 - 11

0-3

46 - 76

0-5

2 Years

4.0 12.0

15 - 35

5 - 11

0-3

0-1

44 - 74

0-5

4 Years

4.0 12.0

23 - 45

5 - 11

0-3

0-1

35 - 65

0-5

6 Years

4.0 12.0

32 - 54

5 - 11

0-3

0-1

27 - 57

0-5

8 Years

4.0 12.0

34 - 56

5 - 11

0-2

0-1

24 - 54

0-4

10 Years

4.0 12.0

31 - 61

5 - 11

0-2

0-1

28 - 48

0-4

12 Years

4.0 12.0

32 - 62

5 - 11

0-3

0-1

28 - 48

0-4

14 Years

4.0 10.5

33 - 63

5 - 11

0-3

0-1

27 - 47

0-5

16 Years

4.0 10.5

34 - 64

5 - 11

0-3

0-1

25 - 45

0-5

18 Years

4.0 10.5

34 - 64

5 - 11

0-3

0-1

25 - 45

0-5

20 Years

4.0 10.5

36 - 66

5 - 11

0-3

0-1

23 - 43

0-5

Adult

4.0 10.5

36 - 66

5 - 11

0-3

0-1

24 - 44

0-4

Information taken from normal range study performed at The Children's Medical Center, Dayton, OH.

Table HE-3. Conditions Affecting Neutrophil Counts

Conditions Causing Neutrophilia (> 8,000 PMNs/mm 3)

Infectious Disease:

Physiological response to stress:

Physical Exercise

Exposure to extreme heat or cold

Following acute hemorrhage or hemolysis

Acute emotional stress

Childbirth

Infectious Disease:

Systemic or severe local bacterial infections

Some viruses (smallpox, chickenpox, herpes zoster, polio)

Some rickettsial diseases (especially Rocky Mountain Spotted Fever)

Some fungi, especially if there is acute tissue necrosis

Inflammatory diseases:

Acute rheumatic fever

Rheumatoid arthritis

Acute gout

Vasculitis and myositis of many types

Hypersensitivity reactions to drugs

Tissue necrosis:

Ischemic damage to the heart abdominal viscera, extremities

Burns

Many carcinomas and sarcomas

Metabolic Disorders:

Uremia

Diabetic Ketoacidosis

Eclampsia

Thyroid Storm

Drugs:

Epinephrine

Lithium

Histamine

Heparin

Digitalis

Many toxins, venoms, and heavy metals

Conditions Causing Neutropenia (<1,500 PMNs/mm3)

Infectious diseases:

Some bacteria (typhoid, tularemia, brucellosis)

Some viruses (hepatitis, influenza, measles, mumps, rubella,
infectious mononucleosis)

Protozoa (especially malaria)

Overwhelming infection of any kind

Chemical and physical agents:

Protozoa (especially malaria)

Dose-related, universal marrow depressants (radiation, cytotoxic
drugs, benzene)
Idiosyncratic drug reactions (numerous)

Hypersplenism:

Liver disease

Storage diseases

Other disorders:

Some collagen-vascular diseases, especially lupus erythematosus

Severe folic acid or vitamin B12 deficiency

Table HE-4. Conditions Affecting Lymphocyte Counts

Conditions Causing Lymphocytosis

(>4,000 lymphocytes/mm3 in adults; >7,200/mm3in children):

Infectious diseases

Bacterial (whooping cough, brucellosis, sometimes tuberculosis,

secondary syphilis)

Viral (hepatitis, infectious mononucleosis, mumps, many

exanthemas, cytomegalovirus)

Other (infectious lymphocytosis, toxoplasmosis)

Metabolic conditions

Hypoadrenalism

Hyperthyroidism (sometimes)

Chronic Inflammatory conditions

Ulcerative colitis
Immune diseases (serum sickness, idiopathic thrombocytopenic
purpura)

Conditions Causing Lymphocytopenia

(<1,000 lymphocytes/mm3 in adults; <2,500/mm3in
children):Immunodeficiency syndromes:

Congenital defects of cell-mediated immunity

Immunosuppressive medication

Adrenal corticosteroid exposure:

Adrenal gland hyperactivity

ACTH-producing pituitary gland tumors

Therapeutic administration of steroids

Severe debilitating illness of any kind:

Congestive heart failure

Renal failure

Far-advanced tuberculosis

Defects of lymphatic circulation:

Intestinal lyphangiectasia

Disorders of intestinal mucosa

Table HE-5 Conditions Affecting Other Circulating White Cells

Conditions Causing Monocytosis (>800 monocytes/mm3in adults):

Infections (tuberculosis, subacute bacterial endocarditis, hepatitis,

rickettsial diseases, syphilis)

Granulomatous diseases (sarcoid, ulcerative colitis, regional

enteritis)

Collagen-vascular diseases (lupus, rheumatoid arthritis,

polyarteritis)

Many cancers, lymphomas, and myeloproliferative disorders

Conditions Causing Eosinophilia (>450 eosinophils/mm 3):

Allergic diseases (asthma, hay fever, drug reactions, allergic

vasculitis, serum sickness)

Parasitic infections (trichinosis, echinococcus, hookworm,

schistosomiasis, amebiasis)

Skin disorders (some psoriasis, some eczema, pemphigus,

dermatitis herpetiformis)

Hypereosinophilic syndromes (systemic eosinophilia associated

with pulmonary infiltration and sometimes cardiovascular disturbances)

Neoplastic diseases (Hodgkins disease, extensive metastases or

necrosis of solid tumors)

Miscellaneous (collagen-vascular diseases, adrenal cortical

hypofunction, ulcerative colitis)

Conditions Causing Basophilia (>50 basophils/mm 3):

Chronic hypersensitivity states in the absence of the specific

allergen (exposure to the allergen triggers cell lysis and rapid drop in
basophil count)

Systemic mast cell disease

Myeloproliferative disorders

Table HE-6 Peripheral Blood Red Cell Abnormalities

Abnormality

Description

Associated Diseases

Anisocytosis

Abnormal variation in

Any severe anemia, e.g.,

size (normal diameter = iron deficiency,

6-8 mm)
megaloblastic
Macrocytosis

Large cells, greater than Megaloblastic anemia,

8 mm (MCV > 100 fl)
liver disease,
hypothyroidism, hemolytic
anemia (reticulocytes),
multiple myeloma,
physiologic macrocytosis
of newborn, myelophthisis

Macroovalocytosis

Large (> 8 mm) oval

cells

Megaloblastic anemia

Hypochromia

Pale cells with decreased

concentration of
hemoglobin (MCHC < 31
g/dL)

Iron deficiency and ironloading (sideroblastic)

anemia, thalassemia, lead
poisoning, transferrin
deficiency, anemia of
chronic disease
(inflammatory diseases,
e.g., rheumatoid arthritis,
collagen diseases,
malignancies)

Poikilocytosis

Abnormal variation in
shape

Any severe anemia, e.g.,

megaloblastic, iron
deficiency,
myeloproliferative
syndrome, hemolytic.
Certain shapes are
diagnostically helpful (see
following, spherocytosis
through teardrop cells)

Spherocytosis

Spherical cells without

pale centers; often
small, i.e.,
microspherocytosis

Hereditary spherocytosis,
Coombs positive
hemolytic anemia; small
numbers are seen in any
hemolytic anemia and
after transfusion of stored
blood.

Ovalocytosis

Oval cells

Hereditary eliptocytosis,
iron deficiency

Stomatocytosis

Red cells with slit-like,

Congenital hemolytic
instead of circular, areas anemia, thalassemia,
of central pallor
burns, lupus
erythematosus, lead
poisoning, liver disease,
artifact

Sickle cells

Crescent-shaped cells

Sickle cell
hemoglobinopathies

Target cells

Cells with a dark center

and periphery and a
clear ring in between

Liver disease, thalassemia,

hemoglobinopathies (S, C,
SC, S-thalassemia)

Schistocytes

Irregularly contracted
cells (severe
poikilocytosis)

Uremia, carcinoma,
hemolytic-uremic
syndrome, disseminated
intravascular coagulation,
microangiopathic
hemolytic anemia, toxins
(lead, phenylhydrazine),
burns, thrombotic
thrombocytopenic purpura

Echinocytes

Cells with long, sharp,

irregularly spaced,
spinous processes

Hemolytic anemias, liver

disease (spur cell anemia)
normal infants, uremia,
microangiopathic
hemolytic anemia,
disseminated intravascular
coagulation,
thrombocytopenic
purpura, pyruvate kinase
deficiency, carcinoma

Acanthocytosis

Small cells with thorny

projections

Abetalipoproteinemia
(hereditary acanthocytosis
or Bassen Kornzweig
disease)

Teardrop cells

Cells shaped like

teardrops

Myeloproliferative
syndrome, myelophthisic
anemia (neoplastic,
granulomatous, or fibrotic
marrow infiltration),
anemia with
extramedullary
hematopoiesis or
ineffective erythropoiesis

Nucleated red cells

Erythrocytes with nuclei

still present; may be
normoblastic or
megaloblastic

Hemolytic anemias,
leukemias,
myeloproliferative
syndrome, polycythemia
vera, myelophthisic
anemia (neoplastic,
granulomatous or fibrotic
marrow infiltration),
multiple myeloma,
extramedullary
hematopoiesis,
megaloblastic anemias,
any severe anemia

Howell-Jolly bodies

Spherical blue bodies

Hyposplenism, pernicious
(Wright stain) within or
anemia
on erythrocytes; nuclear
debris

Heinz inclusion
bodies

Small round inclusions

seen under phase
microscopy or with
supravital staining

Pappemheimer
bodies (siderocytes)

Siderotic granules,
Iron-loading anemias,
staining blue with Wright hyposplenism, hemolytic
or Prussian blue stains
anemias

Congenital hemolytic
anemias (e.g., glucose-6phosphate dehydrogenase
deficiency), hemolytic
anemia secondary to
drugs (dapsone,
phenacetin), thalassemia
(Hb H),
hemoglobinopathies (Hb
Zurich, Koln, Ube, I, etc.)

Cabot rings

Purple, fine, ring-like

intraerythrocytic
structures

Pernicious anemia, lead

poisoning

Basophilic stippling

Punctate stippling when Hemolytic anemia,

Wright-stained
punctate stippling seen in
lead poisoning
(mitochondrial RNA and
iron), thalassemia

Rouleaux

Aggregated erythrocytes Multiple myeloma,

regularly stacked on one Waldenstroms
another
macroglobulinemia, cord
blood, pregnancy,
hypergammaglobinemia,
hyperfibrinogenemia

Polychromasia

RBCs containing RNA,

staining a pinkish blue
color; stains supravitally
as reticular network with
new methylene blue

Hemolytic anemia, blood

loss, uremia, following
treatment of iron
deficiency or
megaloblastic anemias

Table HE-7 Leukocyte Abnormalities and Diseases

Abnormality

Description

Associated Diseases

Leukocytosis

White blood cell count > Any physiological or

11.0 x 106/L
pathological stress,
corticosteroids

Neutrophilic
leukocytosis
(granulocytosis)

Neutrophilic leukocyte
count >8,000/mm3

Infection, intoxication, tissue

necrosis, myeloproliferative
syndromes, leukemia (e.g.,
chronic myelocytic),
leukemoid reaction,
hemorrhage, hemolysis

Neutropenia or
granulocytopenia

Neutrophilic count
<1,500/mm3

Drugs, infection, congenital

megaloblastic anemia,
aplastic anemia, leukemia,
lupus erythematosus,

postirradiation
hypersplenism, myelophthisis
anemia
Toxic granulation

Coarse black or purple

cytoplasmic granules

Infections of inflammatory
diseases

Dohle bodies

Small (1-2 mm) blue

Infections or inflammatory
cytoplasmic inclusions in diseases, burns, myelocytic
neutrophils
leukemia, myeloproliferative
syndromes,
cyclophosphamide therapy

Pelger-Huet
anomaly

Neutrophil with bilobed Hereditary, myelocytic

nucleus or no
leukemias, myeloproliferative
segmentation of
syndromes
nucleus. Chromatin is
coarse and cytoplasm is
pink with normal
granulation.

May-Hegglin
anomaly

Basophilic, cytoplasmic May-Hegglin syndrome

inclusions of leukocytes. (hereditary), includes
Similar to Dohle bodies. thrombocytopenia and giant
platelets.

Alders anomaly

Prominent azurophilic
granulation in
leukocytes. Similar to
toxic granulation.
Granulation is seen
better with Giemsa
stain.

Hereditary, gargoylism

Chediak-Higashi
anomaly

Gray-green, large
cytoplasmic inclusions
resembling Dohle
bodies.

Chediak-Higashi syndrome

Tart cell

Neutrophilic leukocyte
Drug reactions (e.g.,
with a phagocytized
penicillin, procainamide)
nucleus of a granulocyte
that retains some

nuclear structure
Myeloid shift to
left

Presence of bands,
myelocytes,
metamyelocytes or
promyelocytes

Infections, intoxications,
tissue necrosis,
myeloproliferative syndrome,
leukemia (chronic
myelocytic), leukemoid
reaction, pernicious anemia,
hyposplenism

Hypersegmented
neutrophil

Mature neutrophil with

more than 5 distinct
lobes

Magaloblastic anemia,
hereditary constitutional
hypersegmentation of
neutrophils; rarely, iron
deficiency anemia,
malignancy, or infection

Atypical
lymphocytes
Reactive
lymphocytes
Downey cells

Lymphocytes, some with

vacuolated cytoplasm,
irregularly shaped
nucleus, increased
numbers of cytoplasmic
azurophilic granules,
peripheral basophilia, or
some with more
abundant basophilic
cytoplasm

Infectious mononucleosis,
viral hepatitis and other viral
infections, tuberculosis, drug
(e.g., penicillin) sensitivity,
posttransfusion syndrome

Leukemic cells
Presence of
(lymphoblasts,
lymphoblasts,
myeloblasts, etc.) myeloblasts,
monoblasts,
myelomonoblasts,
promyelocytes (none
normally present in
peripheral blood)

Leukemia (acute or chronic),

leukemoid reaction, severe
infectious or inflammatory
diseases, myeloproliferative
syndrome, intoxications,
malignancies, recovery from
bone marrow suppression,
infectious mononucleosis,
myelophthisis

Auer bodies

Acute myelocytic leukemia

Round or rod-like, 1-6

mm long, red-purple,
refractile inclusions in
neutrophils

Smudge cell

Disintegrating nucleus
of a rupture white cell

Increased numbers in
leukemic blood, particularly in
CML or CLL when WBC count
is greater than 100,000/mm3

RBC = Red Blood Cell = jumlah sel darah merah

Hb = Hemoglobin = kalau kebanyakan namanya polisitemia vera, kalo kesedikitan namanya anemia
Hct = Hematokrit = persentase bagian darah yang padat dibandingkan dengan plasma (cairnya)
MCV, MCH, MCHC berkaitan dengan anemia, kalau dijelaskan juga ribet... pokoknya untuk menentukan
jenis anemia
WBC = White blood cell = sel darah putih --> bisa menjadi penanda infeksi pada tubuh..
PLT = platelet = angka trombosit
Hiperinflasi

Barrel chest ( dada barrel )

Bentuk dada yang menyerupai barel,hal ini terjadi karena hasil hiperinflasi

paru.Hiperinflasi paru ialah terjebaknya udara akibat saluran pernafasan yang

sempit/menyempit,pada keadaaan ini terjadi peningkatan diameter anteroposterior,penyakit
yang bermanifestasikan barrel chest ini misalnya asma berat dan PPOK (jenis empisema )
ini terjadi karena paru paru yang kronis overinflated pada udara,sehingga tulang rusuk tetap
sebagian diperluas sepanjang waktu,hal ini membuat pernafasan kurang efisien dan
memburuk setiap sesak nafas.umumnya ditemukan pada pria
Dada barel dapat disebabkan oleh beberapa factor:
1.
Osteoarthritis
2.

Penuaan

3.

Empisema

Dada barel juga berhubungan dengan osteoartihritis yang mempengaruhi sendi dimana
tulang rusuk melekat pada tulang belakang

alveolar infiltrate
Opacification of air spaces, caused by the filling of alveoli with blood, pus, or fluid. Alveolar infiltrates are s
een on the chestradiograph as patchy areas of increased density, often surrounding air bronchograms.
See also: infiltrate

Stock Photo:

film chest x-ray show alveolar infiltrate at lung due to Mycobacterium

tuberculosis infection (Pulmonary Tuberculosis)

Image ID:297114935

Copyright: Tewan Banditrukkanka

Available in high-resolution and several sizes to fit the needs of your project.

Infiltrate is when your alveolar spaces are filled with some sort of fluid, i.e. transudate, exudate.
Consolidation refers to the lung becoming a hard, firm mass, which is very characteristic of
lobar pneumonia. So this can be due to an exudative infiltrate, for example, in lobar pneumonia,
where the cell debris and pus is literally filling up the spaces and instead of giving your lungs
this squishiness that you see on autopsy it makes it hard and less pliable, and less able to fill up
with air.

So consolidation = texture, infiltration = filling up of the lungs. You can have consolidation with
or without infiltration.

The term "pulmonary infiltrate" is considered a context dependent, nonspecific and imprecise
descriptive term when used in radiology reports (plain film or CT).

From a pathophysiological perpestive, the term "infiltrate" refers to an abnormal substance that
accumulates gradually within cells or body tissues or any substance or type of cell that occurs within or
spreads as through the interstices (interstitium and/or alveoli) of the lung, that is foreign to the lung, or
that accumulates in greater than normal quantity within it
While when used with a better anatomic reference, such as alveolar, air space, interstitial, or nodular, it
may occasionally be helpful in suggesting an underlying pathologic basis for the findings on the
radiograph, the use of the term in general is discouraged.
According to a study by Patterson et.al, the use of the term "infiltrate" on its own was not shown to be
very meaningful for the clinician or very beneficial to the patient 1.
According the Fleischer Thoracic Society recommendations, use of the term "infiltrate" remains
controversial and is no longer recommended 3.

Interstitial vs Alveolar Lung Patterns

under construction

Introduction
This page considers all aspects of the appearances of interstitial and alveolar opacity
demonstrated on chest plain film imaging. Radiographers who are able to differentiate
alveolar from interstitial lung patterns are operating at a very high level and will find a whole
new appreciation of chest radiography. An appreciation of the features of these patterns will
prevent you from describing appearances as cloudy, fuzzy etc. You are more likely to gain
the respect of your fellow health professionals and impart meaningful information if you can
describe an appearance using correct descriptors- e.g "there is widespread coarse
interstitial opacity" rather than "the lungs look a bit fuzzy".

Caution
This is not easy- in fact, this is the difficult end of plain film image interpretation. The
interpretation difficulties are as follows

The appearances can be subtle

Interstitial patterns can be mixed (linear, reticular, or nodular)
There can be mixed alveolar and interstitial patterns
There can be other patterns present (tumour, pleural effusion, atelectasis etc)
There can be acute on chronic changes.
The causes of interstitial lung opacity are numerous

Interstitial Opacity on CXR- anatomy, causes and

appearances.
The interstitium of the lung consists of the supporting structures such as pulmonary vessels,
bronchi, and connective tissue. On the normal CXR, the visible interstitium consists
primarily of the pulmonary vessels, which are most pronounced at the hila, and decrease in
prominence towards the periphery (in fact, under normal circumstances, the pulmonary
vessels are not visible in the periphery on a CXR because they are too small to resolve at
this point). Most lung diseases cause an increase in the radiodensity of the lung, and if this
is due to a relative thickening of the interstitium- this will be manifest as increased
prominance of the interstitial markings on the CXR. If generalized or diffuse, this will likely
appear as a linear or reticular pattern, whereas if localized, it may appear as multiple tiny
nodules.
Note that in diseases confined to the interstitium (i.e. sparing the alveoli) the lung will still
appear aeratedthe basic appearance is of an aerated lung that has too many markings.
Common causes of this pattern include pulmonary edema, inflammation, fibrosis, and
tumour.
The interstitium
surrounds bronchi,
vessels, and groups of
alveoli. When there is
disease in the interstitium
it manifests itself by
reticulonodular
shadowing (criss cross
lines or tiny nodules or
both). The main two
processes affecting the
interstitium are
accumulation of fluid
(occurring in pulmonary
oedema or in
lymphangitis
carcinomatosa) and
inflammation leading to
fibrosis (occurring in
industrial lung disease,
inflammatory arthritides
such as rheumatoid

arthritis, inflammation of
unknown cause such as
cryptogenic fibrosing
alveolitis and
sarcoidosis).
Quoted from: source unknown

Causes of Interstitial lung opacity

- Common identifiable
causes:
a) infectious causes, e.g.:
non-tuberculous
mycobacteria & certain
fungal infections
b) occupational causes,
e.g.: asbestos & silica
c) drug reactions, e.g.:
methotrexate &
amiodarone
d) neoplastic causes, e.g.:
metastatic cancer,
bronchoalveolar cell
carcinoma (a form of lung
cancer)
e) radiation pneumonitis
f) hypersensitivity
pneumonitis
g) rheumatologic
diseases
(1) systemic lupus
erythematosis

(2) rheumatoid arthritis

(3) scleroderma
(4) mixed connective
tissue disease
(5) polymyositis

- Diseases of unknown
cause, e.g.: sarcoidosis,
Langerhan's cell
granulomatosis
(eosinophilic granuloma;
histiocytosis X),
lymphangioleiomyomatos
is

- Idiopathic pulmonary
fibrosis
Source: unknown

Causes of Alveolar Opacity

pneumonitis
pulmonary contusion
pulmonary oedema
Aspiration

The Meaning of the Term 'Consolidation'

One of the unfortunate aspects of the term consolidation is that its meaning can be different
depending on who is using the term. When a clinician uses the term consolidation, he/she is
usually referring to a consolidation associated with acute pneumonia. Thus, the term
consolidation and pneumonia have very similar meaning and are almost used
interchangeably. Strictly speaking, the term consolidation does not imply any particular

aetiology or pathology. Acute pneumonia is the commonest cause but not the only cause of
consolidation. (other causes include chronic pneumonia, pulmonary oedema and
neoplasm). Thus when a radiologist has reported a chest X-ray examination and notes the
presence of consolidation he/she is simply stating that some of the lung airspace has been
replaced by a fluid. Sutton, Textbook of Radiology, 2nd ed.,1975,
This is a basic video that explains
consolidation in simple terms

Notes

Consolidation may be complete or incomplete

The distribution of the consolidation can vary widely.
A consolidation could be described as patchy, homogenous, or generalised.
A consolidation may be described as focal or by the lobe or segment of lobe affected
Sutton, Textbook of Radiology, 2nd ed.,1975, p325

Interstitial vs Alveolar Patterns

Recognition of a plain film interstitial pattern is important because it identifies the abnormal
density as being within the supporting tissues of the lung rather than within the air spaces,
pleural space, mediastinum, or outside the thoracic cavity- it indicates the infiltrate's cellular
rather than fluid nature.

Alveolar Opacity
Alveolar Opacity- Definition

Interstitial Opacity
Interstitial Opacity- Definition

Alveolar opacity refers to opacity on The interstitium refers to the supporting

structures of the lung. An interstitial
chest X-ray associated with fluid
opacity on chest X-ray refers to an
filling of the airspaces.
abnormal appearance of the lung
interstitium
Alveolar Opacity- Anatomy

Interstitial Opacity- Anatomy

High-Resolution CT of the Lung, 3rd Edition, 2001 Lippincott Williams

& Wilkins

http://www.ichristianschool.org/anatomy/3rdQuarter/anatom
y23.htm

Well demonstrated normal interlobular

septa in patient with pneumothorax
(pneumothorax causes alveolar
compression and so, the intersitium forms
a larger component of the lung volume).

Alveolar Opacity- Plain Film Pattern

Interstitial Opacity- Plain Film Pattern

Interstitial opacity can be linear, reticular,

nodular or reticulonodular.
Opacity is often described as fluffy,
cotton wool-like, or cloud-like

Alveolar Lung Patterns on CXR

Alveolar pattern results
from flooding of the end
air spaces (acini) with
fluid (pus, blood, edema)
only rarely with cellular
material. As individual
acini become filled the
fluid spreads to adjacent
ones through the
interalveolar pores. This
results in the typical

radiographic pattern of a
poorly margined ("fluffy")
density. The densities
may spread and their
borders coalesce. This
may progress until all
acini within a lung lobe
are filled. There may be a
sharp border at the edge
of a lung lobe due to the
pleura blocking further
spread of the fluid into
the adjacent lung lobe. As
the number of fluid filled
adjacent acini increases,
the air filled, large and
medium sized bronchi
become evident as linear
radiolucent branching
structures (air
bronchogram). The airfilled bronchi are
surrounded by a fluid
density and the bronchial
wall and adjacent vessel
are not seen. When a
bronchus branches
perpendicular to the x-ray
beam it will be seen as a
round radiolucent dot.
Radiographic Diagnosis of Pulmonary
Disease
Norman Ackerman, DVM, DACVR

This
patient
aspirated
IV
contrast
medium.
The postcontrast
image
was
taken
within a
few
minutes
of
aspiratio
n. The
dense
contrast
media
has filled
the
alveoli as
well as
coating
some of
the
larger
airways.
The
whispy/fl
uffy/clou
dy
pattern is
character
istic of
alveolar
airspace
filling.

Interstitial Lung Patterns on CXR

There are 4
basic
interstitial lung
patterns
1.

linearseptal lines
(Kerley lines)
2.
reticularmesh like
appearance,
lines in all
directions
3.
nodulardiscrete
opacities
4.
reticulon
odularcombination of
2 and 3

Pracical Approach to Interstitial Lung Diseases, A. Nour-Eldin

Linear Interstitial
Pattern

Retic Nodular Interstitial

Reticulonodular
ular
Pattern
Interstitial Pattern
Inter
stitia
l

Patte
rn

This is a nodular pattern in Reticulonodular pattern in

a patient with lymphangitis
a patient with COPD
carcinomatosis.

This is a fine linear

interstitial pattern

The linear pattern on chest

radiography consists of
thin linear opacities which
are either 2 to 6 cm long
within the lungs oriented
radially toward the hila or
1 to 2 cm long at right
angles to, and in contact
with, the lateral pleural
surfaces. These linear
opacities have been
referred to as Kerley A and
Kerley B lines, respectively,
although the descriptors
septal thickening or
septal lines are now
preferred for the latter.
Histologically, this linear
pattern represents
thickening of either the
bronchovascular/axial
interstitium (Kerley A) or

The
reticul
ar
patter
n as
seen
on
chest
radiogr
aphy
and
compu
ted
tomog
raphy
(CT or
HRCT)
is
depict
ed by
numer
ous,
small,
linear

The nodular pattern on

chest radiography is
characterized by multiple
small, discrete, rounded
opacities that range in
diameter from 2 to 10
mm.The differential
diagnosis for the nodular
pattern can be separated
into 3 main categories
based on etiology: nodular
metastases, nodular
pneumoconioses and the
granulomatous diseases.
The most common
malignancies resulting in
this pattern are thyroid,
breast and renal-cell
carcinoma, with the
nodules measuring up to
10 mm in diameter.
Scott D. Perrin, MD, Adam Ulano, MD,

the peripheral interstitium

(Kerley B).The linear
opacities may be single or
multiple, regional or
diffuse, and short or long,
depending on the etiology
and severity of disease.

opaciti
es
which,
by
summ
ation,
have
been
The most common cause
descri
of the linear pattern is
bed as
hydrostatic pulmonary
a laceedema, but other
like or
etiologies include
netlymphangitic
like in
carcinomatosis, and
appear
atypical interstitial
ance.4
pneumonias such as those ,5 The
caused bymycoplasma,
reticul
chlamydia, cytomegaloviru ar
s (CMV), and respiratory
patter
syncytial virus (RSV).
n can
Interstitial pulmonary
be
edema tends to be
divide
symmetric in distribution
d into
while atypical infections
3
and lymphangitic
distinc
carcinomatosis may be
t
asymmetrical.
groups
, each
of
Scott D. Perrin, MD, Adam Ulano, MD,
and Todd R. Hazelton, MD
which
Revisiting the pattern approach to
sugges
interstitial lung disease on chest
radiography
ts
Aplied Radiology
differe
Volume 38, Number 12, December
nt
2009
diagno
ses:
periph
eral
reticul
ar
patter
n with
small
lung
volum
es,
diffuse

and Todd R. Hazelton, MD

Revisiting the pattern approach to
interstitial lung disease on chest
radiography
Aplied Radiology
Volume 38, Number 12, December
2009

reticul
ar/cyst
ic
patter
n with
normal
or
increas
ed
lung
volum
es,
and
airway
/centra
l
reticul
ar
patter
n.
Scott D.
Perrin,
MD, Adam
Ulano,
MD, and
Todd R.
Hazelton,
MD
Revisiting
the
pattern
approach
to
interstitial
lung
disease
on chest
radiograp
hy
Aplied
Radiology
Volume
38,
Number
12,
December
2009

1. Linear

A linear
pattern
is seen
when
there is
thickenin
g of the
interlobul
ar septa,
producin
g Kerley
lines
The most
common
cause of
interlobul
ar septal
thickenin
g,
producin
g Kerley
A and B
lines, is
pulmona
ry edema
other
causes

adapted from Medpix

Mit
ral
stenosis
Ly
mphangi
tic
carcinom
atosis
Ma
lignant
lymphom
a

Idi
opathic
pulmona
ry
fibrosis
Pn
eumocon
iosis
Sar
coidosis

Note the
obscurati
on of the
normal
lung
markings
in the
patient
with the
linear
interstiti
al
pattern

2. Reticular

A reticular pattern results from the

summation or superimposition of
irregular linear opacities. The term
reticular is defined as meshed, or in
the form of a network. Reticular
opacities can be
described as fine, medium, or coarse,
as the width of the opacities increases.
A classic reticular pattern is seen with
pulmonary fibrosis, in which multiple
curvilinear opacities form small cystic
spaces along the pleural margins and
lung bases (honeycomb lung)

3. Nodular
A nodular pattern consists of
multiple round opacities, generally
ranging in diameter from 1 mm to
1 cm
Nodular opacities may be
described as miliary (1 to 2 mm,
the size of millet seeds), small,
medium, or large, as the diameter
of the opacities increases
A nodular pattern, especially
with predominant distribution,
suggests a specific differential
diagnosis
This x-ray shows a bilateral
diffuse miliary nodular
pattern involving both lung
fields with no loss of
volume.
Source: Chest Radiology, Pretest USMLE, Part 2, Juzar Ali and Warren R. Summer

4. Reticulonodular

This
patient
has a
primary
lung
cancer
with
lymphat
ic
spread
(lympha
ngitic
carcino
matosis)
. The
lower
zone of
the left
lung
shows a
coarse
reticulo
nodular
pattern.
Compar
e the
appeara
nce of
the
lower
zone of
the left
lung
with an
earlier
CXR on
the
same
patient
(below)

A
reticulo
nodular
pattern
results
from a
combina
tion of
reticular
and
nodular
opacitie
s.
A
reticulo
nodular
pattern
is often
difficult
to
distingui
sh from
a purely
reticular
or
nodular
pattern,
and in
such a
case a
different
ial
diagnosi
s should
be
develop
ed
based
on the
predomi

nant
pattern.
If there
is no
predomi
nant
pattern,
causes
of both
nodular
and
reticular
patterns
should
be
consider
ed.

CXR on
same
patient
2 years
earlier.

Distinguishing Acinar nodules from from interstitial nodules

Acinar

Varying in size
Indistinct edges
Larger than interstitial nodules

Interstitial
Same size
Sharp edges
smaller

A recent chest X-ray showed that I have hyperinflated lungs.

What could cause this?
Answers from Edward C. Rosenow III, M.D.

Hyperinflated lungs can be caused by obstructions in the passages that deliver air to
your lung tissue. Air gets trapped within the lung and causes it to overinflate.
Hyperinflation can also occur when the air sacs in your lungs become less elastic, which
interferes with the expulsion of air from your lungs.
One of the most common causes of hyperinflated lungs is chronic obstructive pulmonary
disease (COPD) a disorder that includes emphysema. Certain lung problems, such
as asthma and cystic fibrosis, also can cause hyperinflation.
In some cases, lungs may appear hyperinflated on X-rays for reasons unrelated to lung
function. If you aren't experiencing shortness of breath, there's probably nothing to worry
about. However, if it isn't clear what is causing the hyperinflation, your doctor may
recommend additional testing.

Hyperinflated lungs
Case contributed by Dr Ian Bickle

Presentation:
Longstanding asthma. Shortness of breath.

Patient Data:
Age: 41
Gender: Female

Modality: X-ray

X-ray

Frontal

Flattened hemidiaphragms.
> 10 posterior ribs in the midclavicular line above the diaphragm.
Hyperlucent lungs

Case Discussion:
Hyperinflated lungs are present in many chronic chest conditions in particular COPD and asthma.
This may be evidenced by:
a. Flattened hemidiphragms
b. Hyperlucent lungs ( less bronchovascular markings per cm2)
c. More than 6 anterior or 10 posterior ribs in the mid-clavicular line at the lung diaphragm level.
Related Articles:

Asthma

Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease with marked hyperinflation

Case contributed by A.Prof Frank Gaillard

Presentation:
Chronic, worsening shortness of breath.
Patient Data:
Age: 60 years
Gender: Female

Chest x-ray
Modality: X-ray

X-ray

Chest xrays demonstrates very marked hyperinflation of both lungs. Over 11 posterior ribs are seen, the
diaphragms are flattened and there is enlargement of the retrosternal airspace. Pulmonary vasculature
not terribly distorted, although there is some prominence of the pulmonary arteries.

3 study questions available

Annotated images (different patient)

Modality: Annotated image

Annotated image

The normal dome of each hemidiaphragm should rise at least 1.5cm above a line connecting the costophrenic angle
posteriorly and sternophrenic angle anteriorly.

Lateral chest x-ray from a different (normal but well inflated) patient.
The thickness of the space between the ascending aorta and the sternum is normally no more than
2.5cm.
The normal dome of each hemidiaphragm should rise at least 1.5cm above a line connecting the
costophrenic angle posteriorly and sternophrenic angle anteriorly
Case Discussion:
This case demonstrates unequivocal and marked hyperinflation secondary to emphysema.

LITFL | Resources | Pulmonary opacities on chest x-ray

Pulmonary opacities on chest x-ray

Reviewed and revised 6 September 2015

Overview

There are 3 major patterns of pulmonary opacity:

1. Airspace filling

Localized = segmental

Diffuse or multifocal

2. Interstitial patterns

Reticularfine or coarse linear shadows

Reticulonodular

Nodularsmall (2 to 3 mm), medium, large, or masses (>3 cm)

3. Atelectasis

Diminished aeration of lung

Associated with signs of volume loss

Causes of pulmonary opacity

Focal airspace disease

Pneumonia

Pulmonary embolism: infarction or intrapulmonary hemorrhage

Neoplasm: alveolar cell carcinoma, lymphoma (usually diffuse)

Atelectasis: opacity accompanied by signs of volume loss

Diffuse or multifocal airspace disease

Pulmonary edema: CHF and non-cardiogenic pulmonary edema

Pneumonia: bacterial, viral, Mycoplasma, Pneumocystis

Hemorrhage: trauma (contusion), immunologic (Goodpastures), bleeding

diathesis, pulmonary embolism

Neoplasm: alveolar cell carcinoma, lymphoma

Desquamative interstitial pneumonitis (DIP), alveolar proteinosis

Bat-wing patternCentral opacification with peripheral clearing

characteristic of pulmonary edema

Fine reticular pattern

Acute:

Interstitial pulmonary edema

Interstitial pneumonitis: viral, Mycoplasma

(Airspace filling often accompanies interstitial pneumonia and pulmonary
edema)

Chronic:

Lymphangitic metastasis, sarcoidosis, eosinophilic granuloma, collagen

vascular diseases, inhalation injuries, idiopathic pulmonary fibrosis (fibrosing
alveolitis), resolving pneumonia

Coarse reticular pattern

Honeycomb lungend-stage pulmonary fibrosis

Also seen when pneumonia or pulmonary edema occurs in patients with

underlying emphysema

Reticulnodular pattern

A common radiographic pattern that encompasses the same disorders as

reticular patterns

Miliary pattern 2 to 3 mm well-defined nodules (micronodular pattern)

Tuberculosis, Fungal, Nocardia, Varicella

Silicosis, Coal Workers lung, Sarcoidosis, Eosinophilic granuloma

Neoplastic (adenocarcinoma, thyroid)

Nodular pattern Margins of the lesions are generally well-defined. Mass: >3 cm

Neoplasm: metastatic, lymphoma; benign tumors

Fungal or parasitic infection, septic emboli

Rheumatoid nodules, Wegeners granulomatosis

References and Links

Journal articles and Textbooks

Schwartz DT, Reisdorff EJ. Emergency Radiology, McGraw-Hill 2000.

CORAKAN BRONKOVASKULER

e. Cor / Jantung (bentuk dan ukuran) --> dengan menggunakan CTR (Cardiothoraco ratio). normalnya pada
orang dewasa adalah 48%-50%, sedangkan pada anak-anak sebesar 52%-53%. Cara menghitungnya
adalah a + b : c

f. Mediastinum
g. Corakan Bronkovaskuler
Untuk corakan bronkovaskuler, normalnya hanya terdapat pada 1/3 lapangan paru dari central pada dewasa,
sedangkan pada anak hanya 1/4 dari lapangan paru. Corakan bronkovaskuler yang meningkat dapat
menjadi suatu tanda suatu proses perandangan paru misalnya pada bronkitis.
h. Lesi Parenkim Paru
erdapat banyak gambaran lesi yang mungkin terjadi. Misal pada Tuberkulosis (TB) bisa terdapat gambaran
infiltrat, fibrotik, kavitas, dan lain-lain. Proses TB aktif ditandai dengan adanya lesi kavitas atau infiltat.
Sementara bekas TB lama atau yang sudah tidak aktif lagi bisa tampak gambaran fibrotik berupa garis-garis
radioopaque dengan batas yang tegas. Bisa juga tampak gambaran metastasis pada parenkim paru dengan
adanya bentukan-bentukan lesi yang noduler, milier, koin, cannon ball, dll
urutan Cara Membaca/Interpretasi photo :
1. Sinus costophrenicus kanan/kiri ....
2. diaphragma kanan kiri ....
3. Jantung bentuk dan ukuran .....
4. Corakan bronkovaskuler kedua paru ... apakah tampak infiltrat, dsb
5. Tulang-tulang costa kanan/kiri ...
Kesan. . .
Contoh :

Photo ini adalah photo thorak posisi AP

sinus costoprenicus kanan dan kiri Lancip
diaphragma kanan kiri normal
Jantung bentuk dan ukuran normal
Corakan bronkovaskuler kedua paru normal
tampak nodul opaque pada bagian media paru kanan disertai kalsifikasi di sekitarnya
Tulang-tulang costa kanan/kiri intact
Kesan --> Tumor jinak paru / Hamartoma

Kemudian nilai juga parenkim paru, keadaan hilus, corakan bronkovaskuler, dan apakah terdapat lesi atau
tidak. Hilus merupakan tempat keluar masuknya arteri dan vena pulmonalis, bronkus, dan juga saluran limfe.
Normalnya diameter hilus sama dengan diameter trakea. Pada foto rontgen, hilus memberikan gambaran
yang padat. Untuk corakan bronkovaskuler, normalnya hanya terdapat pada 1/3 lapangan paru dari central
pada dewasa, sedangkan pada anak hanya 1/4 dari lapangan paru. Corakan bronkovaskuler yang meningkat
dapat menjadi suatu tanda suatu proses perandangan paru misalnya pada bronkitis, pneumonia, dll.
Kemudian lesi pada parenkim paru. Terdapat banyak gambaran lesi yang mungkin terjadi. Misal pada
Tuberkulosis (TB) bisa terdapat gambaran infiltrat, fibrotik, kavitas, dan lain-lain. Proses TB aktif ditandai
dengan adanya lesi kavitas atau infiltat. Sementara bekas TB lama atau yang sudah tidak aktif lagi bisa
tampak gambaran fibrotik berupa garis-garis radioopaque dengan batas yang tegas. Bisa juga tampak
gambaran metastasis pada parenkim paru dengan adanya bentukan-bentukan lesi yang noduler, milier, koin,
cannon ball, dll (masalah lesi pada parenkim paru buanyakkk sangat,,, lengkapnya silahkan browsing lebih
lanjut, okeh ! )

Selanjutnya jantung, nilai besar dan ukurannya, normal atau tidak. Ukuran bisa kita nilai dengan menghitung
CTR (Cardio Thoracic Ratio), normalnya pada orang dewasa adalah 48%-50%, sedangkan pada anak-anak
sebesar 52%-53%. Cara menghitungnya adalah a + b : c. Jelasnya lihat gambar

CTR

Selanjtnya, diafragma, apakah terdapat elevasi, bagaimana bentuknya, dan permukaannya licin atau tidak.
Diaframga letak tinggi misalnya bisa disebabkan oleh desakan massa dari bawah, paralisis m. diafragmatika
atau lumpuhnya n. phrenicus

Hufffff sekian dulu,, chit-chat kita mengenai baca-baca rontgen ya mungkin lain kali disambung lagi
(cieee hahaaa :D ),, semoga bermanfaat ^^V

Membaca Foto Toraks (X-Ray)

Source: http://typo.zib.de/vis-long_projects/x-ray-3d/x-ray-3d.html

Foto Toraks PA (kiri) dan Lateral (kanan)

Syarat foto normal (kelayakan foto):

1. Identitas foto dan marker kiri/kanan ada
2. Kualitas foto baik
3. Simetris
4. Semua bagian terlihat
5. Tidak ada artefak
6. Tidak goyang (inspirasi maksimal dan tahan napas)
7. Waktu pemotretan singkat

Modified from: http://motherhealth.info/2011/03/normal-chest-xray-criteria.html

Langkah-langkah membaca foto toraks:

1. Identitas foto dan marker
2. Baca klinis
3. Kualitas foto, dapat dilihat dari:

- kV (tegangan)

kV dikatakan cukup jika corpus vertebra yang terlihat adalah dari T1-T3.
Di bawah itu, corpus semakin tidak terlihat.

- mAs (kuat arus)

dikatakan cukup jika saat meletakkan jari di balik foto yang berwarna hitam, jari masih terlihat.

4. Baca foto:
a. Simetris/Tidak simetris
Tarik garis khayal sepanjang processus spinosus toraks kemudian tarik garis ke ujung medial
clavicula. Bila sama antara yang kiri dan kanan, dikatakan simetris. Jika asimetris, akan sulit untuk
menilai pembesaran jantung.

b. Cek inspirasi maksimal

Minimal terlihat intercostal space 5 maksimum terdapat pada puncak diafragma

c. Trakea
Harus terlihat dan harus di tengah (berwarna lusen [hitam] berisi udara)
Lihat apakah ada pendorongan atau tidak

d. Jantung
Lihat besar, bentuk, posisi jantung. Apakah ada pembesaran atau tidak.
Hitung cardiothoracic jantung untuk melihat adanya pembesaran.
Caranya:

Source: http://www.indmedica.com/journals.php?journalid=12&issueid=141&articleid=1872&action=article

Cardiothoracic ratio (CTR) = (CR + CL)/TD x 100%

Normal jika <50%
Jika > 50%, jantung membesar.
Ekspertise (laporan penemuan): Cor tidak membesar.

e. Baca sinuses
Sinus costophrenicus normalnya bersudut tajam.
Dapat tumpul pada kelainan seperti pada efusi pleura, emfisema.
Sinus cardiophrenicus normalnya tajam (terlihat pada foto lateral)

f. Baca diafragma
Normalnya yang kanan lebih tinggi dari yang kiri. (Perbedaan tinggi normal: 2-2.5 cm)
Jika bedanya >3cm: abnormal.
Letak diafrgma meninggi ini dapat ditemukan misalnya pada hepatomegali, asites.

Ekspertise sinuses dan diafragma: Sinuses dan diafragma normal.

g. Baca pulmo
Hillus (tempat keluar masuknya pembuluh darah bronkus dan pembuluh limfatik) normalnya yang
kiri lebih tinggi dari kanan (beda 1 kosta). Biasanya 0.6-1.5 cm.

Corakan bronkovaskular normalnya terlihat pada:

Kanan: </= 2/3 medial paru (tarik 2 garis khayal vertikal yang membagi paru menjadi 3)
Kiri: </= 1/3 medial paru.
Corak dapat bertambah atau tidak tampak jika ada kelainan.

Lihat apakah ada bercak atau penampakan abnormal lainnya. Jika terdapat di parenkim, sebutkan
lokasinya di lapang paru sebelah mana. Jika terdapat di pleura, sebutkan lokasi di hemitoraks
sebelah mana.

Lapang paru terbagi atas:

1) Apeks
dari puncak paru sampai batas atas klavikula

2) Lapang atas
dari batas bawah klavikula sampai dengan batas atas costae II anterior
3) Lapang tengah
dari batas bawah costae II anterior sampai dengan batas atas costae IV anterior
4) Lapang bawah
dari batas bawah costae IV anterior sampai dengan batas atas diafragma

h. Skeletal
Apakah ada fraktur atau dislokasi

i. Soft tissue (jaringan lunak)

Contoh ekspertise foto toraks normal:

- Cor tidak membesar

- Sinuses dan diafragma normal
- Pulmo:
Hilli normal
Corakan bronkovaskular normal
Tidak tampak bercak lunak
- Kesan:
Tidak tampak kardiomegali
Tidak tampak TB paru aktif

Sumber:
Kumpulan Kasus dan Ekspertise Radiologi
Catatan kuliah dan bimbingan