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 Hg1-12 months: 70 mm Hg1-10 years: 70 mm Hg + (2 times age in years)

Vital Signs at Various Ages

Age Heart Rate (beats/min)

Blood Pressure (mm Hg)

Respiratory Rate (breaths/min)

Prematur 120-170 * 55-75/35-45† 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 ChildrenBabies 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 Breaths per minute

Newborn to 6 months 30-60

6 to 12 months 24-30

Normal breathing rates for children

Age Breaths per minute

1 to 5 years 20-30

6 to 12 years 12-20

ByHealthwise StaffPrimary Medical ReviewerWilliam H. Blahd, Jr., MD, FACEP - Emergency MedicineSpecialist Medical ReviewerDavid Messenger, MDCurrent as ofJune 4, 2014

Normal Vital SignsIn 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 rateTable 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 rateTable 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 pressureThe 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 98.0°F (36.6°C) and 98.6°F (37°C) when measured orally and about 1°F higher when measured rectally.[2]

Retraksi interkosta

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

BronkiolitisGEJALAGejalanya 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).

DIAGNOSADiagnosis 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 serologismerupakan 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 nafas2. 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 (cracklesatau 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 menimbulkanedema 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

KrepitasiKrepitasi (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 - 14.5 32 - 42 76 - 90 25 - 31 32 - 36

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

 

FemaleAge 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 - 14.5 33 - 43 76 - 90 25 - 31 32 - 36

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 WBCCells x 103/mm3

Segmented Neutrophils (%)

Band Neutrophils (%)

Eosinophils (%)

Basophils (%)

Lymphocytes (%)

Monocytes (%)

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 0 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 0 44 - 74 0 - 5

6 Months 6.0 – 14.0 13 - 33 6 - 12 0 - 3 0 46 - 76 0 - 5

8 Months 6.0 – 14.0 12 - 32 5 - 11 0 - 3 0 47 - 77 0 - 5

1 Year 6.0 – 14.0 13 - 33 5 - 11 0 - 3 0 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/mm3) 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/mm3):

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 (Hodgkin’s disease, extensive metastases or necrosis of solid tumors)

Miscellaneous (collagen-vascular diseases, adrenal cortical hypofunction, ulcerative colitis)

Conditions Causing Basophilia (>50 basophils/mm3):

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 size (normal diameter = 6-8 mm)

Any severe anemia, e.g., iron deficiency, megaloblastic

Macrocytosis Large cells, greater than 8 mm (MCV > 100 fl)

Megaloblastic anemia, 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 iron-loading (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, Coomb’s 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, instead of circular, areas of central pallor

Congenital hemolytic anemia, thalassemia, 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 Abetalipoproteinemia (hereditary

projections 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 (Wright stain) within or on erythrocytes; nuclear debris

Hyposplenism, pernicious anemia

Heinz inclusion bodies Small round inclusions seen under phase microscopy or with supravital staining

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

Pappemheimer bodies (siderocytes)

Siderotic granules, staining blue with Wright or Prussian blue stains

Iron-loading anemias, hyposplenism, hemolytic anemias

Cabot rings Purple, fine, ring-like intraerythrocytic structures

Pernicious anemia, lead poisoning

Basophilic stippling Punctate stippling when Hemolytic anemia, punctate

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

Rouleaux Aggregated erythrocytes regularly stacked on one another

Multiple myeloma, Waldenstrom’s 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 > 11.0 x 106/L

Any physiological or 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 cytoplasmic inclusions in neutrophils

Infections or inflammatory diseases, burns, myelocytic leukemia, myeloproliferative syndromes, cyclophosphamide therapy

Pelger-Huet anomaly Neutrophil with bilobed nucleus or no segmentation of nucleus. Chromatin is coarse and cytoplasm is pink with normal granulation.

Hereditary, myelocytic leukemias, myeloproliferative syndromes

May-Hegglin anomaly Basophilic, cytoplasmic inclusions of leukocytes. Similar to Dohle bodies.

May-Hegglin syndrome (hereditary), includes thrombocytopenia and giant platelets.

Alder’s 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 with a phagocytized nucleus of a granulocyte that retains some nuclear structure

Drug reactions (e.g., penicillin, procainamide)

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 Lymphocytes, some with Infectious mononucleosis, viral

Reactive lymphocytes“Downey cells”

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

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

Leukemic cells (lymphoblasts, myeloblasts, etc.)

Presence of lymphoblasts, 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 Round or rod-like, 1-6 mm long, red-purple, refractile inclusions in neutrophils

Acute myelocytic leukemia

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 priaDada 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 infiltrateOpacification of air spaces, caused by the filling of alveoli with blood, pus, or fluid. Alveolar infiltrates are seen 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 Patternsunder construction

IntroductionThis 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". 

CautionThis 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 aerated—the 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), lymphangioleiomyomatosis 

- 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 PatternsRecognition 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 Interstitial Opacity

Alveolar Opacity- Definition

Alveolar opacity refers to opacity on chest X-ray associated with fluid filling of the airspaces.

Interstitial Opacity- Definition

The interstitium refers to the supporting structures of the lung. An interstitial opacity on chest X-ray refers to an abnormal appearance of the lung interstitium

Alveolar Opacity- Anatomy Interstitial Opacity- Anatomy

http://www.ichristianschool.org/anatomy/3rdQuarter/anatomy23.htm

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

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

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

Interstitial opacity can be linear, reticular, nodular or reticulonodular.

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 air-filled 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 DiseaseNorman Ackerman, DVM, DACVR

This patient aspirated IV contrast medium. The post-contrast image was taken within a few minutes of aspiration. The dense contrast media has filled the alveoli as well as coating some of the larger airways. The whispy/fluffy/cloudy pattern is characteristic of alveolar airspace filling.

Interstitial Lung Patterns on CXR

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

There are 4 basic interstitial lung patterns

1. linear- septal lines (Kerley lines)

2. reticular- mesh like appearance, lines in all directions

3. nodular- discrete opacities

4. reticulonodular- combination of 2 and 3

Linear Interstitial Pattern

Reticular Interstitia

l

Nodular Interstitial Pattern

Reticulonodular Interstitial Pattern

This is a fine linear interstitial pattern

Pattern

This is a nodular pattern in a patient with lymphangitis

carcinomatosis.

Reticulonodular pattern in a patient with COPD

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

The reticular pattern as seen on chest radiography and computed tomography (CT or HRCT) is depicted by numerous, small,

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,

interstitium (Kerley A) or 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. 

The most common cause of the linear pattern is hydrostatic pulmonary edema, but other etiologies include lymphangitic carcinomatosis, and atypical interstitial pneumonias such as those caused bymycoplasma, chlamydia, cytomegalovirus (CMV), and respiratory syncytial virus (RSV). Interstitial pulmonary edema tends to be symmetric in distribution while atypical infections and lymphangitic carcinomatosis may be asymmetrical. 

Scott D. Perrin, MD, Adam Ulano, MD, and Todd R. Hazelton, MDRevisiting the pattern approach to interstitial lung disease on chest radiographyAplied RadiologyVolume 38, Number 12, December 2009

linear opacities which, by summation, have been described as a lace-like or net-like in appearance.4,5 The reticular pattern can be divided into 3 distinct groups, each of which suggests different diagnoses: peripheral reticular pattern with small lung volumes,

and Todd R. Hazelton, MDRevisiting the pattern approach to interstitial lung disease on chest radiographyAplied RadiologyVolume 38, Number 12, December 2009

diffuse reticular/cystic pattern with normal or increased lung volumes, and airway/central reticular pattern.

Scott D. Perrin, MD, Adam Ulano, MD, and Todd R. Hazelton, MDRevisiting the pattern approach to interstitial lung disease on chest radiographyAplied RadiologyVolume 38, Number 12, December 2009

1. Linear

adapted from Medpix

A linear pattern is seen when there is thickening of the interlobular septa, producing Kerley lines

The most common cause of interlobular septal thickening, producing Kerley A and B lines, is pulmonary edema

other causes

Mitral stenosisLymphangitic carcinomatosisMalignant lymphomaIdiopathic

pulmonary fibrosisPneumoconiosisSarcoidosis

Note the obscuration of the normal lung markings in the patient with the linear interstitial 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

Source: Chest Radiology, Pretest USMLE, Part 2, Juzar Ali and Warren R. Summer

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.

4. Reticulonodular

This patient has a primary lung cancer with lymphatic spread (lymphangitic carcinomatosis). The lower zone of the left lung shows a coarse reticulonodular pattern.

Compare the appearance of the lower zone of the left lung with an earlier CXR on the same patient (below)

A reticulonodular pattern results from a combination of reticular and nodular opacities.A reticulonodular pattern is often difficult to distinguish from a purely reticular or nodular pattern, and in such a case a differential diagnosis should be developed based on the predomi

nant pattern. If there is no predominant pattern, causes of both nodular and reticular patterns should be considered.

CXR on same patient 2 years earlier.

Distinguishing Acinar nodules from from interstitial nodules

Acinar

Varying in sizeIndistinct edgesLarger than interstitial nodulesInterstitial

Same sizeSharp edgessmaller

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 lungsCase contributed by Dr Ian Bickle

Presentation:

Longstanding asthma. Shortness of breath.

Patient Data:

Age: 41

Gender: Female

Modality: X-ray

X-ray

FrontalFlattened 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 hyperinflationCase 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 availableAnnotated 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 anteriorlyCase 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

Reticular—fine or coarse linear shadows Reticulonodular

Nodular—small (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 (Goodpasture’s), bleeding diathesis, pulmonary

embolism Neoplasm: alveolar cell carcinoma, lymphoma Desquamative interstitial pneumonitis (DIP), alveolar proteinosis Bat-wing pattern—Central 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 lung—end-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 Worker’s 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, Wegener’s 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. Mediastinumg. Corakan BronkovaskulerUntuk 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 Paruerdapat 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, dsb5. Tulang-tulang costa kanan/kiri ...Kesan. . .

Contoh : 

Photo ini adalah photo thorak posisi APsinus costoprenicus kanan dan kiri Lancipdiaphragma kanan kiri normalJantung bentuk dan ukuran normalCorakan bronkovaskuler kedua paru normaltampak nodul opaque pada bagian media paru kanan disertai kalsifikasi di sekitarnyaTulang-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