Transcript Cm * cardiopulmonary exam 3 lectures 26-40

107 title slides
285 total slides
This one’s a real bitch
1
1.
2.
3.
4.
5.
Nose bleed anatomy
Indications for antibiotics in sinus infections
Symptoms of rhinitis medicamentosa
Treatment options for perennial rhinitis
Treatment for orbital cellulitis
2
1. Nose bleed anatomy
3
Anatomy/Physiology of Epistaxis


Anatomy

Vascular organ
 Nasal cavity
 heating
 Vascular supply
 humidification
Physiology

 Vascular nature
 Mucosa

Vasculature runs just under
mucosa (not squamous)
Arterial to venous
anastomoses
4
ICA and ECA blood flow
External Carotid Artery
Internal Carotid Artery

Sphenopalatine artery

Anterior Ethmoid artery

Greater palatine artery

Posterior Ethmoid artery

Ascending pharyngeal
artery

Posterior nasal artery

Superior Labial artery
5
Anterior vs. Posterior

Maxillary sinus ostium

Anterior: younger, usually septal vs. anterior ethmoid,
most common (>90%), typically less severe

Posterior: older population, usually from Woodruff’s
plexus, more serious.
6
Kesselbach’s
Plexus/Little’s Area:

Anterior Ethmoid (Opth)

Superior Labial A (Facial)

Sphenopalatine A (IMAX)

Greater Palatine (IMAX)
Woodruff’s Plexus:

Pharyngeal & Post. Nasal AA of
Sphenopalatine A (IMAX)
7
8
2. Indications for antibiotics in sinus
infections
9
Acute Rhinosinusitis … sinus infection

Facts:
 Viral sinusitis - 1 billion viral URIs per year
 Bacterial sinusitis – only 0.5% - 2%  secondary bacterial
infection of the sinuses.1,2

Indication for use of antibiotics
 Symptoms have not resolved after 10 days or worsen
after 5 to 7 days (see chart on next slide)
1. Gwaltney Clin Infect Dis 1996;23:1209
2. Berg et al. Rhinology 1986;24:223-5
10
11
3. Symptoms of rhinitis medicamentosa
12
13
4. Treatment options for perennial rhinitis
14
1st line therapy
 Avoid the offending allergen
Therapeutic options:
 Decongestants
 Mucolytic treatment
 Intranasal steroids
 Antihistamines
 Saline irrigation
 Leukotriene antagonists
 Intravenous immune globulin
http://www.medscape.com/viewarticle/560619
15
Adjunctive Therapy

Decongestants
no good controlled studies

Mucolytic treatment
Wawrose et al. Laryngoscope 1992;102:1225
1 double blinded study
○ 2400 mg of guaifenesin or placebo with chronic sinusitis
○ improvement in congestion and thick secretions

Topical steroids
○ Cochrane Database Syst Rev. 2013. Intranasal steroids for
acute sinusitis. Zalmanovici Trestioreanu A, Yaphe J.
16
Adjunctive Therapy

Antihistamines
 may play a role in allergic rhinitis patients with sinusitis

Saline irrigation
 may help mucociliary clearance
 mild vasoconstrictor of nasal blood flow
 excessive use can remove beneficial mucus

Leukotriene antagonists … allergies
 Useful in patients with CRS with nasal polyps

Intravenous immune globulin … infectious disease docs
 indicated in patients with impaired humoral immunity
17
5. Treatment for orbital cellulitis
18
http://emedicine.medscape.com/article/12178
58-treatment
Medical Therapy:
 Immediate hospitalization
 Broad-spectrum IV antibiotics – start immediately
 Identify pathogen – start narrow spectrum IV antibiotics
 IV antibiotics continued up to 1-2 weeks and then followed by Oral antibiotics for an
additional 2-3 weeks.
 Oral antibiotics (eg, ampicillin, cefpodoxime, cefuroxime, cefprozil) for aerobic infections
or to metronidazole for anaerobic infections
Surgery:
 Surgical drainage indications:
 If the response to appropriate antibiotic therapy has been poor within 48-72 hours or if
the CT scan shows the sinuses to be completely opacified.
 Ocular symptoms progress: 1) decreased vision, 2) development of afferent pupillary
defect develops, 3) progression of proptosis
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1.
2.
3.
4.
5.
Indications for tonsillectomy
Evaluation of hoarseness
Cord cysts vs. polyps vs. nodules vs. edema
Evaluation of airway foreign bodies
Tonsillectomy #1 indication
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Pearls … straight from lecture 27, slide 91








Tonsils hypertrophy due to acute and chronic infections
SDB (sleep disorder breathing) most common reason for
tonsillectomy
Paradise criteria for recurrent tonsillitis
Foreign body symptoms based on location
Vocal cord paralysis: malignancy or surgical trauma
Hoarseness 2 weeks or more needs evaluation
Etiology of hoarseness usually benign
Best test for voice- videostroboscopy
21
1. Indications for tonsillectomy
22
When is surgery appropriate?
Sleep disordered breathing (#1) – most common
 Airway compromise (unresponsive to medical Tx)
 Recurrent infections (#2)
 Chronic tonsillitis (#3)
 Peritonsillar abscess, recurrent
 Risk of malignancy

23
Paradise Criteria for Tonsillectomy
Paradise JL, Bluestone CD, Bachman RZ, et al. Efficacy of tonsillectomy for recurrent throat infection in severely affected children: results of parallel
randomized and nonrandomized clinical trials. N Engl J Med. 1984;310:674-683.
Baugh R F et al. Otolaryngology -- Head and Neck Surgery 2010;144:S1-S30
Copyright © by American Academy of Otolaryngology- Head and Neck Surgery
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2. Evaluation of hoarseness
25
When to pursue workup?

“Any patient with hoarseness of two weeks duration
or longer must undergo visualization of the vocal
cords”
26
Hoarseness
Considered a symptom of a disease.
 Definition:

 Rough, abnormal harsh quality
 Rough or noisy quality of voice
 Perception of voice with breathy quality
 Abnormal quality
27
Evaluation of Hoarseness: HISTORY

Hoarseness persisting for more than
two weeks requires evaluation

 occupation or livelihood depends on the normal use of
the voice
 need earlier and more aggressive intervention
 often require more specialized care.
 exception: upper respiratory tract infection
 history of tobacco use
○ head and neck cancer is the first diagnosis to
consider, as hoarseness is often the only
presenting symptom.

Voice use pattern
Nature and timing of the dysphonia
 Associated symptoms

 pain, dysphagia, cough or shortness of breath
 amount and style of voice use
 gastroesophageal reflux
 recent voice use (such as screaming at a
baseball game)
 vocal environment (where the patient uses
his or her voice—such as talking while
wearing earmuffs on an assembly line)
 history of hearing loss in the patient or in a
family member
Professional voice user
 sinonasal diseases (allergic rhinitis or chronic
sinusitis)





Medications that dry the upper airway mucosa
Tobacco and ethanol use must be determined
Other irritant exposure
Surgery on the head and neck
Intubation.
28
Physical Exam



Head and neck exam
Cranial nerve exam
Tongue
Incisions
Hearing acuity

Visualization of larynx



http://youtu.be/ajbcJiYhFKY?t
=9s
 Mirror
 Laryngoscopy
 Videostroboscopy
○ Best test for diagnosis

EMG
Drs. Zeitels (left) and Hillman (middle) examine a voice
patient (seated) using digital videoendoscopy with
stroboscopy
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3. Cord cysts vs. polyps vs. nodules vs.
edema
30
Benign growth on vocal cords









Nodules – callous
Cyst
Polyps - blister
Varices
Granulomas
Papillomas
Laryngocele
Polypoid Corditis/ Reinke’s
edema
Granular cell tumor
http://fauquierent.blogspot.com/2011/10/how-do-vocalcord-cysts-polyps-and.html
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3a. Cord cysts
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Cyst





http://www.ghorayeb.com/VocalCordCyst.html
Epithelial lining covering cyst
Results from misuse or overuse
Midcord
Found in the lamina propria,
Reinke’s space
May cause fibrosis to
contralateral cord
33
Cyst

Treatment:
 Medical - modified voice use, vocal hygiene, steroid taper,
anti-reflux
 Surgical - vocal cysts typically do not respond to
conservative therapy
○ Goal is preservation of the mucosal cover with minimal
disruption of underlying tissue
 Lateral vs. medial flap
 Triamcinolone acetate at the end
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3b. polyps
35
Polyp … 3rd most common
“Blister”
 Sessile or pedunculated
 Fibrotic, vascular or mixed
 Not uncommon to find
contralateral prenodule
 Not symmetric

36
Polyp

Treatment can be different based on type of polyp
 Sessile – microflap and resect
 Pedunculated – may retract, small flap and amputate
http://youtu.be/wrsHxE9bRzA
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3c. nodules
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Nodules
“calluses”
 overuse/misuse

 hard glottal attacks
females and children
 free edge

 anterior & middle third
bilateral and symmetric
 hourglass wave on strob

39
Nodules
Three Stages
 Inflammatory phase
 increased vascularity and protein accumulation (SP
involved early)
Localized swelling on the edge of the vocal cord that
appears as grayish, translucent thickening
 Replacement of thickening by fibrotic tissue

40
Nodules

Treatment:
 Voice rest
 Speech therapy
 Surgery (secondarily and rare)
41
3d. edema
42
Reinke's edema
Polypoid degeneration
 smoking, chronic irritation,
hormones

43
VC (Varices) – Reinke’s Edema

Treatment
 Smoking cessation
 Speech Therapy
 Antireflux medication
 Surgery
○ Epithelial microflap (lateral/Hirano flap) elevation with SLP
contouring and reduction using either cold instruments,
Microspot CO2 laser, or both
44
4. Evaluation of airway foreign bodies
45
Foreign Bodies

Children
 Safety pins
 Coins
 Food
○ nuts
○ seeds
○ carrot
○ beans
○ sunflower seeds
○ watermelon seeds
 Disc Batteries
 Toys
 School supplies

Adults
 Food
○ Meat
○ Vegetable matter
46
See a ring
- Must R/O a disc battery
- Medical emergency – eats through
whatever it touches
http://www.aaemrsa.org/communication/modernre
sident/2011/aug-sept.php
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Presentation

If patient was coughing like crazy,
Not any more coughing … BE WORRIED
Initial phase
 choking and gasping, coughing, or airway obstruction

Asymptomatic phase … DANGER ZONE
 relaxation of reflexes, acute inflammation reduces
 results in a reduction or cessation of symptoms
 lasting hours to weeks

Complications phase
 erosion or obstruction leading to pneumonia, atelectasis, or
abscess
48
Symptoms based on location

Esophagus
 drooling, dysphagia, odynophagia, retching,
refusing po, fussy
 10 percent have airway symptoms

Larynx
 airway obstruction, hoarseness, aphonia

Trachea
 similar to laryngeal foreign bodies but
without hoarseness or aphonia
 wheezing similar to asthma

Bronchus
 cough, unilateral wheezing, and decreased
breath sounds
 65% of patients present with this classic
triad.
If FB in esophagus
(cricopharyngeus), it pushes
forward on trachea
UNILATERAL PNEUMONIA
(decrease breathe sounds,
wheezing)
49
Location of Ingested Foreign
Body
Cricopharyngeus
15-17 cm (C6)
Aorta
22-24 cm
Left mainstem bronchus
28-30 cm
Gastroesophageal junction
40 cm (T11)
Intrinsic narrowing
stricture, tumor
Extrinsic
tumor
Histology for Pathologists, 3rd Edition, 2007 Lippincott Williams & Wilkins
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Workup at Hospital
Chest X-ray
AP & lateral
Inspiration and expiration
**Most important primary test
Flouroscopy
CT scan
virtual bronchoscopy
Bronchoscopy – definitive after
Rigid vs flexible
Foreign Bodies in the Chest: How Come They Are Seen in Adults?
Kim TJ, Goo JM, Moon MH, Im JG, Kim MY - Korean J Radiol (2001 Apr-Jun)
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5. Tonsillectomy #1 indication
52
When is surgery appropriate?
Sleep disordered breathing (#1) – most common
 Airway compromise (unresponsive to medical Tx)
 Recurrent infections (#2)
 Chronic tonsillitis (#3)
 Peritonsillar abscess, recurrent
 Risk of malignancy

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1.
2.
Symptoms, timing of symptoms and treatment of croup
Micro of epiglottitis
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1. Symptoms, timing of symptoms and
treatment of croup
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1a. Symptoms of croup
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Larygotracheobronchitis
AKA “Croup”
“steeple sign” on x-ray
•
The most common cause of stridor outside the
neonatal period
• Peak incidence is ages 6mo – 3yrs
• Seasonal distribution: fall & early winter months
• Viral: parainfluenza, RSV, rhinovirus, and human
bocavirus
57
Classifying Croup by symptoms
•
•
•

Mild: occasional barking cough, no stridor, mild to no
retractions, no agitation or distress
Moderate: frequent barking cough, easily audible
stridor at rest, +chest wall retractions at rest, little
agitation or distress
Severe: frequent barking cough, prominent inspiratory
stridor and occasional expiratory stridor, marked
sternal retractions, +agitation and distress
CLINICAL JUDGEMENT / ASSESSMENT SKILLS!
58
1b. Timing of croup symptoms
59
Larygotracheobronchitis
AKA “Croup”
•
The most common cause of stridor outside the
neonatal period
• Peak incidence is ages 6mo – 3yrs
• Seasonal distribution: fall & early winter months
• Viral: parainfluenza, RSV, rhinovirus, and human
bocavirus
60
1c. Treatment of croup
61
Treating Croup
RACEMIC EPINEPHRINE




For moderate to severe croup
Do not use Albuterol as β-agonists cause
vasodilatation and can increase airway edema
Observe for approx 3hrs
Studies have shown that approx 38% of patients
with Croup refractory to treatment expressed this in
the 2nd-3rd hours of observation
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Treating Croup
CORTICOSTEROIDS
 Dexamethasone 0.6mg/kg IM or PO
 Reduces severity & duration of symptoms
HELIOX (mix of 70%helium & 30%oxygen): may improve
laminar gas flow / ventilation but not definitively proven
The majority of children w/ Croup are readily managed with
Dexamethasone and anti-pyretics / cough & cold
preparations.
63
2. Micro of epiglottitis
64
Epiglottitis
•
•
•
“thumbprint sign” on x-ray
An ACUTE inflammatory process of the epiglottis
which can lead to a life-threatening airway obstruction
Primary causative agent is H.influenzae type B;
which, has been largely eradicated due to
immunization
Other potential causative agents: Staph & Strep,
Candida (immunocomp.), thermal injury/burns, direct
trauma
65
1.
2.
3.
Rash causes after amoxicillin
Symptoms of peritonsillar abscess
Retropharygeal vs. peritonsillar vs. Ludwigs
66
1. Rash causes after amoxicillin
67
If a patient is placed on antibiotic (PCN) for a
presumed pharyngitis and a scattered, faint,
morbilliform rash occurs….what is another
possible diagnosis?
68
Amoxicillin rash, differential dx
1.
2.
PCN Allergy
Infectious mononucleosis secondary to EBV
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2. Symptoms of peritonsillar abscess
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Retropharyngeal Abscess (RPA)
•
•
Believed to be due to suppuration of lymph nodes found
within/between the anatomical space between the post.
pharyngeal wall & prevertebral fascia
These nodes tend to regress by age 4; hence, increased
potential in children <4yo
Also can be due to trauma/penetration into the space
•
Symptoms:
•
• Lack of or very mild URI
• Neck pain & swelling
• Increased drooling
• Tripoding
RPA
“tripoding”
• Pleuritic chest pain (ominous sign of extension into the thoracic
cavity/mediastinum)
71
3. Retropharygeal vs. peritonsillar vs.
Ludwigs
72
3a. Retropharygeal Abscess (RPA)
73
Retropharyngeal Abscess (RPA)
•
•
•
•
Believed to be due to suppuration of lymph nodes found
within/between the anatomical space between the post.
pharyngeal wall & prevertebral fascia
These nodes tend to regress by age 4; hence, increased
potential in children <4yo
Also can be due to trauma/penetration into the space
Symptoms: lack of or very mild URI, neck pain & swelling,
increased drooling, tripoding, pleuritic chest pain is an
ominous sign of extension into the thoracic
cavity/mediastinum
74
RPA Anatomically speaking
75
RPA Diagnosis
•
Lateral neck X-ray
 Retropharyngeal space at C2 is 2x diameter of the
vertebral body width OR > ½ width of C4 vertebral body
 CT scan is near 100% sensitive
•
Need to be clinically astute as this can cause
severe airway compromise – be prepared, airway
equipment, steroids to reduce inflammation
76
RPA on X-Ray
(L) normal
(R) abnormal
77
RPA on CT
78
RPA Treatment
•
•
•
•
Airway management!
ENT consultation for possible Incision & Drainage
Often mixed flora: S.aureus, S.pyogenes,
S.viridans, gram-negative rods, oral anaerobes
Ampicillin/sulbactam or Clindamycin
79
3b. Peritonsillar Abscess
80
Peritonsillar Abscess (PTA)
•
•
•
•
Deep OROPHARYNGEAL infection/abscess
Can occur at ANY age; however, most common in
adolescents & young adults
Typically is the propagation of a superficial infection
that progresses to an accumulation of pus between
the tonsillar capsule the superior constrictor
muscle
Most are UNI-lateral (<10% BI-lateral)
81
Trismus – cannot open mouth d/t pain
PTA Diagnosis & Treatment
•
•
•
•
•
Sore throat, fever / chills, trismus, voice
change (“hot potato”), increased salivation
Exam reveals UNI-lateral peritonsillar edema,
deviation of the uvula away from the side of
infection
Abscess vs. Cellulitis can often be difficult to
discern: more ill appearing = ?PTA, CT scan
can identify
Antibiotic for polymicrobial coverage:
Amoxicillin/clavulanic acid or Clindamycin
Needle Aspiration
82
PTA Aspiration
Complications:
Compliance of patient to
participate
 Hemorrhage
 Puncture of the Carotid artery;
needle should not penetrate
>1cm as the Carotid lies
lateral & posterior
 Aspiration of purulent material

83
3c. Ludwig’s Angina
84
Ludwig’s Angina
•
•
•
•
•
•
Infection of the submental, sublingual, and submandibular
spaces
Clinical findings: 1) poor dentition/dental hygiene, 2) dysphagia,
odynophagia, 3) trismus, 4) edema of the upper midline neck and
floor of the mouth
85% of cases arise from an odontogenic source (abscess)
Need to consider in patients with recent dental
instrumentation/procedures
Rapidly progressing Infection/inflammation  cause the
posterior displacement of the tongue  airway compromise
Treatment: airway management, steroids, IV antibiotics,
ENT/surgical consultation
85
Ludwig’s Angina
86
Ludwig’s Angina on the Inside
Tongue can fall posterior and can block airway
87
1.
2.
3.
4.
5.
Promoter and synergistic agents of head/neck cancers
What to do with hoarseness > 2 weeks
Sinus cancer presentation
Why do supraomohyoid dissection
Etiology of sinus cancers
88
Conclusions
Head and neck cancer is the 8th leading cause of death
worldwide
 Tobacco use is the most significant risk factor for developing a
head and neck cancer
 Most common sites include





Tongue
Floor of mouth
Tonsil
Vocal cord
Early detection and smoking cessation lead to the best longterm outcomes
 Cancer of the nose and sinuses are very rare and require a
high index of suspicion for diagnosis

89
Conclusions
Status of cervical lymph nodes is an important
prognostic indicator
 The benefit of elective therapy outweighs the risks, if the
prevalence of micrometastases is >20% … neck
dissection (early removal can prevent mets)
 Neck dissections are divided into 3 main categories
(RND, MRND, SND)
 Selective neck dissection is based on lymphatic
drainage of the primary site
 Recurrence rates are comparable in appropriately
selected patients

90
1. Promoter and synergistic agents of
head/neck cancers
91
Head and Neck Cancer
All tobacco products –
cigarettes, pipes,
cigars, smokeless
tobacco, betel quids
(nut), reverse smoking,
secondhand smoke
Tobacco and alcohol are considered the most
common factors associated with the development of
head and neck cancer
 This relationship is synergistic

 Alcohol serves as a promoter for the carcinogenic
effects of tobacco
92
Head and Neck Cancer

Tobacco
 1.9 fold risk for males
 3.0 fold risk for females
 Risk directly proportional to the number of cigarettes smoked and
number of years smoked (dose dependant relationship)

Alcohol
 Alone confers a 1.7 fold risk

Combination
 At least 15 fold risk
 35 fold risk for 2 pack per day and 4 drinks per day
93
2. What to do with hoarseness > 2 weeks
94
Hoarseness (side note)


Hoarseness lasting >2 weeks
with little or no improvement
needs laryngeal exam
URI is most common cause of
hoarseness
 Often lasts several weeks


Hoarseness lasting >6 weeks in
an adult should be considered
cancer until proven otherwise
Acute Hoarseness in any
smoker should be considered
cancer until proven otherwise
 Rarely lasts 6 weeks
95
Evaluation (laryngeal exam)
Complete history and physical







Laryngosocpy
Videostroboscopy
CT neck with contrast
CXR
Labs including LFTs
FNA neck mass
Biopsy / Exam under
anesthesia

Consultations









Head and neck surgeon
Radiation oncologist
Medical oncologist
Internal medicine
Dentist / Oral surgeon
Speech pathologist
Nutritionist
Psychologist
Tobacco cessation
96
Evaluation
Flexible fiberoptic nasopharyngoscope
Videostroboscopy
97
3. Sinus cancer presentation
98
Cancer of the Paranasal Sinuses
Very rare: 3% of Head and Neck Cancers
 Delay in diagnosis due to similarity to benign conditions (i.e.
usually present in advanced stages [88% at T3/T4])
 Nasal cavity neoplasms

 ½ benign
 ½ malignant

Paranasal Sinuses
 Malignant
99
Presentation

Oral symptoms: 25-35%
 Pain, trismus, alveolar ridge fullness, erosion

Nasal findings: 50%
 Obstruction, epistaxis, rhinorrhea

Ocular findings: 25%
 Epiphora, diplopia, proptosis

Facial signs
 Paresthesias, asymmetry
100
Epidemiology
Predominately disease of older males
 Exposure:

 Wood working, nickel-refining processes
 Industrial fumes, leather tanning

Cigarette and Alcohol consumption
 No significant association has been shown

HPV may play role in malignant degeneration of inverting
papillomas
101
Location

Maxillary sinus
 70%

Ethmoid sinus
 20%

Sphenoid
 3%

Frontal
 1%
102
Inverted Papilloma





UNILATERAL “SINUS INFECTION”
- Think inverting papilloma
- Will turn into SCC 10% if untreated
4% of sinonasal tumors
Site of Origin: lateral nasal wall
Unilateral
Malignant degeneration in 2-13% (avg 10%)
Must rule out IP for any CT showing unilateral sinusitis
103
4. Why do supraomohyoid dissection
104
Introduction
One of the most important prognostic indicators for patients
with squamous carcinomas of the upper aerodigestive tract
is the status of the cervical lymph nodes
 Local metastatic disease (spread to cervical lymph nodes)
can be managed with surgery, radiation, or both

 i.e. Goal is to remove cancer that may have spread to the neck
105
Supraomohyoid Type
Used for oral cavity cancer: lip, buccal mucosa,
upper & lower alveolar ridge, RMT, hard palate,
anterior 2/3 tongue, FOM
 Tumors in this region, especially oral tongue & FOM,
metastasize early
 20% risk occult disease
 >90% of occult metastatic disease in oral cavity
cancer involves Levels I, II, and III

106
Supraomohyoid Type



En bloc removal of node
levels I-III
Posterior limit: posterior
border SCM
Inferior limit: superior belly
of omohyoid m. where it
crosses the IJ
107
5. Etiology of sinus cancers
108
Epidemiology
Predominately disease of older males
 Exposure:

 Wood working, nickel-refining processes
 Industrial fumes, leather tanning

Cigarette and Alcohol consumption
 No significant association has been shown

HPV may play role in malignant degeneration of inverting
papillomas
109
1.
2.
3.
4.
5.
Injuries with associated internal injuries
Clavicle injuries with Surgical repair required
When to intubate a trauma
Most easily seen injuries on plain x-ray
Define flail chest
110
1. Injuries with associated internal injuries
111
Blunt Chest Trauma

Chest Wall Injuries
○ Rib, clavicle, sternal fractures
○ Chest wall contusions

Cardiac Injuries
○ Cardiac Tamponade*
○ Myocardial Contusions*

Pulmonary Injuries
○ Pulmonary contusion
○ Pneumothorax*/Hemothorax*
○ Flail Chest

Vascular Injuries
○ Aortic Rupture*



Esophageal Rupture*
Tracheal/Bronchial Injuries*
Diaphragmatic Rupture*
112
2. Clavicle injuries with Surgical repair
required
113
Clavicle Fractures


Most common newborn/childhood fracture
Mechanisms
 Force directly to clavicle or to outer end
 Most pts have history of direct fall onto shoulder
 Football, bike accidents, wrestling, hockey, MVC

Classification of fractures
 Based on dividing clavicle into thirds
 Proximal (5%), Middle (80%), Distal (15%)

Presentations
 swelling, loss of normal contour, skin tenting, head turned towards affected
side, open fx possible

Complications
 Brachial plexus injury, pneumothorax, non-union (0.1-15%)
 Vascular Injury: subclavian artery/vein, internal jugular, axillary artery
114
Lateral (Distal) Third Fractures



15% of clavicle fractures
Mechanism – direct blow to top of shoulder
Fracture lateral to the coracoclavicular ligament
Integrity of
CC Ligament
Fx Displaced?
Treatment
Type I
Intact
No
Non-operative: sling, ice, pain control, early
ROM exercise
Type II
Torn
YES
Medial fragment pulled
superiorly
Ortho consult within 72 hrs -possible
surgical repair
Risk of non-union
Type III
Intact
No
Fx through articular
surface of AC joint
Non-operative: sling, ice, pain control, early
ROM exercise
Risk of OA of joint
What type of fracture
is this?
115
3. When to intubate a trauma
116
Pulmonary Contusion

Treatment
 Maintenance of adequate oxygenation & ventilation
○ Endotracheal intubation may be necessary
 Pain control, encourage deep breaths, incentive spirometry
 Generally require admission – contusions tend to worsen
over 24 hrs
 Avoid excessive IV fluid - may worsen contusions

May lead to ARDS, pneumonia, respiratory failure
http://www.trauma.org/index.php/main/image/1002/
117
Flail Chest

Management
 Oxygenation, ventilation, pain control
 Manual stabilization initially
 Detection & treatment of underlying injuries
○ CT scan indicated
○ Chest tube if PTX of hemothorax
 Positive pressure ventilation - endotracheal intubation often
required
○ Provides splinting
 Pain Control - IV narcotics, regional nerve blocks, epidural
anesthesia
 If no hypotension, hypovolemia, blood loss limit IV fluids
118
4. Most easily seen injuries on plain x-ray
119
Hemothorax
 Pneumothorax
 Pulmonary contusion
 Vascular injury

120
5. Define flail chest
121
Flail Chest

Three or more adjacent ribs, each fractured in 2 or more places
 Chest wall unstable & segment lacks continuity with rest of thoracic cage

Paradoxical motion of chest wall
 Segment moves IN during Inspiration & OUT during Exhalation
 May not be obvious initially (splinting, muscle spasm)
122
1.
2.
3.
Secondary pneumothorax causes
Symptoms (it’s not shortness of breath),Tx and imaging of simple PNX
Treatment of tension PNX
123
Summary Points - PTX







Primary ptx occurs in pts without lung disease
Pain, not dyspnea may be the chief complaint in primary ptx
Secondary ptx occurs in pts with underlying lung disease - COPD
most common
Tension pneumothorax is an immediate life threat and if suspected
must be treated emergently before x-ray confirmation.
A CXR is the initial test to detect ptx in a stable patient.
An open ptx must be sealed and then a chest tube placed
A needle decompression may be performed in an emergent
situation as a temporizing measure in suspected tension
pneumothorax. A chest tube must be placed following needle
decompression.
124
1. Secondary pneumothorax causes
125
Secondary Pneumothorax

PTX in setting of underlying
lung disease
 1/3 – 1/2 of all spontaneous ptx
(o)

Most common risk factor?
 COPD
Peak age is 60-65 years; male
to female 3:1
 More likely to present with
dyspnea & more severe
symptoms . Why?
 Much higher mortality than
PSP


Don’t
Memorize!
Other diseases associated
with SSP
 HIV
 Other Airway Disease – asthma;




CF
Infections - necrotizing
bacterialpneumonia/ abscess; TB
Interstitial lung disease –
sarcoidosis; idiopathic pulmonary
fibrosis
Neoplasms - primary lung ca;
pulmonary/pleural metastasis
Miscellaneous - connective tissue
dx; pulmonary infarction
126
2. Symptoms (it’s not shortness of
breath),Tx and imaging of simple PNX
Simple pneumothorax is a non-expanding collection of
air around the lung. The lung is collapsed, to a variable
extent. Diagnosis on physical examination may be very
difficult.
127
2a Symptoms (it’s not shortness of breath)
simple PNX
128
Primary Pneumothorax

Clinical Manifestations - Chest pain & dyspnea
 Chest pain
○ Acute onset, ipsilateral
○ Often pleuritic
 Symptoms often mild – rarely life threatening (l) Why?

Physical Exam Findings
 Vital signs often normal (l)
 Most common physical finding - tachycardia (o)
 Ipsilateral Chest findings
○ \/ movement with respiratory cycle
○ Hyperresonant to percussion
○ \/ Breath sounds
○ \/ fremitus
 Chest exam findings may be absent in small ptx
129

Symptoms of PTX
 Sudden onset of ipsilateral chest
or shoulder pain
 Dyspnea - variable
 Cough



Reduced air entry
Resonance to percussion are
often difficult or impossible to
appreciate.
Careful palpation of the chest
wall and apices may reveal

Signs of PTX
 Mild resting tachycardia
 Tachypnea
 Unilateral \/ breath sounds
○ Caution: Often normal with small
ptx
 Other possible findings
○ Hyperresonance to percussion
○ Unilateral enlargement of
hemithorax
○ \/ chest excursion with
respiration
 Subcutaneous emphysema
 Rib fractures as the only sign of
an underlying pneumothorax.
130
2b. Tx simple PNX
131
Observation
 Oxygen

132
2c. Imaging of simple PNX
133
Summary Points - PTX







Primary ptx occurs in pts without lung disease
Pain, not dyspnea may be the chief complaint in primary ptx
Secondary ptx occurs in pts with underlying lung disease - COPD most common
Tension pneumothorax is an immediate life threat and if suspected must be
treated emergently before x-ray confirmation.
A CXR is the initial test to detect ptx in a stable patient.
An open ptx must be sealed and then a chest tube placed
A needle decompression may be performed in an emergent situation as a
temporizing measure in suspected tension pneumothorax. A chest tube must be
placed following needle decompression.
134
3. Treatment of tension PNX
135
EXAM … Management – Tension Pneumothorax



Emergency!
Clinical diagnosis – don’t wait for cxr!
Immediate needle decompression
 Must follow w/ chest tube

Needle Decompression





Temporizing measure
Insert 14-16 gauge IV catheter over rib at 2nd ICS, midclavicular line
Advance catheter & remove needle
Rush of air is confirmatory
Tube Thoracostomy




28-36F in Trauma
16-20F for Spontaneous
4th-5th ICS (about nipple level)
Mid to anterior axillary line
136
Case – Patient A Resolution
Occlusive dressing placed over wound
Needle decompression followed by 36 F chest tube
Pt dramatically improved after chest tube and was taken to the OR for exploration of his abdomen due to a
GSW to the abdomen
137
1.
2.
3.
4.
5.
Dermoid vs. 1st branchial cleft cyst
Symptoms of thyroglossal duct cyst
Tx of thyroglossal duct cyst
Anatomy of 3rd branchial cleft cyst
Micro / appearance of scrofula
138
1. Dermoid vs. 1st branchial cleft cyst
139
Congenital – by Location
Lateral
Branchial Cleft Cyst
 Laryngocele

Frequently Cross midline


Lymphangiomas (Cystic
Hygromas)
Hemangiomas
Midline
 Thyroglossal
Duct Cyst
 Plunging Ranula
 Thymic Cysts
 Dermoid Cysts
 Teratomas
140
1a. Dermoid
141
Dermoid cysts
Present at birth
 Moves freely, feels “doughy”
 Has Epidermal and dermal components
 Simple excision for treatment

142
1b. 1st branchial cleft cyst
143
Branchial Cleft Cyst




Most common lateral congenital neck mass
Originate from cervical sinus of His vs.
Waldeyer’s ring tissue
Along the sternocleidomastoid muscle
(anterior)
Always superficial to CN XII
144
1st Branchial Cleft Cyst


Near or above the angle of the
mandible
Can be seen as duplicate external
auditory canal or as pits
145
2. Symptoms of thyroglossal duct cyst
146
Thyroglossal Duct Cyst
Most common central congenital neck mass
in children
 Persistent thyroid descent tract, beginning at
the foramen caecum of the tongue
 Midline mass, mobile with swallowing
(superiorly)
 Asymptomatic unless large (obstruction) or
infected

147
Thyroglossal Duct Cyst


Can contain ectopic thyroid tissue (benign or malignant)
Treatment – excision
 Sistrunk procedure
 10% recurrence after surgery
148
3. Tx of thyroglossal duct cyst
149
4. Anatomy of 3rd branchial cleft cyst
150
3rd Branchial Cleft Anomalies
VERY RARE
 Lower neck – near the upper pole of
the thyroid gland
 Deep to sternocleidomastoid
 Can displace common carotid artery
and/or the internal jugular vein
 Ends in thyrohyoid membrane OR
pyriform sinus

151
5. Micro / appearance of scrofula
152
Scrofula: Cervical Mycobacteria

Atypical mycobacterial

Typical myco
 M. avium-intracellulare,
 M. Tuberculosis
scrofulaceum
 Pediatric population
 Isolated cervical involvement
 Treatment: Excision (consider
2 months of clarithromycin
first)
 Immunocompromised Adult




population
Multiple post. triangle nodes
Positive PPD test noted
Manifestation of disseminated
disease
Treatment: anti-TB drugs
BOTH: Painless, enlarging or persistent mass in the neck.
153
1.
2.
Distinguish metabolic acidosis / alkalosis / respiratory acidosis /
alkalosis / gapped
Treatment for high CO2
154
1. Distinguish metabolic acidosis / alkalosis
/ respiratory acidosis / alkalosis /
gapped
155

STEP 1

 Acidosis (pH < 7.35)
 For metabolic acidoses, calculate the
 Alkalosis (pH > 7.45)
anion gap
 (Na++K+)-(Cl+HCO3)
 Is there an elevated anion gap (normal
is 10-16)?
 Normal (pH in the range of 7.35-
7.45)

STEP 3
STEP 2
 Respiratory? (pCO2 out of range?)

STEP 4
 Look for compensation – the alternate
 Metabolic? (HCO3 out of range?)
value will stray from normal to try to
normalize the pH
 Both?

STEP 5
 Determine oxygen status
○ While the oxygen status will not affect
pH, it provides information on the
ventilation / perfusion status of the lungs
156
Direct Measurements
pH
 PaO2
 PaCO2
 SaO2
 HCO3

NORMAL VALUES LISTED
7.35-7.45
75-100 mm Hg
35-45 mm Hg
94-100%
22-26 mEq/L
157
1a. metabolic acidosis
158
ABG Practice #2
A six year old boy is taken to the
emergency department with vomiting
and a decreased level of consciousness.
 His breathing is slow and deep
(Kussmaul breathing), and he is
lethargic and irritable in response to
stimulation.
 He appears to be dehydrated—his eyes
are sunken and mucous membranes are
dry—and he has a two week history of
polydipsia, polyuria, and weight loss.









pH 7.20
pO2 100
pCO2 25
HCO3 - 10
Na+ 126
K+ 5.0
Cl- 95
Glucose 538
Diagnosis = metabolic acidosis with respiratory compensation
159
STEPS
1) Acidotic
2) Metabolic
3) Compensation – only partial compensation, not enough to bring back to normal; low
CO2 (normally gives alkalosis)
4) Anion gap – 26 (elevated)
5) Oxygen – normal
Diagnosis = metabolic acidosis with partially respiratory compensation
- Secondary to diabetic ketoacidosis
- Primary metabolic condition, is the respiratory component going away from normal to
compensate (away from normal, decreased CO2, slow deep respirations)
Treatment
- Insulin
- Body can use glucose present
- Before insulin, glucose not used, used FFA  ketone bodies  metabolic acidotic
buildup
160
1b. metabolic alkalosis
161
ABG Practice #4




An 80 year old woman presents
with a two day history of persistent
vomiting.
She is lethargic and weak and has
myalgia.
Her mucous membranes are dry
and her capillary refill takes >4
seconds.
She is diagnosed as having
gastroenteritis and dehydration.





pH 7.5
pO2 85
pCO2 45
HCO3 - 37
Normal anion gap
162
Steps
1) Alkalosis (vomited acid)
2) Metabolic alkalosis (CO2 45 is upper range of normal; HCO3- 37 is high)
3) Respiratory compensation beginngin (slower, shallower breathing  higher CO2)
4) Anion gap – normal
5) Oxygen status – normal
Diagnosis
- Metabolic alkalosis with partial respiratory compensation
Treatment
- During compensation, oxygen will go down – needs some oxygen
- Antiemetic – slow the N/V
- Hydration
- Monitor respiratory rate for decreased oxygenation
Serious complications
- Arrhythmias d/t poor electrical conduciton
163
1c. respiratory acidosis
164
ABG Practice #1
A 60 year old man with a history of
chronic obstructive pulmonary
disease presents to the emergency
department with increasing
shortness of breath, pyrexia, and a
cough productive of yellow-green
sputum.
 He is unable to speak in full
sentences. His wife says he has
been unwell for two days.
 On examination, a wheeze can be
heard with crackles in the lower
lobes; he has a tachycardia and a
bounding pulse.







pH 7.20
pCO2 70
HCO3 - 27
pO2 59 mm Hg
O2 saturation 84%
Normal anion gap
165
Diagnostic STEPS:
1) Acidosis
2) Respiratory – really high CO2
3) Compensation? – nope, elevated bicarb would
show compensation (renal compensation takes
days to improve the acid/base balance) … bicarb
on its way up
4) Anion gap? Not as helpful
5) Determine O2 status – hypoxic
DIAGNOSIS:
Pyrexia (fevers),
RESPIRATORY ACIDOS with HYPOXIA
- Acute decompensation
Long standing COPD, will have increased pCO2 (blood) –
- Baseline is high (CO2 retainers)
- High baseline bicarb is high
- Higher residual dead space, pockets of space, rotten air
(high CO2) d/t dead alveoli
- Cannot blow off CO2 (poor exhalation)
Treatment
- Primary respiratory drive is high CO2
- COPD patients have oxygen related drive or equal to CO2
drive
- HIGH FLOW OXYGEN with NON-REBREATHER MASK
(POSTIVE PRESSURE VENT)
-
Slower breathing
Retain more CO2 in response
CO2 in 90-100  lethargic, airway compromise
DEFINITIVE TREATMENT
- TIDAL VOLUME (decreases dead space) = BIPAP
166
1d. respiratory alkalosis
167
ABG Practice #3




A 12 year old girl attends the
emergency department after falling
and hurting her arm.
In triage she is noted to be tachycardic
and tachypneic.
She is given some pain killers.
While waiting to be seen by the doctor,
she becomes increasingly hysterical,
complaining that she is still in pain and
now experiencing muscle cramps,
tingling, and paresthesias.





pH 7.5
pO2 115
pCO2 29
HCO3 - 24
Normal anion gap
168
Steps:
1) Alkalosis
2) Respiratory alkalosis (low CO2)
3) No compensation
4) Normal anion gap
5) Oxygen is high (hyperventilation)

Diagnosis
- Respiratory alkalosis secondary to hyperventilation
- pH up with CO2 out
Treatment
- Brown bag
169
1e. gapped
170
Anion Gap Metabolic Acidoses
ELEVATED (Gapped)









Methanol
Uremia
Diabetic ketoacidosis
Propofol Infusion
Isoniazid/iron toxicity
Lactic Acidosis
Ethanol / ethylene glycol
Rhabdomyolysis
Salicylates
DECREASED





Hypoalbuminemia
Plasma cell dyscrasias
Monoclonal protein
Bromide toxicity
Normal variant
171
Calculated Measurements

Anion Gap
normal = 8-16
 (Na+) – (Cl- + HCO3-)

Base Excess normal = -2 to +2 = 0
 0.93 x ([HCO3] – 24.4 + 14.8 x [pH – 7.4])
172
2. Treatment for high CO2
173
DEFINITIVE TREATMENT
- BIPAP
- Decreases dead space
- Increases tidal volume
174
1.
2.
3.
4.
5.
Inspiratory cough anatomy
Treatment of epiglottitis
Diagnosing laryngomalacia
Diagnosing croup with imaging
Diagnosing vocal cord dysfunction
175
1. Inspiratory cough anatomy
176
Evaluation
Location of stridor:
 Supraglottic region →
Inspiratory stridor
 Glottic and Subglottic →
Biphasic (inspiratory and expiratory)
 Intrathoracic trachea →
Expiratory stridor (wheeze)
 Bronchi/Bronchioles →
Expiratory fine wheeze
177
2. Treatment of epiglottitis
178
EVALUATE ONLY WITH ENT DOCTOR IN OR UNDER
GENERAL ANESTEHSIA
Do NOT examine by yourself in office or ER
179
EPIGLOTTITIS
“Tripod Position”: Sitting upright and leaning forward
with the chin up mouth open while bracing on the
arms.
 Invest: Lat. X-ray “Thumb Sign”
 Dx: Cherry-red swollen epiglottis
 Rx: ET Intubation (in OR by Anesthesia)
 Antibiotics

180
3. Diagnosing laryngomalacia
181
LARYNGOMALACIA
 Diagnosis:
Flexible Laryngoscopy (The gold standard)
 Visualizing supraglottic structures getting sucked into the glottis during
inspiration
 Treatment:
- Wait and watch
- Treat GERD
- Tracheostomy
- Surgery (severe – must do laryngoscope)
182
182
4. Diagnosing croup with imaging
183
EXAM:Croup “Laryngotracheobronchitis”
Soft tissue neck x-ray
“Steeple Sign”
(observed on PA Xray
What is characterisitc to croup = steeple sign of Xray (PA)
184
5. Diagnosing vocal cord dysfunction
185
EXAM:
VOCAL CORD DYSFUNCTION
A.k.a. Paradoxical Vocal Cord Motion
Disordered movement of vocal cords
Vocal cords involuntarily close during inspiration
and
sometimes exhalation
Mistaken as asthma
Onset: Respiratory distress with physical or emotional
stress
Diagnosis: spirometery and laryngoscopy
Treatment: calming technique and speech therapy
186
1.
2.
3.
4.
5.
Etiology of VTE
Origin of PE clots
EKG findings in PE
Definitively diagnosing PE
Length of tx for PE
187
1. Etiology of VTE
189
(Long plane flights)
Do NOT need all 3 risk factors to have thrombus or
embolus
2. Origin of PE clots
200
Where?
- Deep veins of leg (most common
thrombus)
3. EKG findings in PE
203
EKG – S1Q3T3 phenomenon
- If seen, chance is high for PE
- S wave in lead 1 on QRS
- Lead 3 – dipped Q wave and inverted T wave
4. Definitively diagnosing PE
206
5. Length of tx for PE
209
1.
2.
3.
4.
5.
Define pulmonary hypertension
pulmonary function tests of pulmonary hypertension
treatment plans for pulmonary hypertension
diagnose Goodpasture syndrome
lab findings of Goodpasture syndrome
213
EXAM
Gold Standard … he emphasized this.





Right heart catheterization is the gold standard for
diagnosis of PH.
mPAP greater than or equal to 25
Rules in or out the presence of left sided heart disease.
Rules out L > R atrial shunt
Allows evaluator to perform a vasodilator challenge.
 If referred patients comes back on cardizem only (not a new
drug), it is b/c the patient responded well to vasodilator challenge

Gives a baseline to determine response to treatment
1. Define pulmonary hypertension
215
Pulmonary Hypertension
Definition
An elevation in the mean pulmonary artery pressure –
mPAP greater than or equal to 25 mmHg at rest.
 This is determined by Right Heart Catheterization
 Once it is determined that Pulmonary Hypertension is
present it can be classified by placing in a World
Health Organization – WHO PH Category.
 This is the new nomenclature and will be discussed
later.

2. Pulmonary function tests of pulmonary
hypertension
217
Additional Testing
Additional testing can be targeted by clinical suspicion
 Pulmonary Function Testing – can help identify
underlying obstructive or restrictive lung disease.
Lung volumes less than 50% predicted have been
shown to contribute to pulmonary hypertension.
 PH can be seen as an isolated decrease in diffusion
capacity on PFTs.

3. treatment plans for pulmonary
hypertension
219
EXAM
Treatment

WHO Functional Class II
 Bosentan or Sildenafil

WHO Functional Class III
 Bosentan and/or Sildenafil +/- Flolan

WHO Functional Class IV
 Flolan
Treatment
Primary therapy is always directed at the underlying
cause
 Group 1 patients – idiopathic PAH have no underlying
cause thus treatment is always advanced therapy.

Treatment
Supplemental oxygen, cpap, optimize pulmonary
function
 Diuretics – be careful
 Digoxin
 Anticoagulation
 Pulmonary Rehabilitation

Improved WHO functional class and oxygen consumption.
Did not improve hemodynamic measures
Treatment

Prostanoids
 Prostacyclin is a potent vasodilator
 Iloprost, epoprostenol or flolan
 Ultrashort half lives, systemic hypotension
 Continuous inhalation, infusion or subdermal
Treatment

Endothelin Receptor Antagonist
 Endothelin is a vasoconstrictor and smooth muscle mitogen
 Bosentan and Ambrisentan
 Side effects hepatotoxicity and edema
Treatment

Phosphodiesterase 5 Inhibitors
 Sildenafil, tadalafil, vardenafil
 Prolong vasodilatory effects of NO
4. diagnose Goodpasture syndrome
226
Symptoms
Patients with pulmonary renal syndromes usually
present with a rapidly progressive onset of cough,
dyspnea, fever and hemoptysis
 They will present like a patient with pneumonia in
ARDS. Unless there is a known history of connective
tissue disease such as lupus you will have only subtle
hints that a pulmonary renal syndrome is present
 The physical diagnosis is non specific. Findings are
usually positive if there is a known vasculitis or
connective tissue disease

Goodpasture’s
Rapidly progressive glomerulonephritis secondary to
circulating antibodies against the basement
membrane.
 The glomerulonephritis is associated with a crescent
formation (COMLEX / USMLE)
 Younger adults <30 typically present with full
constellation of symptoms whereas older adults > 50
have primarily glomerular disease.

Goodpastures - Presentation
The history and physical findings are non specific.
 The patient presents in respiratory failure and will
resemble someone with pneumonia with ARDS.
 When intubated you may notice frothy sputum in the
endotracheal tube. You may note an absence of
purulent sputum in a patient whom you suspected
had pneumonia

5. lab findings of Goodpasture syndrome
230
Laboratory Findings









CXR with diffuse patchy alveolar infiltrates
Leukocytosis (High WBC)
Falling hemoglobin (Hb 10 today, Hb 7 tomorrow AM)
Elevated creatinine (bad kidney function)
Active urine sediment (glomerulus is not working well)
+ ANCA, cANCA
Anti GBM Ab
Anti DNA
Drug Screen
Goodpasture’s - Clues


Subtle clues may be present on initial laboratories
An elevation of the serum creatinine indicating acute kidney injury may initially be
thought of as secondary to dehydration or sepsis.
 It will not recover as expected with supportive care.
The patient may be mildly anemic on presentation. This will worsen with treatment
and further hemorrhage into the lungs.
 Bronchoalveolar lavage (bronchoscope)

 Place 120cc saline in lungs + 100% O2
 Pull back syringe = pink frothy sputum
 Add 60cc saline
○ Remove Red fluid
 60 more cc saline
○ Remove Dark red fluid




You are flushing out blood and removing it
Send VAL culture (-) for bugs,
Tx as soon as it is not microbial infectious
Call nephrologist
○ r/o Wegner’s, Goodpasteur’s
Goodpasture’s - Labs
Serum anti GBM Ab
 Followed by kidney biopsy if medically stable
 Immunofluresence will reveal linear deposition of IgG

1.
2.
3.
4.
Management of CF hemoptysis
Differential Newborn with no poop
Lab findings in CF
Testing for CF
234
1. Management of CF hemoptysis
235
Treatment of Pulmonary Complications

Atelectasis
 Aggressive intravenous therapy with antibiotics and
increased chest PT

Hemoptysis
 vitamin K , Bronchoscopy, Lobectomy, Bronchial artery
embolization

Pneumothorax
236
2. Differential Newborn with no poop
237
Intestinal Tract






Meconium ileus
Meconium peritonitis- intrauterine rupture of the bowelperitoneal or scrotal calcifications
Meconium plug syndrome- distal intestinal obstruction
syndrome (DIOS)- cramping abdominal pain and abdominal
distention
Evidence of maldigestion from exocrine pancreatic
insufficiency-frequent, bulky, greasy stools.
Intussusception, fecal impaction of the cecum with an
asymptomatic right lower quadrant mass
Prothrombine, dementia, peripheral neuropathy, hemolytic
anemia, bone density, and night blindness- ADEK
238
Clinical Manifestations
Acute or persistent respiratory symptoms 45%
 Failure to thrive, malnutrition 37%
 Abnormal stools 28%
 Meconium ileus, intestinal obstruction 19%
 Newborn Screening 6.4%
 Electrolyte, acid-base abnormality 4%
 Rectal prolapse 3%

239
3. Lab findings in CF
240
Diagnosis and Assessment

Sweat Testing- pilocarpine iontophoresis to collect sweat and
performing chemical analysis of its chloride content
 > 60 mEq/L of chloride in sweat is diagnostic of CF plus

Presence of typical clinical features (respiratory, gastrointestinal, or
genitourinary) or
 A history of CF in a sibling or
 A positive newborn screening test

PLUS - Laboratory evidence
 for CFTR (CF transmembrane regulator) dysfunction or
 Two elevated sweat chloride concentrations obtained on separate days
or
 Identification of two CF mutations or
 Abnormal nasal potential difference measurement
241
4. Testing for CF
242
DNA Testing

Test for 30-96 of the most common
CFTR mutations.
Identifies ≥90% of individuals who carry 2 CF
mutations.
 Some laboratories perform comprehensive mutation
analysis screening for all of the >1,500 identified
mutations.

243
Diagnosis
Appropriate investigations
 Chest radiographs- nonspecific

 bronchovascular markings, crowding of bronchi, and loss
of lung volume
 cystic spaces, occasionally with air-fluid levels and
honeycombing
 Gold standard- thin-section HRCT scanning
○ include cylindrical (“tram lines,” “signet ring appearance”)
○ varicose (bronchi with “beaded contour”),
○ cystic (cysts in “strings and clusters”), or mixed forms
244
1.
2.
3.
4.
5.
6.
Preventing and treating pertussis
Micro of bronchiolitis
When to hospitalize bronchiolitis
Define RDS
Etiology of RDS
Symptoms of primary ciliary dyskinesia
245
1. Preventing and treating pertussis
246
1a. Preventing pertussis
247
Pertussis Prognosis
Most children- complete healing of the respiratory epithelium and have
normal pulmonary function after recovery
 Young children can die from pertussis and are more likely to be
hospitalized
 Most permanent disability is a result of encephalopathy
PREVENTION
 Active immunity- acellular pertussis
 Macrolides are effective in preventing secondary cases
 Under 7 years of age who have received only four doses of vaccine

 Should receive a booster dose of DTaP + macrolide antibiotic for 10 to 14
days

7 years of age and older
 Should receive prophylactic macrolide antibiotic for 10 to 14 days + Tdap
248
1b. Treating pertussis
249
Treatment





Erythromycin, clarithromycin, or azithromycin are recommendedtrimethoprim and sulfamethoxazole
Early treatment eradicates nasopharyngeal carriage of organisms
within 3 to 4 days and lessens the severity of symptoms
Limit spread of infection
Treatment is not effective in the paroxysmal stage
Major complications
 include hypoxia, apnea, seizures, encephalopathy, and malnutrition
 Pneumonia- Pertussis itself or Streptococcus pneumoniae, Haemophilus
influenzae, and Staphylococcus aureus
 Atelectasis
 pneumomediastinum, pneumothorax
 epistaxis; hernias; and retinal and subconjunctival hemorrhages
250
2. Micro of bronchiolitis
251
Bronchiolitis- Definition
Inflammation of the bronchioles
 Usually is caused by an acute viral infection
 The most common lower respiratory tract infection in
infants and children who are 2 years
 The most commonly identified infectious agent is the
respiratory syncytial virus (RSV)
 BUT adenovirus, human metapneumovirus, influenza
virus, and parainfluenza virus

252
3. When to hospitalize bronchiolitis
253
Epidemiology
90,000 hospitalizations annually
The cost children <1 year of age - $700 million
Bronchiolitis is a self-limited disease
Increasing over the past decade
Young patients and patients who have pre-existing
medical conditions form a vulnerable population that may
require inpatient admission
 RSV-associated deaths are rare, accounting for fewer
than 500 deaths per year in the United States
 Most RSV-associated deaths occur in children who have
no pre-existing medical conditions.





254
4. Define RDS
255
ARDS (Acute Respiratory Distress Syndrome)


RDS = Respiratory Distress Syndrome
Respiratory Failure
 Pulmonary system is unable to maintain adequate gas exchange to meet
metabolic demands
○ Paco2 >50 mm Hg- inadequate alveolar ventilation
 decreased minute ventilation (tidal volume × respiratory rate)
 or an increase in dead space ventilation
○ Pao2 <60 mm Hg- ventilation-perfusion mismatch
○ No intracardiac shunt


ALI- acute onset, bilateral pulmonary edema, no clinical evidence of
elevated left atrial pressure, and a ratio of PaO2 to FiO2 between 201
and 300 mm Hg
ARDS- with more severe hypoxemia- PaO2/FiO2 of ≤200 mm Hg
256
5. Etiology of RDS
257
ARDS

ARDS triggered by a variety of insults







sepsis
Pneumonia, the most common cause
bronchiolitis (RSV- 5% of patients), asthma
Shock
Burns
Traumatic injury
Upper airway obstruction
Resulting in inflammation and increased vascular
permeability
 leading to pulmonary edema

258
6. Symptoms of primary ciliary dyskinesia
259
PCD

Newborn period- respiratory distress
 Tachypnea
 hypoxemia
 respiratory failure requiring mechanical ventilation
Early infancy- chronic cough and persistent rhinosinusitis,
poor feeding and growth delays
 Chronic sinusitis and nasal polyposis
 Chronic otitis media- conductive hearing, myringotomy
tube placement, and recurrent otorrhea
 Recurrent pneumonia or bronchitis- bronchiectasis

260
1.
2.
3.
Intrinsic vs. Extrinsic causes of restrictive lung
PFTs in restrictive dz
Asbestosis vs. sarcoid vs. hypersensitivity vs. pneumonia
261
1. Intrinsic vs. Extrinsic causes of restrictive
lung
262
Categories of Restrictive Lung Disease

Intrinsic lung diseases (diseases of the lung
parenchyma)

Extrinsic disorders (extra-parenchymal diseases)
1a. Intrinsic causes of restrictive lung
264
Intrinsic Lung Diseases

These diseases cause either:
 Inflammation and/or scarring of lung tissue (interstitial lung
disease)
or
 Fill the air spaces with exudate and debris (pneumonitis).

These diseases are classified further according to the
etiological factor.
►THE GAS EXCHANGER, There is a multitude
of diseases that effect this area of the lung. You
can expect changes in compliance, possible
hypoxemia at rest or with exercise, an abnormal
diffusion capacity for Carbon Monoxide, and at
times a relentless progression of the disease
1b. Extrinsic causes of restrictive lung
267
EXTRINSIC CAUSES
THE RESPIRATORY CONTROLLER OR THE
VENTILATORY PUMP
Any entity that may affect the CNS
may ultimately effect the lungs. Think
of  CNS bleeds, CNS masses,
Encephalitis, Meningitis, Head trauma,
Strokes, ischemic or hemorrhagic, or
Drug effects.
► These processes can cause
changes in the Respiratory
rate, the depth of breathing,
and can cause non cardiogenic
pulmonary edema, hypoventilation,
aspiration, pneumonia, hypoxemia,
and Resp. Failure and death.
Extrinsic Causes
By their very nature, severe kyphoscoliosis and massive obesity are easily recognizable.
 The pleural disorders are associated with decreased tactile fremitus, dullness or
hyperesonance upon percussion, and decreased intensity of breath sounds.


In cases of neuromuscular diseases, the physical examination findings may indicate
accessory muscles usage, rapid shallow breathing, paradoxical breathing, and other features
of systemic involvement. *

External trauma may be evident and/or the patient may have minor trauma but be massively
obese that his/her respiratory function may be compromised.

 Final Result a restrictive defect!!!
Extrinsic Lung Diseases
Neuromuscular diseases
• Amyotrophic lateral sclerosis
• Poliomyelitis
• Myasthenia Gravis
• Spinal Cord Lesions
• Guillain-Barre’ syndrome
• Bilateral Diaphragm paralysis
Non-neuromuscular
• Obesity!!!!
• Chest wall trauma
• Kyphoscoliosis
• Pleural diseases
• Pneumothorax
2. PFTs in restrictive dz
271





Due to the effects of accumulation of mineral dust in the lungs
Silicosis- exposure to crystalline free silica; ACUTE silicosis causes
pulmonary
alveolar proteinosis; CHRONIC- simple nodular silicosis to progressive
massive fibrosis
PFT’s- Normal obstructive or restrictive pattern.
CXR- “Eggshell nodal calcifications”

Asbestosis- Shipyard workers, insulators, construction, pipe fitters, fibrosis of
lung and pleural disease; asbestos bodies of long and short fibers; symptoms
related to extent and duration of exposure; MESOTHELIOMA, Lung CA,
Pleural Plaques; restrictive PFT’s

Berylliosis- rare metal, acute and chronic form which is more of a
granulomatous disease and hard to differentiate from Sarcoidosis, RxCorticosteroids, avoid further exposure
3. Asbestosis vs. sarcoid vs. hypersensitivity
vs. pneumonia
273
3a. Asbestosis
274

Asbestosis- Shipyard workers, insulators, construction,
pipe fitters, fibrosis of lung and pleural disease; asbestos
bodies of long and short fibers; symptoms related to extent
and duration of exposure; MESOTHELIOMA, Lung CA,
Pleural Plaques; restrictive PFT’s
275
3b. sarcoid
276
Sarcoidosis
A disease characterized by the presence of granulomatous tissue.
This is a systemic disease which involves eyes, brain, heart, lungs, bones and
kidneys, skin, liver and spleen. 90% of patients have lung involvement.
On pathology a non-caseating granuloma composed of histiocytes, giant cells and
lymphocytes. In advanced lung disease fibrotic changes are seen.
3c. hypersensitivity
278
Hypersensitivity Pneumonitis
Also known as extrinsic allergic alveolitis.
Hypersensitivity reaction in the lung occurs in response to
inhaled organic dust.
Example is farmer’s lung.
The exposure may be occupational or environmental.
The disease occurs from type III (immune complex mediated)
and type IV (delayed hypersensitivity) hypersensitivity
reactions.
Farmer’s lung is due to thermophilic actinomyces in moldy hay.
Bird fancier’s lung is caused by avian antigen.
Bronchoalveolar lavage lymphocytic alveolitis, 'CD-8 T cells ;
there is infiltration of the alveolar walls with
lymphocytes, histiocytes, and plasma cells. May see
loosely formed granulomas. All this may lead to fibrosis.
Look for precipitating antibodies to specific antigens
Dx by transbronchial biopsy or open lung biopsy.
Rx avoid exposure, corticosteroids
Hypersensitivity
Pneumonitis
3d. pneumonia
281
Diffuse Interstitial Pulmonary Fibrosis

Synonyms: idiopathic pulmonary fibrosis, interstitial pneumonia,
cryptogenic fibrosing alveolitis.
Pathology
 Thickening of interstitium.
 Initially, infiltration with lymphocytes and plasma cells.
 Later fibroblasts lay down thick collagen bundles.
 These changes occur irregularly within the lung.
 Eventually alveolar architecture is destroyed – honeycomb lung
 Etiology
 Unknown, may be immunological reaction.
Clinical Features
Uncommon disease, affects adults in late middle age.
Progressive exertional dyspnea, later at rest.
Non-productive cough, dry in nature
Physical examination, fine inspiratory crackles (VELCRO
crackles) throughout both lungs.
 Patient may develop respiratory failure terminally.
 The disease progresses insidiously, median survival 4-6
years.
 Wheezing is an uncommon manifestation but can occur
in patients with lymphangitic carcinomatosis, chronic
eosinophilic pneumonia, and respiratory bronchiolitis.
Chest pain rare!





Morbidity/Mortality Depends on the underlying
cause of the disease process. Median survival time
for idiopathic pulmonary fibrosis (IPF) is 3 years.

Factors that predict poor outcome in (IPF) include :
older age, male gender, severe dyspnea, history of
cigarette smoking, severe loss of lung function,
appearance and severity of fibrosis on radiologic
studies, lack of response to therapy, and prominent
fibroblastic foci on histopathologic evaluation.
Treatment








Each patient is individually assessed.
Patients are treated if they have symptoms or progressive
dysfunction on pulmonary function tests.
Corticosteroids (Prednisone 1 mg/kg) is standard therapy.
Prednisone dose is lowered over 6-8 weeks and continued at
15 mg for 1-2 years.
Addition of Imuran may benefit survival.
Cyclophosphamide occasionally used.
Antifibrotics such as colchicine may be used.
Ancillary therapies such as oxygen, pulmonary rehabilitation,
psychosocial aspects are helpful.