W2P3 Flashcards
Febrile Neutropenia
- diagnostic temperature
PLUS what?
Fever ≥ 38.3 oC oral in a single measurement ≥ 38 oC in two measurements within 1 hour PLUS Low absolute neutrophil count (ANC) ≤ 500 cells/μL
Could be axillary or oral NEVER RECTAL for people who have cancer/ have low neutrophils
Who gets Febrile Neutropenia
- *Cancer patients get fever
- Up to 50% in solid tumour cancers
- More than 80% with hematologic cancers
Usually after a week after their last chemotherapy (nadir of ANC)
Less than half have a documented infection
PHYSICAL EXAM and CLINICAL SUSPICION are key
Protocols exist in order to not miss things
What should you think of for Neutropenia
Secondary to Cancer Chemotherapy
- Think of denuded gut secondary to chemotherapy
- Including mucositis
- Usually Gram negative enteric rods - Think of central line infections
- Usually Gram positive cocci (CoNS, MSSA/MRSA)
- Pseudomonas aeruginosa - Think of fungal organisms
- Candida spp (from gut, from central line(s))
- Aspergillus spp (from lungs) - Finally, think of common organisms causing fever
- S. pneumoniae, respiratory viruses, C. difficile
What should you think of with Fever in Cancer Patients In the absence of obvious symptoms
- Think first of bacteria coming from a denuded gut
SO CHEMOTHERAPY IS KEY
- Please note: Fever in a NEWLY diagnosed cancer patient (no chemotherapy yet) is due to either the tumour/cancer or community stuff (eg. S. pneumoniae, respiratory viruses etc) - Then think of community acquired sources
- Pneumonia
- Respiratory viruses
If persistent fever: especially while on very extensive and broad spectrum antibiotics, THEN think of fungal illness
Candida spp, Aspergillus spp
What should you think of with Fever in Cancer Patients With specific symptoms
Think of central line sepsis especially if IV site is red and/or painful
MOST COMMON CAUSE OF BACTEREMIA IN CANCER CHEMOTHERAPY PATIENTS = CoNS
If diarrhea: think of C. difficile
What to think of with Fever in Cancer Patients With symptoms of mucositis and/or shock
Think of all of the above AND:
Streptococcus viridans
This relatively benign respiratory tract organism has been increasingly associated with shock and ARDS in cancer patients on chemotherapy
Risk factors include:
“strong” chemotherapy which may lead to mucositis
High dose Ara-C
recall these are IMMUNE SUPPRESSED PATIENTS so commensal organisms are dangerous in this group
What are the Empiric Antibiotic Choices for Fever in Cancer Patients
Overall at minimum must cover all of the following:
- Bacteria from the gut (including anaerobes)
- Pseudomonas spp
- Staphylococcus aureus
IF there is the presence of mucositis or shock, must cover Streptococcus viridans also
IF you know or suspect resistance, what organisms should you think of?
MRSA, ESBL, VRE
Empiric Therapy for NEWLY diagnosed patient coming in with fever
Any antibiotic that covers community organisms causing pneumonia, and sepsis
e.g. Ceftriaxone IV
+/- “atypical” organism coverage
If signs of viral illness
Oseltamivir?
Acyclovir?
Empiric Therapy
KNOWN cancer patient coming in with febrile neutropenia
Broad spectrum beta-lactams \+/- aminoglycosides IV \+/- vancomycin IV depending on clinical condition Line sepsis Septic shock Known MRSA colonization Sometimes oral therapy is used eg. Ciprofloxacin + Clindamycin
What should you think of in: Fever that persists with neutropenia, on broad spectrum AB
THINK FUNGAL INFECTION
- give empiric antifungal treatment
Fever in cancer patients Empiric antifungal treatment?
Usually not given empirically IN THE BEGINNING unless there is clinical evidence for a fungal infection:
- Characteristic rash
- Lung nodules on CXR
- Positive blood culture for yeast or fungus.
A minority of patients (~4%) will have invasive fungal disease
KEY: Antifungals are started if fever persists past 4 days in cancer patients with febrile neutropenia
Or sooner as needed (clinical and/or lab evidence)
Once you think of fungal infection, what else should you recommend (investigations)
Need to see where the supposed Candida spp has caused disease:
Need liver and spleen imaging
Need retinal exam
Chest CT
Usually Candida spp will infect the above tissues first before any blood tissue
i.e. blood is the last tissue to get infected
Imaging studies are most sensitive when neutropenia has resolved as abscesses will then form (especially for hepatosplenic candidiasis).
* so you WAIT till neutrophils is back UP before chest CT**
Fever in cancer patients : A quick note about invasive aspergillosis
Patients with severe (ANC <100 cells/mL) AND prolonged neutropenia (> 10 days)
- Usually bone marrow transplant patients
- Patients with AML (“strong” chemotherapy)
Invasive pulmonary aspergillosis
- Blood vessel and alveolar invasive disease
- High mortality rate
Treatment is usually with Voriconazole IV (best results of all antifungals for this) until radiographic resolution (may take 1 – 2 months, AT LEAST).
Fever in Cancer patients; Thoughts on Empiric Antiviral treatment?
There is NO ROLE for empiric antiviral treatment unless there is an obvious clinical need:
- Characteristic rash
i. e. varicella/shingles or herpes - Severe respiratory illness
i. e. influenza, COVID (VERY IMPORTANT)
What is the Duration of Therapy for Cancer Fever Neutropenic patients on Antimicrobials/virals
Antimicrobials/virals are continued: For the duration of a specific illness treatment - At least 10 – 14 days AND - Until no fever AND - At least until ANC >500 cells/mL
If NO bacteremia and/or source identified
- Until no fever AND
- At least until ANC >500 cells/mL
What is the Duration of Therapy for Cancer Fever Neutropenic patients on Antifungals
If antifungals are started:
Documented fungal invasive disease
- Need to rule out liver and eye disease (Candidiasis)
- Treat at least until radiographic improvement (eg. Aspergillosis)
- Usually at least 1 month
No documented disease
- Treat until you can rule out hepatosplenic candidiasis and candidal retinitis
How to treat fever in BONE MARROW transplant patients?
read the three slides
Take home points for Febrile neutropenia in cancer patients
- when is empiric use of vancomycin needed
High morbidity and mortality
Swift and empiric therapy is required
Must cover: Gut organisms (including anaerobes) Pseudomonas aeruginosa Staphylococcus aureus Respiratory organisms
Empiric use of vancomycin is not needed unless:
Shock
Mucositis
Line sepsis
Known MRSA
Known bacteremia with gram positive cocci
Febrile neutropenia in cancer patients Take Home Points on Empiric Use of
a. Antifungals
b. Antivirals
Empiric use of antifungals is not needed unless:
- Clinical presentation of invasive fungal disease
- Antifungals are ADDED if fever persists after 4 days
Empiric use of antivirals is not needed unless:
Clinical presentation of a treatable viral illness
*Especially symptoms of INFLUENZA
Signs of Odontogenic Infections
Face DISTORTED
Hand on the swelling because it is painful
REDNESS
ESPECIALLY IF: The mouth is OPEN, if tongue is protruded = airway issue
think of painting
How does facial swelling and facial space involvement occur secondary to an odontogenic infection?
These lectures will consider infections arising from the pulp ( the nerve) , although the same manifestations can arise from infections of:
- Periodontal Origin ( gum infection)
- Peri-coronal Origin (semi impacted wisdom tooth)
- Traumatic Origin
- Post-dental /surgical Origin
Odontogenic Infections can spread via:
4 & #5 occur if infection is draining into the mouth
- DIRECT EXTENSION***** [most common way, rest you think of in immunocompromised patients]
- Lymphatic spread
- Hematologous spread
- Ingestion (rare-HCl acidity in stomach)
- Aspiration
The outcome of the odontogenic infection is dependant on:
- The virulence of the organisms
- The host’s resistance [ patient’s ability to fight plays a significant role]
- The anatomical pathways of the spread of infection via direct extension
Immunodepressed or compromised patients Include:
Malnourished, especially secondary to alcoholism
Cancer / radiation / chemotherapy
Poorly controlled diabetic
Steroids or other immunosuppressive drugs
3 routes of the spread of Infection, Dental Abscess
There are 3 routes of the spread of this infection by DIRECT EXTENSION
Infection perforates the cortical plates of the maxilla or mandible , and the periostium and:
- Drains into the oral cavity [ideal, safely drains]
- Drains onto the skin [on cheek, mandible]
- Tracts into deeper fascial planes and spaces
Infraorbital Space (Canine Space) clinical picture
Clinical picture:
swelling pointing toward eye
no trismus- not able to open your eye fully
From the maxillary canine tooth
Eye tooth
top right canine of patient (1, 3)
INFECTION here leads to inability to open right eye
Buccal Space
- Clinical picture
Bound medially by the buccinator muscle
Bound laterally by subcutaneous tissue and skin
Clinical picture:
cheek swelling (as if they are holding their breath)
no trismus
Sublingual Space
Submandibular Space
related to lower teeth esp wisdom teeth
2 spaces separated by the Mylohyoid line
infection draining above this mylohyoid muslce: gets into sublingual space
- swelling here will impair talking because TONGUE is infected by this
- tongue may even protude out of the mouth
Sublingual Space
- Clinical Picture*
Occupies the floor of the mouth between the mucosa and the mylohyoid muscle
Clinical Picture:
elevation of the tongue (difficult to speak)
elevation floor of mouth
- has their mouth involuntarily open because of tongue elevation
Communicates with the submandibular space posteriorly
Submandibular Space
- clinical picture
Lies below the mylohyoid muscle
Clinical picture:
Firm, ill –defined swelling below the anterior border of the mandible
Tender to palpation
Trismus: is difficulty opening the mouth
Ludwig’s Angina
Aggressive rapidly spreading cellulitis involving:
Bilateral Submandibular Spaces
Bilateral Sublingual Spaces
And the Submental Space
Emergent situation, loss of airway eminent
need to treat immediately to avoid DEATH
Parapharyngeal Spaces
Divided into 3 spaces:
Pterygomandibular Space Lateral pharyngeal Space Retropharyngeal Space
Fascial Spaces of the Head and Neck
- The fascial layers of the head and neck represent connective tissue sheaths that surround and enclose potential spaces
- These potential spaces offer little resistance to the spread of infection
- These spaces are all potentially interconnected to eventually reach the brain or the mediastinum
The clinical findings of an acute odontogenic infection are based on the cardinal signs of inflammation:
Pain Swelling Warmth over the affected area Loss of function: (e.g. trismus [can't open wide], dysphagia [difficulty swallowing], dysphonia [difficulty pronouncing words] ,dyspnea [difficulty breathing]) Redness
Acute Inflammatory Reaction
- Inoculation of bacteria
- Cellulitis in the pulp, then
- Abscess in the pulp, then
- Cellulitis, or abscess at the peri-apical area, then
- Cellulitis of the surrounding soft tissue spaces, then
- Abscess of the surrounding soft tissue spaces
This is the evolution of the infection, in order
without treatment
Infection develops in 4 Stages:
- Inoculation
- Cellulitis( 1-2 days)
- Abscess ( 2-3 days)
- Resolution
if they say they had swelling for 4 days, then you should be looking for PUS (Abscess stage)
Cellulitis vs Abscess
Cellulitis: diffuse inflammatory reaction with bacteria
abscess: PUS anaerobic stages - defines which antibiotics you’re giving the patient
Explanation for the 4 stages in infection development
Once the bacteria gain access to a potential space, colonization will trigger an inflammatory reaction
The space and area becomes soft and spongy and mildly tender to palpation. This can occur in hours or can take up to 1 to 2 days
Cellulitis occurs once a full inflammatory response is mounted.
Clinically, the area is proorly localized, reddened, indurated, and tender to palpation
Typical cellulitis is necrotic tissue with fluid. (I.e. diffuse inflammation)
Antibiotic therapy and dental treatment may or may not prevent the progression of cellulitis to the abscess stage
Abscess formation occurs once the bacteria, necrotic tissue and WBC’s coalesce within the surrounding soft tissue (pus).
When is Cellulitis present? When is Abscess present?
- what is happening
Classically, the patient gets a throbbing pulsating type of pain in the offending tooth.
Pain is usually severe: patient can’t eat nor sleep.
After 24 to 48 hours, pain will start to subside but swelling in face will appear
cellulitis: 1-2 days
abscess: 2-3 days
What is happening:
The infection and abscess and pressure have spread to the soft tissue
Initially, the spread of the bacteria will cause an inflammatory response before any pus is formed. This is cellulitis.
There must be a history of 48 to 72 hours of swelling for pus to be present. (2 to 3 days after initial toothache). Pus collection should be suspected to be present after the third day from the onset of the symptoms
Pus is confirmed clinically by the presence of fluctuance. This is abscess.
Management of Odontogenic infections
We use a combination of medical and surgical therapies
- Patient Care
- Incision and Drainage
- Antibiotic Therapy
- Removal of the cause:
Extraction
Endodontic treatment
Management of odontogenic infections:
Patient Care
a. Airway management***
b. Medical problems
c. Rest and nutrition
d. Presence of Fever
Symptoms and Signs of Airway Embarrassment
Difficulty managing own secretions Use of accessory muscles of respiration Respiratory rate, rhythm, depth Dysphagia Dysphonia Dyspnea
** first priority is to CLEAR AIRWAY if obstructed
Securing the airway from odontogenic infection
***Airway embarrassment impingement can rapidly proceed to airway obstruction (sometimes within hours).
The above conditions necessitate immediate hospital admission
Maintenance of airway can be via: intubation, surgical
decompression, and/or tracheotomy.
Management of odontogenic infections:
step 2: Incision and Drainage (I&D)
Presence of Facial Swelling – i.e. soft tissue involvement:
INCISION and DRAINAGE (I&D) of the soft tissue space involves:
- Placing incisions through soft tissue in an area of localized abscess, allowing the pus to drain.
- Then placing a CONDUIT to encourage drainage.
Functions of I & D:
I & D = Incision and Drainage
- Relieve the pressure and pain symptoms
- Removal of pus (to allow antibiotics to be more efficient).
- Antibiotics cannot penetrate pus, therefore with less pus, easier for the blood flow to reach the infection
- Facilitate microbial elimination, reducing the tissue bacterial load.
- Decompresses the swollen area. (Concern: both comfort and airway)
- Changes the micro-environment, alters the oxygen tension.
Antibiotics on PUS
does nothing, it does not penetrate the pus
you NEED to drain it
Management of odontogenic infections:
step 3: Antibiotic Therapy
- Odontogenic infection are POLYMICROBIAL, I.e Aerobic and anaerobic.
- 75 % anaerobes, 25 % aerobes.
- The first stage of infection: Cellulitis is caused by aerobic bacteria.
- The second stage of the infection: Abscess formation is caused by anaerobic bacteria.
- One should always try to perform a C&S (culture and sensitivity) but must treat the patient empirically
Antibiotics as the ADJUNCT for odontogenic infections
Remember: Antibiotics assist the patient to eliminate the infection.
Antibiotics are the adjunct: The antibiotic will kill off a certain number of the microorganisms or change the consistency of the flora but ultimately, the patient’s immune system will do the rest.
What is the most important factor for oral antibiotics
The patient’s compliance is the most important factor
for oral antibiotics.
This is the variable most likely to affect the blood concentration of an orally administered antibiotic.
What types of ABs are used for oral infections?
- two main ones
Ideally, use specific narrow spectrum antibiotics
Penicillin:
Bactericidal (against all common major pathogens associated with odontogenic infections)
Innexpensive
No or little toxicity
Well adsorbed taken PO
Allergy: 3-5% of the population
- however a lot of people have been on it clinically and could be resistant
- people are also allergic to penicilin
Amoxicillin:
Extended spectrum penicillin
What types of ABs are used for oral infections?
- Clindamycin
- Metronidazole
Clindamycin:
Bactericidal
Metronidazole (Flagyl)
Narrow spectrum: Anti-anaerobes only
Never used as a single agent because it has no clinical activity against aerobes.
Alcohol and flagyl=vomiting (flagyl inhibits the oxidation of acetaldehyde, the primary metabolite of alcohol).
What is the antibiotic of choice for Odontogenic infections
- patient response to AB timeline
- if there is no change…
Penicillin is still the antibiotic of choice for odontogenic infections.
The patient will not respond immediately to the antibiotic
It takes at least 24 to 48 hours before any significant change will occur
If after 48 hours, there is no change:
Look at results of the C&S
Change antibiotics
Look for pus to I&D.
Role of Hydration in odontogenic infections
If a patient cannot tolerate PO fluids, need IV intake
Especially in the face of fever and trismus as poor or no PO intake for a few days is common.
What are complications of unresolved odontogenic infections
Osteomyelitis Airway obstruction Intracranial extension Mediastinitis Systemic sepsis involvement
Mucositis
Mucositis is a mucosal barrier injury characterized by erythemia, ulceration and pain.
Mucositis affects the quality of life of patients in their ability to swallow, eat, and talk.
The Effect of Mucositis and Stomatitis is related to Therapeutic Measures and Patient Factors:
1) Therapeutic Measures
Type and duration of pharmacologic agent used, dose and field of irradiation
2) Patient Factors
a) Local Factors – Poor fitting dentures and rough restorations increase irritations and plaque accumulation
b) Systemic Factors – Immunosuppressed patients have increased microbial invasion.
Index for Oral Mucositis
Grade 3 = SEVERE, this is a medical emergency
Multiple ulcerations with severe pain
and inability to eat
What type of infection is common in immunocompromized oral palliative care patients?
Herpes infections are commonly seen in immunocompromized palliative care patients.
Treat with: Acyclovir (Zovirax) 200 mg 5x’s/d for 7d
Decrease pain: Kaopectate and Benadryl Elexir 50:50 painted onto lesions provide relief
Herpes Zoster
Herpes zoster is caused by the reactivation of the varicella zoster virus within the sensory ganglia. Once activated it follows a unilateral dermatone.
The CDC has estimated that 32% of the USA will have a shingles
What can be used as an alternative for patients not able to use a conventional tooth brush?
A chlorhexidine soaked foam brush is as effective as a toothbrush in removing plaque
It is recommended for patients not able to use a conventional toothbrush
Chlorhexidine Substantivity:
Binds to oral tissues (30% retained)
Slowly released over time providing a prolonged effect
Inhibits bacterial growth
What does Upper Respiratory Tract Infections [URTI] include?
What does Upper Respiratory Tract Infections [URTI] include?
Upper respiratory tract infections (URTI): Infections of the respiratory mucosa from the nose to larynx.
Include: The common cold “Strep throat” = Pharyngitis Ear infections = otitis Sinusitis Laryngitis
LRTI include?
Lower respiratory tract infections (LRTI): from trachea down to airways and alveoli
Bronchitis
The Flu [influenza]
Bronchiolitis
Pneumonia
CORYZA
- transmission
The common cold: CORYZA
The same viruses can cause asthma flare-ups and severe illness in some patients
more than 200 viruses can cause coryza i.e. rhinovirus, coronovirus, adenovirus
Less likely to catch a cold in the summer
transmission:
Spread by:
direct contact (person-person or contaminated objects)
droplets from airways (expelled during coughing, sneezing)
small particle aerosolization for some viruses (ex influenza)
The first event: infection of nasal epithelium rhinitis
Most common agent of CORYZA
Rhinovrisu = 50% of cass Influenza = 35% Adnovirus = 10%
Management steps for URTI
- possible complication*
Differentiate from non-infectious causes: allergic rhinitis (where can have itching of nose and conjunctivae)
Exclude more serious condition such as lower tract infection
No specific diagnostic tests or treatment
Can detect viruses by PCR or culture but no benefit for management
Possible complications: otitis media (with 30% of colds), acute sinusitis (with 8%)
Acute rhino-sinusitis
- most likely pathogen
- acture vs chronic duration
Sinusitis = inflammation of tissue around sinus cavity
Viral causes»_space; bacterial »_space;» fungi or mycobacteria
acute = <4 weeks chronic = > 8 weeks
Management of Sinuisitis
History:
Possible irritants and allergens?
Duration and nature of symptoms?
Presence of other symptoms (sore throat, cough, aches, malaise, fever)?
If fever and purulent (thick greenish) nasal secretions: more indicative of bacterial infection
if NO FEVER, unlikely to benefit form ANTIBIOTICS
Acute pharyngitis
- common bacterial causes include?
Fever, sore throat and inflammation of pharynx
Most (25-45%) caused by respiratory viruses and accompanied by other symptoms of URTI: tend to be benign, self-limited
GAS, strep group C and G too
N. GONORRHEA
CORYNEBACTERIUM- DpT
Strep Throat
- organism
- clinical presentation
GAS, and if untreated -> Rheumatic fever
this is a B hemolytic pathogen
Acute onset sore throat, with difficulty swallowing
Fever
+/- headache and GI symptoms
**Pharyngeal erythema, tonsillar enlargement, grey-white exudates
**Tender nodes at angle of jaw
+/- Rash from trunk spreading to arms and legs, sandpaper-like: scarlatiniform
Usually NO COUGH
- * Complications of Strep Throat*
- what are the two types?
Suppurative vs Non Suppurative
Suppurative complications of strep throat
- 1 abscess where?
- 3 infections where?
- 1 unpredictable one
Suppurative complications:
- Para-pharyngeal abscess
- otitis
- mastoiditis
- Bacterial sinusitis
- Invasive infection (necrotizing fasciitis “flesh eating disease”, toxic shock syndrome)
**Non Suppurative Complications of Strep Throat*
RHEUMATIC FEVER** [ rare but common in indigenous] and Glomerulonephritis (kidney)
RF likely result of immune system turning on self because of “mimicry” (Ag-Ab response) – occurs 3-4 weeks after untreated Strep infection
Affects: heart (carditis), joints (arthritis), skin (rash and nodules), nervous system (uncontrolled movements: chorea)
Treatment of STEP THROAT
Penicillin active against GAS (and most other strep species)
Penicillin, amoxicillin, 1st generation cephalosporins
Treat for 10 days to prevent complications
For penicillin-allergic: clindamycin, macrolides
No need to give broad-spectrum antibiotics promote emergence of drug-resistant bacteria
Patients with previous attacks of RF will need long-term prophylaxis with antibiotics to prevent recurrence of attacks
Diphteria
- organism
Corynebacterium diphteria
Sore throat, malaise and low-grade or no fever
Sticky white-grey membrane which can spread
Extensive adenopathy (Lymph nodes) “bull’s neck”
Epiglottis
- EMERG when…
- Caused by which organism?**
- clinical presentation
Inflammation of epiglottis: high risk of complete obstruction of airway
Caused by bacteria: Haemophilus influenza type b
Now rare because of Hib vaccination
EXTREMELY RAPID ONSET, very ill: sitting leaning forward, muffled voice, anxious, DROOLING, pain, fever
AIR RAID
A: Airway closed
I: Increased pulse
R: restlessness
R: retractions
A: anxiety
I: inspiratory stridor
D; Drooling
Extremely rapid onset, very ill: sitting leaning forward, muffled voice, anxious, drooling, pain, fever. Inspiratory Stridor*
DIAGNOSIS:
Epiglottitis
- H.influenza b
Management of Epiglottitis
DON’T EXAMINE THROAT
will see thumb sign on X ray
Children: need to secure airway quickly so insert endotracheal tube Adults: may need direct visualization of epiglottis for diagnosis (Xray not great and cause of delay in diagnosis) Labs: elevated white blood cells, growth of Hemophilus influenza (type b) in cultures of blood and epiglottis Antibiotics IV (3rd generation cephalosporin
Cause of insipratory stridor
epiglottitis or CROUP: Laryngo-tracheo-bronchitis
CROUP
- clinical presentation
- organism cause
- age group at risk
- DIAGNOSIS
- management
Laryngo-tracheo-bronchitis
Upper and lower tract involved; subglottic area inflammed
Sharp stridulous voice …(like) the crowing of a cock… Barking cough, hoarseness, inspiratory stridor
Viruses are most common causes, rarely bacteria
- Parainfluenza viruses (4 types)*8
Often very young kids: 6 months to 3y**
Onset of stridor can be 12-24h after sore throat, rhinorrhea and fever
Often onset at night, with improvement during the day; generally lasts 3-4d
Diagnosis is clinical - avoid doing any testing (throat swabs) that can worsen the condition
Management according to severity (score); no antibiotics; supportive care +/- steroids
Hospitalization in about 4%
Clinical suspicion of flu
- diagnosis
- treatment ( one of the few viral infections where treatment is given*)
- vary variable symptoms
- just always think flu during flu season
Testing for virus useful if management will be affected (admission, infection control, antivirals); CXR to rule out pneumonia
Antiviral medication (oseltamivir = neuraminidase inhibitor) for cases at risk of severe disease (asthma, COPD, cancer, obesity, pregnancy, extremes of age)
***Complete resolution within 7d even if no treatment
What are complications of influenza
primary influenza pbeumonia
Secondary bacterial pneumonia (initial improvement then worsening
bronchitis vs bronchioloitis
bronchitis: linked to many resp viruses AND bacteria
bronchiolitis: linked to specific VIRUSES and mostly occurs in infants
What is the most common LRTI of kids <2 years
- which pathogen is the leading cause?
- clinical presentations
- Diagnosis
BRONCHIOLITIS
- RSV is the leading cause, then influenza
Chest wall retractions, flaring of nose, grunting (signs of increased work of breathing)
On auscultation: wheezing and/or crackles (difficult to differentiate from asthma) decreased sounds herald obstruction and impending respiratory failure
CLINICAL diagnosis (xray and labs are not helpful)
What is the management of bronchiolitis
- *Symptom relief
- *Maintain hydration
- Maintain oxygenation
Steroids and bronchodilator therapy in some select cases
*No effective antiviral therapy
Some children candidates for preventative therapy using an antibody to RSV
Most common cause of mortality related infection
- diagnosis
- causative pathogen
Acute Pneumonia
Requires Xray for diagnosis
Many potential microbial causes and no single drug to treat pneumonia
how is Pneumonia Classified and Characterized by?
3 categories:
Organisms: bacterial (typical vs “atypical”), viral
(strep pneumoniae, staph aureus, H. influenza)
Pathogenesis: Community acquired pneumonia (CAP) Nosocomial/HAI (occuring > 72h after admission) Ventilator-associated (VAP) Aspiration
Anatomic distribution: lobar vs multifocal; bronchopneunomia vs interstitial
* Epidemiology of Pneumonia by age*
Infants
young Adults
Older adults
Infants and young children
Gr B strep
RSV, parainfluenza, influenza
S. pneumonia and H. influenza type B (now less frequent since vaccines)
Young adults
Mycoplasma, chlamydophyla (“atypicals”)
Influenza
Older adults
S. pneumo, H. influenza, S. aureus, gram negatives
TB
Epidemiological risk factors for Pneumonia based on ETOH/Alcohol consumption: Aspiration: COPD*: Hospitalization*: Post-influenza*: Sickle cell: Immunocompromised:
ETOH: S. pneumonia, H. influenza, Klebsiella, anaerobes, TB
Aspiration: mixed flora with anaerobes; staphylococcus and G(-) in hospitalized
***COPD: H. influenza, S. pneumonia, Moraxella, Legionella
**Hospitalization: G(-) pathogens
*****Post-influenza: Staphylococcus, S. pneumonia, H. influenza
Sickle cell: S. pneumonia
Immunocompromised (HIV, chemotherapy, transplant,..): bacterial, fungal, mycobacterial (TB
which bug causes highest mortality in pneumonia
TYPICALS:
S. aureus 32%
gram negatives up to 605
Atypicals: legionella
