CASE PRESENTATION

Santosh Kishor Chandrasekar

 GENERAL DATA

• P.M.
• 30
• Female
• Lives in Davao
• Christian
• Informant : patient
• Date of admission: June 4th, 2017
 CHIEF COMPLAINT

COUGH
 HISTORY OF PRESENT ILLNESS

• 6 days prior to admission, patient had onset of productive

cough, nonbloody, without fever.
• Patient increased fluid intake and took Vitamin C
• 4 days prior to admission, patient had persistence of symptoms
associated with fever (Tmax = 40’C). Patient took paracetamol
with temporary relief from fever.
• 2 days prior, patient consulted a doctor in DDH due to
persistence of fever and started cefuroxime 200mg twice a day
with no relief.
 HISTORY OF PRESENT ILLNESS

• Morning PTA, pt had 2 episodes of vomiting, nonbilious,

nonbloody with headache.
• Due to persistence of cough, fever and headache patient opted
for admission.
 PAST MEDICAL HISTORY

(+) hypertension for 11 years – good maintenance meds

compliance

Amlodipine 5 mg tab OD

Losartan 100mg tab OD

(+) sinusitis

(-) Diabetes

(-) Bronchial Asthma

 FAMILY HISTORY

• (+) Hypertension – paternal

• (-) Diabetes

• (-) Heart defects

• (-) Bronchial asthma

• (-) Cancer
 PERSONAL AND SOCIAL
HISTORY
• Patient works as a Nurse

• Non-smoker, (-) alcoholic beverage drinker

• Single

• Eats rice, chicken, fish and vegeetables

 REVIEW OF SYSTEMS
• General:(-)fever,(-)weight change,(-)fatigue

• Skin: (-)rash, (-)itching, (+)diaphoresis

• Head: (-)injury, (-)dizziness

• Eyes: (-)hyperopia,(-)discharge

• Ears: (-)discharge, (-)tinnitus

• Nose: (-)epistaxis, (-)loss of smell, (-) sinusitis

• Mouth: (-)ulcer,(-)lesions

• Neck: (-)swelling, (-)lesions

• Cardiac: (+)chest DISCOMFORT (-
)orthopnea, (-)PND

(-)palpitations, (-)syncope, (-)edema

• GI: (-)diarrhea (-)melena, (-)hematochezia.

• GU: (-)dysuria,(-)polyuria, (-)oligouria

• Musculoskeletal: (-)joint pain, (-)cramps,

• Endocrine: (-)diabetes, (-)thyroid

• Neurologic: (-)weakness

• Psychiatric: (-)anxiety,(+)conscious.
 PHYSICAL EXAMINATION

General: awake, febrile, conscious, co-operative, not in respiratory

distress
Temp: 40.3’C
Respiratory rate: Pulse: 142
Blood pressure: 130/90
Wt: 60kg
Ht: 160cm
BMI : 23.4
• Skin: Dry and warm, non erythematous

• Head: normocephalic, non traumatic

• Eyes: anicteric sclera, pale palpebral conjunctiva

• Ears: symmetric with no discharge

• Nose: midline septum, no discharges

• Mouth: pink moist oral mucosa, moist lips, (-)ulcers

• Neck: midline trachea, no palpable lymph nodes, (-)neck veins

engorgement
• Thorax: Inspection: Equal chest expansion
Percussion: Resonant
Palpation: Equal tactile and vocal fremitus
Auscultation: clear breath sounds

Cardiac: Inspection: Adynamic precordium

Palpation: Apex beat at 5th ICS mid-clavicular
line, (-)heaves, (-)thrills
Auscultation: S1 and S2 distinct, (-)murmurs
• Abdomen: Inspection - Round, Flabby, No scars seen

Auscultation - normoactive bowel sounds

Percussion - Tympanitic on all quadrants, (-) Hepatomegaly

(-) Splenomegaly

Palpation - No tenderness on both light and deep palpation

• Extremities- Full pulses, (-) Bipedal edema, (-) Cyanosis

 NEURO EXAM
• Musculoskeletal: (-)Joint deformities, Good range of motion

• MSE: Conscious, Coherent, Cooperative, Oriented to time, place and person

• Cranial nerves:

I. Smells Soap when closed eyes

II. Good visual acquity

III. intact EOM range of motion,

IV. intact EOM range of motion,

V. (+) Corneal reflex

VI. Intact EOM range of motion,

VII. Can raise both eyebrows, (-)facial asymmetry

VIII. Good hearing

IX. Patient is able to swallow

X. Patient is able to swallow

XI. Can shrug shoulders against resistance

XII. (-)tongue deviation

• Motor: 5/5 strength in all extremities

• Sensory: 100% sensitivity

• Reflex: no pathologic reflex

 SALIENT FEATURES
• 30 year old female
• Productive cough
• Fever
• Headache
• (+)Crackles on bibasal lung fields
• Dry and warm skin
• Works as a nurse in a hospital setting
• Hypertensive
 ADMITTING IMPRESSION

• Lower respiratory tract infection

 DIFFRENTIAL DIAGNOSIS
Diagnosis Rule in Rule out

PNEUMONIA Productive Cough Cannot be ruled out

Fever
Chills
Chest wall discomfort

BRONCHITIS Productive cough Crackles heard through

Throat irritation auscultation
Fever
Tachycardic

PULMONARY EMBOLISM COUGH NO CHEST PAIN

NO SUDDEN DYSPNEA

NO RISK FACTORS
COURSE IN THE WARD
 DAY 1 OF HOSPITALISATION

• S - Patient had fever, headache • P – Venoclysis – IV rehydration

8/10 in pain scale and productive therapy done.
cough. - Ampicillin sulbactam was started.
• O - T – 40.3’C, Pulse rate – 142bpm, - Supplementary therapy – Zykast,
BP - 130/90 mm/Hg, Respiratory Ventolin expectorant was started.
rate – 23 - Other maintenance medications
was continued – Losartan, Vitamin
- patient was warm to touch, had clear
E, Amlodipine.
breath sounds.
- creatinine – 72.1, Na – 134, K – 4.1, Ca- - Norgesic Forte was given for
2.17 Headache as needed.

• A – Lower respiratory tract infection

 DAY 2 OF HOSPITALISATION

urinalysi Value
• S - Patient had fever, 19 to 21 cpm s

headache 10/10 in pain - patient was warm to touch, WBC 4

RBC 21
scale and productive had bibasal crackles. EPI. 3
CELLS
cough; patient started to - Xray revealed Right sided CASTS 0
feel chest discomfort and basal pneumonia. BACTERI 20
A
throat itching worsened • A – Community acquired COLOR L. YELLOW
due to repeated coughing. pneumonia – moderate CLARITY CLEAR
SPEC. 1.010
• O - T – 38.3 to 39.5 ’C, risk GRA.
GLUCOS +
Pulse rate – 76 to 115 bpm, • P – The medications were E
PROTEIN NEGATIVE
BP - 100-120/70-90 continued.
mm/Hg, Respiratory rate –
 DAY 3 OF HOSPITALISATION
• S - Patient had fever, • A – the fever trend did
headache 10/10 in pain not improve stating the
scale and productive ineffectiveness of
cough; Patient was able ampisulbatam
to expectorate only Community acquired
after so many forceful pneumonia – moderate
coughs risk
• O - T – 38.5 to 39.3 ’C, • P – Levofloxacin was
Pulse rate – 86 to 105 added.
bpm, BP - 110-130/60- The medications were
80 mm/Hg, Respiratory continued.
rate – 19 to 22 cpm
- patient was warm to
touch, had enlarged
tonsils, bibasal crackles.
 DAY 4 OF HOSPITALISATION

• S - Patient’s fever did not improve. Headache relapsed in 3 to 4

hours after norgesic intake; productive cough; Patient felt weak
and malaise due to forceful coughing.

• O - T – 38 to 40.2’C, Pulse rate – 94 to 103 bpm, BP - 100-110/60-

80 mm/Hg, Respiratory rate – 19 to 22 cpm
- Patient was warm to touch, had dry lips, had bibasal crackles,
decreased breath
sounds at lower lung fields.
- Dengue test and typhi dot test came out negative.
- Sputum GS results revealed gram(+) cocci in clusters, chains and
pairs, gram (-) bacilli;
Epithelial cells <25/OIF; Pus cells >25
 DAY 4 OF HOSPITALISATION

• A – PSEUDOMONAS infection was suspected because of no

response to ampisulbactam based on fever.
• Community acquired pneumonia – moderate risk

• P – AMPISULBACTAM was shifted to CEFEPIME

• Ipratropium bromide + salbutamol nebulizer was also added to
the current medications
• IV hydration rate was increased.
• A repeat CBC was ordered.
 DAY 5 OF HOSPITALISATION

• S - Patient’s fever, chest pain due to coughing

and ability to expectorate started to improve.
Headache still remained same, but was
relieved by norgesic forte. Patient felt better
and less weak.
• O - T – 37 to 39.6’C, Pulse rate – 88 to 103 bpm,
BP - 90-110/60-70 mm/Hg, Respiratory rate –
19 to 20 cpm
- Patient was warm to touch, had bibasal crackles,
decreased breath sounds at lower lung fields.
- Chest xray revealed bilateral pneumonia with
consolidation
 DAY 5 OF HOSPITALISATION

• A – Cefepime Day1, Levofloxacin day4.

• Patient’s infection is responding to cefepime treatment by
showing a decrease in fever trend.
• Community acquired pneumonia – moderate risk

• P – Cefepime course should be completed for 7 days ad

levofloxacin for 10 days
IV flow rate was decreased
 DAY 10 OF HOSPITALISATION

• S - Patient became afebrile in day 6 and the patient felt better

in the consecutive days of hospitalization .
• O - T – 36.4 to 38’C, Pulse rate – 76 to 102 bpm, BP - 90-
130/60-90 mm/Hg, Respiratory rate – 19 to 23 cpm
-Patient’s crackles became less severe as the days progressed
- Patient had stable vital signs
- SPUTUM CS results showed a light growth of streptococcus
proving our streptococcus.
- A repeat chest x ray was ordered which showed resolving
pneumonia.
 DAY 10 OF HOSPITALISATION

• A – Cefepime Day 6, Levofloxacin day 9.

• Patient’s infection has almost resolved and chest radiograph
showed resolving pneumonia
• Community acquired pneumonia – Moderate risk

• P – Ventolin expectorant and ipratropium nebulizer were

asked to discontinue after consumption.
• IVF flow rate was tapered off.
 DAY 11 OF HOSPITALISATION

• S - Patient is free of fever and headache and was discharged

on this day
• O - T – 36.4 to 37’C, Pulse rate – 76 to 98 bpm, BP - 90-130/60-
90 mm/Hg, Respiratory rate – 19 to 21 cpm
-Patient had no crackles or any other pertinent abnormal findings in
physical exam

• A – Cefepime day 7 (last day), levofloxacin day 9

• Community acquired pneumonia – Moderate risk

• P – HOME MEDS
• Levofloxacin 500mg tab OD x7days
 FINAL DIAGNOSIS

• Community acquired pneumonia – Moderate risk

• Hypertension
 PNEUMONIA
Infection of Pulmonary Parenchyma
 pneumonia

HCAP

CAP HAP VAP

HEALTH CARE ASSOCIATED PNEUMONIA

COMMUNITY ACQUIRED PNEUMONIA
HOSPITAL ACQUIRED PNEUMONIA
VENTILATOR ASSOCIATED PNEUMONIA
 PATHOPHYSIOLOGY
• Pneumonia results from the proliferation of microbial
pathogens at the alveolar level and the host’s response to those
pathogens.
• Many pathogens are inhaled as contaminated droplets.
 PATHOPHYSIOLOGY

• Small-volume aspiration
ASPIRATION • in patients with decreased
levels of consciousness.

HEMATOGENOUS • E.G. Tricuspid endocarditis

• infected pleural Space

CONTIGUOUS
• mediastinal space.
 PATHOPHYSIOLOGY
MECHANICAL FACTORS
• Hairs and Turbinates
• Tracheobronchial tree
• Gag reflex and the cough mechanism
• Normal flora – mucosal cells of the Oropharynx
IF THEY CROSS THE BARRIER OR
SMALL SIZED,

ALVEOLAR
MACROPHAGES
WILL KILL OR CLEAR THEM
 PATHOPHYSIOLOGY
MACROPHAGES
• Assisted by proteins by alveolar epithelial cells
• intrinsic opsonizing properties
• Antibacterial activity.
• antiviral activity.

• Killed or expelled

• Capacity is overcome – CLINICAL PNEUMONIA

INFLAMMATORY RESPONSE
Tr iggers the clinical syndrome of pneumonia
 Alveolar
Neutrophil
fever capillary
recruitment
leak

IL-1 &
TNF

FEVER
 Alveolar
Neutrophil
fever capillary
recruitment
leak

PERIPHERAL
LEUKOCYTOSIS
NEUTROPHIL
IL – 8 & GCSF
RECRUITMENT
PURULENT
SECRETIONS
INCREASED
 Alveolar
Neutrophil
fever capillary
recruitment
leak

CHEMOKINES
FROM ALVEOLAR
SIMILAR TO ARDS
NEUTROPHIL AND CAPILLARY LEAK
MACROPHAGES

ERYTHROCYTES
HEMOPTYSIS
LEAK

RADIOGRAPHIC
RALES HYPOXEMIA
INFILTRATES
 INTERFERENCE BY
BACTERIAL
PATHOGENS IN
HYPOXEMIC
VASOCONSTRICTION

SEVERE
HYPOXEMIA

RESPIRATORY
ALKALOSIS

INCREASED
RESPIRATORY
DRIVE
PATHOLOGY
Edema, red hepatization, gray hepatization,
resolution
 Edema Red Gray resolution
hepatization hepatization

• With the presence of a proteinaceous exudate in

the alveoli.
• This phase is rarely evident in clinical or
autopsy specimens because of the rapid
transition to the next phase
 Edema Red Gray resolution
hepatization hepatization

• The presence of erythrocytes in the cellular

Intra-alveolar exudate
• Neutrophil influx
• Bacteria are occasionally seen in pathologic
specimens collected during this phase.
 Edema Red Gray resolution
hepatization hepatization

• no new erythrocytes are extravasating

• The neutrophil is the predominant cell,
• fibrin deposition is abundant
• Bacteria have disappeared.

• This phase corresponds with successful

containment of the infection and improvement
in gas exchange.
 Edema Red Gray resolution
hepatization hepatization

• the macrophage reappears as the dominant

cell type in the alveolar space
• the debris of neutrophils, bacteria, and fibrin
has been cleared, as has the inflammatory
response
Patient is
still a nurse
when she
got the
infection

Patient is
still a nurse
when she
got the
infection
COMMUNITY ACQUIRED
PNEUMONIA
ETIOLOGY
 ETIOLOGY
TYPICAL ATYPICAL
• S. pneumoniae • Mycoplasma pneumoniae

• Haemophilus influenzae, • Chlamydia pneumonia

• S. aureus • Legionella species

• gram-negative bacilli such as • respiratory viruses

• influenza viruses
• Klebsiella pneumoniae and
Pseudomonas aeruginosa. • Adenoviruses
• human metapneumovirus
• respiratory syncytial
viruses.
 ETIOLOGY - ANAEROBES

• Anaerobes play a significant role only when

an episode of aspiration has occurred days
to weeks before presentation of pneumonia.
• The combination of an unprotected airway
(e.g., in patients with alcohol or drug
overdose or a seizure disorder) and
significant gingivitis
 ETIOLOGY - MRSA

• the spread of MRSA from the hospital setting to the community

• The emergence of genetically distinct strains of MRSA in the
community.
CLINICAL MANIFESTATION

indolent fulminant

mild fatal
 CLINICAL MANIFESTATION

• Febrile • Pleuritic chest pain.

• Tachycardia • Up to 20% of patients may
have gastrointestinal
• Chills / sweats
symptoms
• Cough • nausea, vomiting,diarrhea.
• nonproductive
• symptoms may include
• productive of mucoid,
fatigue, headache, myalgias,
purulent, or blood-tinged
sputum. and arthralgias.

• Gross hemoptysis
 CLINICAL MANIFESTATION – PE
FINDINGS
• An increased respiratory rate and use of accessory
muscles
• Palpation may reveal increased or decreased tactile
fremitus,
• the percussion note can vary from dull to flat,
• Crackles, bronchial breath sounds, and possibly a
pleural friction rub
DIAGNOSIS

Is this pneumonia

Likely etiology
 DX- IS THIS PNEUMONIA?

• Radiography
• Clinical methods
 RADIOLOGY - CXR

• A new parenchymal infiltrate

• confirmatory
• unless
• • Healthy individuals or those with stable co-morbid conditions, and
• • Normal vital signs and physical examination fi ndings, and
• • Reliable follow-up can be ensured.

• essential in assessing the severity of disease and the presence

of complications.
 RADIOLOGY - CXR

• Standing Posteroanterior view

• Lateral view

• An initial “normal” chest x-ray may connote a radiographic lag

phase.
 DX- ETIOLOGY?

• The conditions which can alter response to standard antibiotic

management are the presence of:
• 1) a bacterial etiology not covered by the empiric antibiotic
• 2) drug resistance
• 3) etiologies other than bacteria (e.g., Mycobacterium
tuberculosis, fungi, and viruses).
 DX- ETIOLOGY – CAP LR

• Since the bacterial etiology is predictable and the mortality

risk is low, sputum Gram stain and culture may not be done
• when there is failure of clinical response to previous antibiotics
• the patient has clinical conditions in which drug resistance may
be an issue.
 DX- ETIOLOGY – ATYPICAL

• When possible, tests to document the presence of Leginella

pneumophila are recommended in hospitalized patients with
CAP.
• urine antigen test (UAT) to detect serotype 1 and
• Direct fluorescent antibody test (DFA) of respiratory specimens
• And other atypical organisms
• serology [a fourfold increase in IgG or IgM titers or an initially
high initial IgG or IgM titer]
• Culture
• PCR of respiratory specimens.
 PSEUDOMONAS AERUGINOSA

• Patients who are at risk of infection with P. aeruginosa include

those with history of chronic or prolonged (>7 days within the
past month) use of broad-spectrum antibiotic therapy, with
severe underlying bronchopulmonary disease (COPD,
bronchiectasis), malnutrition or chronic use of steroid
therapy>7.5mg/day2.
 PSEUDOMONAS AERUGINOSA

• For these patients, the recommended empiric therapy should

include regimens with
• a parenteral antipneumococcal, antipseudomonal β-lactam plus a
parenteral extended macrolide and aminoglycosides
• a combination of a parenteral antipneumococcal,
antipseudomonal β-lactam plus either parenteral ciprofl oxacin or
high dose levofl oxacin.
• Antipneumococcal, antipseudomonal cephalosporins include
cefepime and cefpirome.
 PSEUDOMONAS AERUGINOSA

• Carbapenems such as meropenem or imipenem-cilastatin

have anaerobic activity.
• Parenteral antipseudomonal β-lactams with β-lactamase
inhibitors include piperacillin-tazobactam, ticarcillinclavulanic
acid and cefoperazone-sulbactam.
 INITIAL THERAPY ASSESSMENT

• Temperature, respiratory rate, heart rate, blood pressure,

sensorium, oxygen saturation and inspired oxygen concentration
should be monitored to assess response to therapy.
• Response to therapy is expected within 24-72 hours of initiating
treatment.
• Failure to improve afer 72 hours of treatment is an indication to
repeat the chest radiograph.
• Follow-up cultures of blood and sputum are not indicated for
patients who are responding to treatment.
 INDICATIONS FOR STREAMLINING
OF ANTIBIOTIC THERAPY
• Resolution of fever for > 24 hours
• Less cough and resolution of respiratory distress (normalization of respiratory
rate)
• Improving white blood cell count, no bacteremia.
• Etiologic agent is not a high-risk (virulent/resistant) pathogen e.g. Legionella, S.
aureus or Gram- negative enteric bacilli
• No unstable comorbid condition or life-threatening complication such as
myocardial infarction, congestive heart failure, complete heart block, new atrial
fibrillation, supraventricular tachycardia, etc.
• No sign of organ dysfunction such as hypotension, acute mental changes, BUN
to creatinine ratio of >10:1, hypoxemia, and metabolic acidosis
• Patient is clinically hydrated, taking oral fl uids and is able to take oral
medications
TREATMENT DURATION
 RECOMMENDED HOSPITAL
DISCHARGE CRITERIA
• 1. temperature of 36-37.5o C

• 2. pulse < 100/min

• 3. respiratory rate between 16-24/minute

• 4. systolic BP >90 mmHg

• 5. blood oxygen saturation >90%

• 6. functioning gastrointestinal tract