Lecture 5

PNEUMONIA

DEFINITION
Pneumonia is a non-suppurative inflammation in the lung parenchyma,distal to the
terminal bronchioles, characterized by exudative alveolitis with/or inflamatory interstitial
infiltrate.

POSITIVE DIAGNOSIS
-clinical signs :fever, cough, expectoration, thoracic pain,dyspnea,pulmonary physic
signs;
-radiological signs: alveolar or interstitial images localizated or difused.

DIAGNOSIS OF GRAVITY
The gravity of a pneumonia can be estimated by implication over the vital functions
(respiration, circulation,excretion) and by analysing the associated diseases.All the infectious
pneumonia must be considered potential grave when it occurs on a weakly patient:
imunodepresion, alchoholism,diabetes mellitus, cardiac failure, chronic respiratory insufficiency,
chronic renal failure, elderly patient.

CLINICAL SIGNS OF GRAVITY

- cyanosis and/or polypnea more then 30 respiration/min. -signs of acute respiratory
insufficiency;
- marbled skin ,cold extremities, hypotension( decreased the blood pressure with more
than 40 mm Hg., diastolic blood pressure less then 60 mm Hg.) olygulia.This means a shock
status:
-an acute renal failure usually functional can appears because of the shock and
dehydratation;
-mental confusion (alterated consciousness) is always a sign of gravity , indifferently
which is its mechanism. Is necessary a lombar punction for eliminate an associated meningitis,
especially in case of pneumococal pneumonia;
- the elderly patients are in particulary exposed to dehydratation with important clinical
consequences.
The presence of one or more clinical signs of gravity require to perform paraclinical
investigations: blood gases, ureea, creatinine, ionic balance,blood bicarbonate.

BIOLOGICAL SIGNS OF GRAVITY

-hypoxenia (decreased pO2<60 mm Hg.);
-leukoneutropenia;
-increased values for creatinine and urea(renal failure).

HOSPITALIZATION INDICATIONS
-uncertainty of the diagnosis;
-clinical signs of gravity;
-imunodepresion;
-associated pleural liquid syndrome

CHRONIC OBSTRUCTION PULMONARY DISEASE - COPD

DEFINITION:
COPD is a chronic and persistent airway obstruction, mainly in bronchioles, determined
by obstructive chronic bronchitis and emphysema.
COPD has a chronic and permanent evolution with exacerbation periods determined by
inflammatory airway modifications. These changes increase the pre-existent obstruction degree
and produce acute respiratory failure.

POSITIVE DIAGNOSIS
Positive diagnosis of COPD is based on:
- clinical findings:
-increased dyspneea, tachypneea over 30 respirations /min;
-increased cyanosis, visible at nails, lips, ear lobe with a particular tint (associating
erythrosis with cyanosis because of pre-existent polyglobulia );
-possible fever;
-decreasing cough and sputum;
-purulent sputum;
-hypercapnial crisis (encephalopathy) with headache, daily drowsiness and night
agitation, flapping tremor, confussional syndrome, coma;
-signs of decompensated cor pulmonale:
-xifoidian galop rhythm and murmurs of functional tricuspid failure;
-signs of systemic stasis: jugular distention, hepatojugular reflux, painful
hepatomegaly, oedema.
- certainty diagnosis: is given by the blood gases modifications:
-hypoxemia: O2 PaP(oxygen partial pressure) < 50 mm Hg or with 10-15 mm Hg less
than previous values (out of exacerbation periods).Normal value is over 95 mm Hg.At
patients with COPD, O2 PaPis arround 70 mm Hg;
-hypercapnia: CO2 PaP> 50 mm Hg. Normal: under 45 mm Hg;
-pH < 7,3 in the absence of metabolic acidosis (the chronic hypercapnia in COPD involve
the renal compensatory mechanism, with pH maintaining).

In practice, any hypercapnia with arterial pH under 7,3 and without metabolic acidosis
must be considered as an acute respiratory failure.

GRAVITY CRITERIAS OF ACUTE EPISODES OF COPD

-alteration in mental status (confusional syndrome, coma) hypercapneea crises;
-weakness of accessor muscles of respirations: paradoxal respiration, bradypneea; excessive
tahypneea
-“silent chest”: decreasing of vesicular murmur, without listening other sounds, decreasing or
disappearance of the wheezing;
- arterial hypotention till colapse;
- paO2 under 40;
- paCO2 over 60;
- pH under 7,25.
If these signs are present, the patient will be hospitalized in intensive care unit.
The appearance of an acute episode at patients with COPD emphysemal type (pink
puffer) or chronic bronchitic type (blue bloater) represents a severity index.

TREATMENT OF ACUTE EPISODE OF COPD

Once the diagnosis is confirmed, treatment has three objectives:
1.maintaing a satisfying oxygenation and ventilation;
2.relief bronchial obstruction;
3. treatment of complications.

1. OXYGENATION
The acute episodes of COPD initiate acute respiratory failure with decreased values of O 2
PaP(under 50mmHg) and increased CO2 PaP(over 50mmHg).
Hypoxemia is the main stimulus for respiratory center and represent a life- threateninf
factor
Giving oxygen is the first and the essential therapeutic manouvre; via face mask or via
nasal tube,with small concentration (24-28%), equivalent to an air flow around 1-2 l oxygen/
min.

2. RELIEF OF AIRFLOW OBSTRUCTION

* Bronchial drainage by:
-cought stimulation: postural drainage, thoracic tapotement , chest percussion;
-aspiration of secretions with tracheal tube;
-good hydration : 1 litter at 3-4 hours, but cautions in those patiens with cardiac failure;
-humidifying the atmosphere , inhalation with salted water;
-2-agonists that enhance mucociliary transport;
-mucolitic agents( nitrigen-acetyl -cysteine)
*Relief bronchospasm by:
-2-agonists
-anticholinergic drug: ipratropium-bromide;
-aminophilline,

2-Actions: -bronchodilators;
-decreasing muscular effort;
- increasing bronchial drainage;
-diuretic;
-cardiotonic.
Administration:
-beta2- agonists by inhalation using nebuliser or spicer devices;
 -non-cholinergic substances like ipratropium bromide are basic for bronchitis and are
used by nebuliser ( 1 ml in 3 ml salted solution) or puff (2 puffs at 6 hours);
-beta2 agonists in parenteral administration
-amynophylline is for intravenous use; the dose is 10 mg/ kg.b.w., twice a day.
The dose of amynophylline will be decreased in case of anterior treatment or right -
ventricular failure.
*Corticosteroids
In severe crises are used big doses 2-3 days :
-methylprednisolone hemisuccinate = Solu- Medrol-40 mg/ phial;
Dose: 125 mg daily, intravenous.
-hydrocortisone hemisuccinate= HHC - 25 mg/phial;
Dose :200 mg at 8 hours.
And then a quick decreasing doses till 2 weeks.
*Antibiotics with large spectrum
-ampicilline 2-4 g/day, i.m.
-penicilline 4-10 mil/day + aminoglycoside
-cephalosporines;
-eritromicine (when mycoplasma or legionalla are involved);
Duration : 10-14 days.

3. TREATMENT OF COMPLICATIONS
* Right-ventriculare congestive failure:
-oxygen;
- bronchodilators;
- corticosteroides;
- antibiotics;
- dietary sodium restriction
If the oedema doesn’t disappear in 48 hours, we use diuretics:
-furosemide 20-40 mg daily, 1 phial=20 mg
-if furosemide is insufficient and urinary ionograme reveals hyperaldosteronism, we can
associate aldactone 100 mg/day

If signs of left ventricular failure are present we use digoxin (it increase the contractility
of right ventricule; it may determine vasoconstrictions and increase the arytmogen risk).
CONCLUSION: We don’t use digoxin and diuretics in right ventricular failure treatment.

*Left ventricular failure

-usually associated with coronary atherosclerosis, arterial hypertension, valvular diseases,
is not always easy for diagnosis when is present chronic cor pulmonale.
When oxygenation is good but the signs of heart congestive failure persists, we may
suspect an left ventricle-failure (LVF).
LVF is an indication for cardiotonics and diuretics.

* Arrhythmias
Most frequent arrythmias which can appear are:
- supraventricular tachycardia;
 -sinusal tachycardia;
-paroxistic atrial fibrillation.
These are determinated by: -hypoxia;
-bronchodilators abuse (myophyllin);
-2 agonists abuse.
Treatment includes: - treatment of favorising factors
- specific treatment of arrythmia
* Pulmonary embolism
Can be a trigger of the acute episode, but also a frequent complication.
Diagnosis is difficult ,so preventive heparinotherapy is required.
Dosage: 50 mg at 8 hours - 10 days ,then 50 mg at 12 hours 10 days.
* Superior digestive hemorrhage
Is determinated by stress ulceration of gastric mucous membrane.
The treatment includes:
-antisecretors;
-antiacides;
-gastric protectors ( sucralphate);
-gastric aspiration.