May. Pathology #2. part. Rahaf Al-yousef. Mohammad Al-Qudah

Transcription

1 8 th May Pathology #2 nd Pneumonias 2 part Mohammad Al-Qudah Rahaf Al-yousef

2 In the first part of our lectures today, we will define pneumonia clinically and pathologically(which is an infection of the parenchyma distal to the bronchioles). So, at the beginning the patient must be diagnosed clinically. Diagnosis: For diagnosis we need: History The patient will mention that he suffers from fever, cough, shortness of breath, etc. Keep in mind that: *The causative agents of pneumonia are usually the same as those in the upper respiratory infections. In many cases the pneumonia will be preceded with an upper respiratory infection. *The upper respiratory infections may develop leading to lower respiratory infections (e.g. pneumonia); which are more dangerous, because we notice that all the immune defense mechanisms were for the lower respiratory infections. This means that it is a severe condition if the microbe enters the lower part. *It is considered a more serious condition if the patient suffers from pneumonia than an upper respiratory infection. Examination: The percussion and auscultation sounds will be different in patients suffering from pneumonia; because the cavity of the chest is now filled with fluid instead of air like in the normal condition. Blood picture: *CBC and acute phase reactants:the most important thing to do is to confirm the diagnosis by doing a CBC test. If the patient does suffer from pneumonia you will find the following: WBCs, CRP, ESR, platelets (because platelets are a part of the acute phase reactants). 1 P a g e

3 *Any acute disease affecting the body might cause an increase in the acute phase reactants. So whatever the relation to the disease, the platelets will increase, as they are part of the acute phase reactants. You know, don t you?. ) Isolation of microbe: -Sputum: ask the patient to produce a cough with sputum. The microorganism previously found inside the lung isnow in the sputum, identifying this microorganism helps us reshape the management plan, but how? This done by changing the drug which is inappropriate to another one which is appropriate for the microorganism that we found in the sputum. -Blood culture: this is done when sputum cannot be obtained. -Pleural fluid -Serology -Chest X ray: used clinically to confirm the diagnosis 100%. **So we can't diagnosepneumonia clinicallyuntil a chest X-ray is done** Morphological patterns of pneumonia: -We said that the most classical/anatomical types of acute bacterial pneumonia are: *LOBAR PNEUMONIA * BRONCHO-PNEUMONIA - However, there are other types that will be seen with different types of microorganisms other than bacteria such as: *INTERSTITIAL PNEUMONIA: it is one of the morphological patterns of pneumonia. *MILIARY (usually TB): it is tuberculosis (TB) related pneumonia.(to be discussed next week). 2 P a g e

4 B D A C Lobar pneumonia: which involves the whole lobe. A: black area is the normal appearance of the lung. B: Dense white area which is abnormal, due to fluid accumulation in the alveolar space. Why does fluid accumulate? Because of edema, or certain microorganisms. and because of whatever reactions that occurred, we have this pattern. C: the lobe which is completely affected by pneumonia D: normal lung tissue Bronchopneumonia: the infection and irritation will follow the bronchial tree, so you won't see a strong lobar involvement. But you will see more opacities with each bronchial tree. In the picture on the right, you see that the whole patches are affected by bronchopneumonia. But there's a problem with Bronchopneumonia. Because the whole patches that are affected by bronchopneumonia will become larger and larger and eventually open into each other and give us a picture which is the same as that seen in Lobar pneumonia. Q: *Bronchopneumonia what's the difference tries between to confuse Lobar us in andbronchopneumonia? the diagnosis, so we decide to classify pneumonia by a different pattern, in order to have a proper treatment for the patient. 3 P a g e

5 *There's no huge difference, but it will give you a hint about the microorganism or the severity of the disease. So, if more than 1 or 2 lobes are involved in the case of lobar pneumonia,this means that we have a serious condition. **Usually bronchopneumonia is less severe than lobar pneumonia. Classification of pneumonias Pneumonia can arise in seven distinct clinical settings, and the implicated pathogens are reasonably specific to each category; so depending on the clinical settings, which we talked about in the previous lecture, we classify the pneumonia into seven categories. We have to classify the pneumonia in our case into one of these categories in order to provide the patient with the proper treatment. You have to give your patient, who has pneumonia, therapy and not let him leave the hospital without it. Then later, when the culture is ready, you will confirm the medication that you have previously prescribedor you have to prescribe different medication which is more appropriate for the microorganism found in the culture. Community- Acquired pneumonia, which is 2 types: - Acute Pneumonia. - Atypical Pneumonia: which is a hospital acquired pneumonia -Nosocomial Pneumonia - Aspiration Pneumonia -Lung Abscess - Chronic Pneumonia - Pneumonia in animmunocompromised host: the type of pneumonia which occurs in immunocompromised patients. So you have to put your patient in one of these categories. Once you do that, you will narrow down the group of causative agents and this will make it easier to choose the proper medication. 4 P a g e

6 Community-Acquired Pneumonia: In general, it causes lobar pneumonia and bronchopneumonia, which is caused by bacteria. (**streptococcus pneumonia: the most common microorganismto cause pneumonia**) Risk factors: -Dependent on organism: some organisms are more virulent than others. - Alcoholism, asthma, immunosuppression, age >70, smoking, COPD, dementia, seizures, congestive heart failure. ** So if a non-smoker young patient comes to you, it's unusual for them to have pneumonia. However, if you confirm the diagnosis (in this casepneumonia) by a different procedure, you have to look for an anatomical defect. **So, Community-Acquired Pneumonia is caused by either a virulent organism or problems in the patient himself. Etiology: *Bacteria: it is the usual cause *fungi, viruses, parasites: they are less common causative agents *S. pneumoniaeand H. Influenzae(the most common cause of pneumonias). *Might be caused by s. aureus, m. pneumoniae, c. pneumoniae, influenza, adenoviruses, respiratory syncytial virus. 5 P a g e

7 *Whatever the causative agent, the patient may come to the ER with a clinical picture like that of acute bacterial pneumonia, the causative agent is sometimes a virus or fungi but will have the same presentation of acute bacterial pneumonia. So we put them under the umbrella of Community-Acquired Acute Pneumonia and based on the history & chest X-ray (that will be either bronchopneumonia OR lobar pneumonia) of the patient we classify the pneumonia into those previous categories. *Sometimes, you make a bacterial culture for this patient and you may not find any MO.at all, this means that he had a previous viral infection. *Sometimes, you will have a severe viral infection sub-added to a normal microflora infection; I mean the virus is the main pathogen, followed by a microflora infection which will worsen the scenario. When you look at the culture, you will be confused because you know this type of bacteria will not cause this pathological condition. But why does this happen?due to a previous viral infection. Pathology of Pneumococcal (streptococcus) Pneumonia: CONSOLIDATION: Hardening of the lung parenchyma due to the presence of exudates in the alveolar spaces. So the most important thing to see in the Community- Acquired acute Pneumoniachest X-rayis the pattern ofthe lobar pneumonia or bronchopneumonia, otherwise we can't diagnose the patient as having Community- Acquired acute Pneumonia. 6 P a g e

8 - The manifestation: acute onset of fever, cough, rust colored sputum, chest pain, pleurisy; that occurs when the patient,during inspiration, expand his cavity so he will push the foci of infection or the foci of pneumonia to be attached with the pleura, this the cause of the pain. - Many things will happen, all of them are the same in patient of pneumonia, but you have to do a chest X-Ray in order to know the pattern of pneumonia that your patient has. - Pathology: Usually strep. Pneumonia causes LOBAR, but bronchopneumonia can happen also. There are 4 stages of evolution (lobar); stages of bacterial pneumonia After you diagnose your patient that he has Community-Acquired acute Pneumonia, this means that his lungs will go through 4 stages. 1- CONGESTION 1-2 days: there are neutrophils, bacteria and fluids No proper gas exchange occurs in the alveolar space, so the patient will suffer from shortness of breath, he will even try to cause tachypnea, and he won't get the proper amount of oxygen; because the alveolar spaces are filled with fluids and neutrophils. -Heavy red lungs -Severe vascular congestion - Intra alveolar exudate with neutrophils -Watery sputum; not concentrated; all the fluid in the circulation will accumulate in the alveolar space. - Bacteria +++; if you take any drop from the sputum, it will be filled with neutrophils and bacteria. 7 P a g e

9 2- RED HEPATIZATION 2-4 days -It will look like the hepatic structure / free hepatic structure. There is a little absorption of fluid, so the things will be slightly organized and more solid, it's not watery at all. -Firm airless, liver-like lung -Fibrinopurulentpleuritis -Intra alveolar exudate : **Organisms ++ (The organisms will be fewer; there is an immune response and the macrophages start eliminating these organisms) **Cells: * Erythrocytes * Neutrophils * Fibrin * Rusty sputum The alveolar spaces are filled with Neutrophils and microorganisms. The patient still suffer from the same symptoms; because the alveolar space is still filled with cells and fluids. 8 P a g e

10 More solid and lesser amount of fluid 3- GREY HEPATIZATION 4-8 days -Dry grey brown cut surface - intra alveolar fibrin & macrophages - Disintegrating neutrophils & RBC s There is more absorption of fluid, more sputum concentrated, decrease in the amount of Neutrophils and increase in amount of macrophages; so the microorganism will decrease in number. The alveolar spaces are filled with fibrotic tissue, solid tissue. No sputum will be produced or there is a decrement in its amount, this means we are in the healing process. 9 P a g e

11 4- RESOLUTION 8-9 days: -It's the healing process and digestion of the whole contents inside the alveolar space by enzymes to get rid of the fluids, MO. and macrophages that were in the alveolar space. -It's a cleaning process, so the patient will resume normal gas exchange and he will breath normally again. -Enzymatic digestion of exudate resorption, phagocytosis, sometimeswith residual adhesion So: **The highest fluids and MO. Will be in? The congestion stage. **The highest amount of macrophages will be in?? Greyhepatization. **If fibrotic tissue and grey hepatizationare still present, this is a problem, we need to control the fibrosis; because if the process of fibrosis continues, this means that the alveolar space will be filled with fibrotic and solid material not water.so we need the resolution phase in order to prevent the obstruction of the alveolar space and to be able to perform gas exchange properly. **Normally, the body will adapt in order to have phases for those 4 stages. The I-L and fibroblastic materials that get out at specific times and stages. Our bodies know what to do with this material in order to clean the alveolar space from fibrosis. *(In the next lectures we will talk about fibrosis, which won't disappear directly, the lung will return to normal after six month) *(Fibrotic process occurs depending on the pro and anti-fibrotic agents) Bronchopneumonia -Patchy consolidation involving one or several lobes. -Usually affects lower & posterior portions of lung. -Neutrophilic exudate centered in bronchi & bronchioles with spread to adjacent alveoli. 10 P a g e

12 Clinical Manifestations Typical Symptoms : -Fever -Cough -Expectoration of sputum -Pleuritic chest pain -Chills, rigors -Shortness of breath Physical signs: -Tachypnea -Single most useful sign for assessing severity: RR >30 bpm -Dullness to percussion. Other common causes of acute pneumonias in the community - H. influenzae and M. catarrhalis (both associatedwith acute exacerbations of COPD). - S. aureus (usually secondary to viral respiratory infections). - K. Pneumoniae (observed in patients who are chronic alcoholics and drug abusers). - P. aeruginosa (seen in patients with cystic fibrosis, in burn victims, patients with neutropenia). - L. pneumophila, seen particularly in organ transplant recipients. (Go over them, remember them; because each one has its own features) ** (Take this information: everybodyis able to get rid of pneumonia by themselves, however, because pneumonia is a very bad disease and a very stressful event, we need to give therapy in order to speed up the process of healing.because the organism might be more virulent nowadays and our immunityis decreased; we have to give therapy to each patient.) 11 P a g e

13 B- Community acquired (Atypical) *Usually can't manifest as lobar orbronchopneumonia. *The classical finding in the X-Ray of an atypical pneumonia patient is: interstitial pattern. Interstitialpneumonia A group of pneumonias caused by atypical bacteria or nonbacterial agents: -Mycoplasma Pneumoniae: the most common - Viruses - Resp.syncitial virus, measles parainfluenza, adenoviruses, CMV. - Chlamydia - Psittacosis - Rickettsiae *Nearly all of these agents, that cause atypical pneumonia, can also cause a primary upper respiratory tract infection ( common cold ). *If not treated properly when they are still in the phase of upper respiratory tract infection ( common cold ), the infection may go down and the patient can develop pneumonia. Usually this condition precedes with upper respiratory infection one or two weeks before. *Mycoplasma pneumonia being the most common. *Mycoplasma infections are particularly common among children and young adults. 12 P a g e

14 *They occur sporadically or as local epidemics in closed communities (schools, military camps, and prisons) may have upper or upper lower infection. Pathology: *Inflammatory process predominantly involving the interstitium: which is the clinical pattern of atypical pneumonia. *May be patchy or diffuse *Alveolar septa contains infiltrate of lymphocytes of the predominant type, not Neutrophils, macrophages, plasma cells *Little exudate in alveoli *lymphocytes inside interstitium might compromise the blood vessels. Compromising vascular space means a problem in the gas exchange process. *Why do we call it atypical pneumonia? Usually pneumonia causes cough, fever, sputum and the signs and symptoms are dependent on the severity of pneumonia. Otherwise, in atypical pneumonia the patient will have severesigns and symptoms, and it's just an interstitial pneumonia. Why was the patient having severe symptoms? Because of the blood vessels which are compromised. So, in atypical pneumonia there is no clear space in the chest X-Ray and the signs and symptoms are not at the same level of the x-ray finding. Clinical picture : -Insidious onset, minimaldry cough, minimal expectoration, minimal WBC s, NO Consolidation. - Radiological picture: Transient ill-defined patches, mainly in lower lobes - In case of viruses, viral inclusions are seen. - In mycoplasma: cold agglutinin present. 13 P a g e

15 Because the edema and exudation are both in a strategic position to cause an alveolocapillary block, there may be respiratory distress seemingly out ofproportion to the physical and radiographic findings. It's wrong to admit every patient to the hospital; because every hospital will increase the chances to have an infection and other complications. Try to treat the patient outside as much as you can; because some times the patient comes to you suffer from influenza and he will leave the hospital with pneumonia due to infection!!! *Hospital-Acquired (Nosocomial) Pneumonia *Pneumonia occurring at least 48 hrs after admission: the patient is clear in the first 48hrs, then he develops pneumonia. *Bacterial not viral. *Incidence 6-20x higher among mechanically ventilated patient. *Atypical pneumonia caused by bacteria, because the viruses are weak and can't survive outside the human body, even HIV virus -AIDS virus. Otherwise, bacteria is stronger and can survive outside the human body, you may find it in each palace in the hospital. Even if you want to do an intubation for the patient, the MO. may get inside his lungsthrough the tube causing Hospital-Acquired (Nosocomial) Pneumonia.There's an organism in each single room in the hospital, we can't eliminate them because they develop resistance for all antibiotics. 14 P a g e

16 Pathogenesis -Poor infection control measures -Prolonged & inappropriate use of antibiotics spread of antibiotic resistant virulent organisms, try to avoid the up use of antibiotics. -Endotracheal intubation Serves as direct bacterial conduit. -Prevents effective coughing. -Damages tracheal epithelium. -Accumulation of oropharyngeal secretions. Etiology Causative organism: *Mostly gram-negative bacilli : P. aeruginosa, K. pneumoniae *Gram positive:s. aureus is the most common cause of nosocomial pneumonia in the US. 15 P a g e

17 Nosocomial Pneumonias -Pseudomonas aeruginosa pneumonia: there is an abscess formation and necrosis that will damage the tissue. -Bronchopneumonia, high mortality. -Patients: neutropenic cancer patients, burn patients, ventilator associated **Pathology: abscess formation &empyema with prominent vascular invasion vasculitis, hemorrhage & necrosis (Necrotizing Pneumonia) ^^ CYSTIC FIBROSIS patients with pneumonia are presumed to have PSEUDOMONAS until proven otherwise. Staphylococcal pneumonia : *Severe abscessing broncho; Staphylococcal because it has enzymes that will destroy the lung tissue--->> pneumonia with destruction. *Risk: children - cystic fibrosis or post viral Adults - COPD, IV drug addicts. Aspiration Pneumonia: means -->> takea fluid or a foreign bodyinto the respiratory tract. -Aspiration from oropharyngeal secretions or acid gastric contents. -Patient:weak, with depressed sensation &control of hypopharynx, repeated vomiting. E.g. post anesthesiaandparalyzed patient. -Mixed bacterial infection + Acid Chemical damage + consolidation. -Severe Necrotizing Pneumonia *It may exacerbate other lung diseases but does not lead to pneumonia. *Micro-aspiration, by contrast, occurs in many people, especially those with gastro-esophageal reflux. 16 P a g e

18 *Patient who have a major surgery, and are given anesthesia - this means there is no contraction-. So, in order to prevent gastro-esophageal reflux we prevent the patient from eating, starting a day before the operation. By doing this we prevent the reflex of the gastric acid upwardsinto the esophagus then into the trachea until it reaches the lung tissue, causing a type of pneumonia which is partially due to infection and partially due tothe chemical material present in the gastric acid. *These chemical materials will digest the lung tissue and the alveolar space, which already has pneumonia and is filled with MO, causing necrosis and spreading of pneumonia, and at the end forming lung abscess. Lung abscess *Lung abscess refers to a localized area (filled with abscess formation) of suppurative necrosis within the pulmonary parenchyma, resulting in the formation of one or more large cavities. It could be the end result of acute pneumonia, could be a hospital acquired infection, or could be caused by an infection or by aspiration pneumonia. *Lung abscess may occur in patients who come very late to the hospital. Due to this delay; the aspiration pneumonia will be more severe and developed forming lung abscess. *Once we have abscess formation in the lung, the patient will produce very bad, rusty,fowl smelling sputum when he cough. 17 P a g e

19 Pathogenesis : 1-Aspiration of infective material. 2-Aspiration of gastric contents: that causes aspiration pneumonia, once we can't control it-->> it will cause lung abscess. 3-Post pneumonic. 4- Bronchial obstruction. (Tumor): remember when you receive a patient with recurrent lung abscess, think about tumors. Because once we have a tumor, it will obstruct the whole area where it presents, and the nearby areas. So, there is no air and secretion passage. This causes stagnation of fluid, recurrent infections and abscess. 5- Infection in existing cavities or cysts. 18 P a g e

20 6- Septic embolism. 7- Bacteremic seeding. **In aspiration cases -aspiration is the cause of lung abscess- : the abscess will be more onright; because it is wider and vertical, single & upper. **In the pneumonia cases -pneumonia is the cause of lung abscess- :more basal, multiple. **lung abscess is very localized, doesn't involve whole lobe. The manifestation sometimes will be less than lobar pneumonia. Keep in mind you need to do a biopsy in order to confirm the lung abscess diagnosis. **if you receive a patient with consolidation, and there is no MO. in the culture that you did, one of the causes might be lung abscess. Fate and complications of lung abscess: *It might open into the pleural space or lung space, so we need a procedure to treat this lung abscess instead of waiting for this abscess to rupture and cause further complications. *The complications of pneumonia could be diffusion from lung tissue into the pleura, could causeformation of massive fibrosis or septicemia or emphysema without healing and many other complication could occur. 1- Healing by fibrosis leaving a sterile cavity. 2- Rupture with partial drainage of material: *Radiological picture Air- Fluid level *Rupture into pleura Empyema *Rupture into bronchus Bronchopneumonia 3- Bronchopleural fistula Pneumothorax 4- Septic emboli. 5- Lung hemorrhage from vessels in fibrous wall 19 P a g e

21 Complications of bacterial pneumonias: *The complications of pneumonia could be diffusion from the lung tissue into the pleura, could cause a massive fibrosis, could cause septicemia or emphysema without healing and many other complications may occur. 1- Pleural effusion 2- Non resolution and organization of exudate fibrosis 3- Abscess formation 4- Bacteremic dissemination meningitis, arthritis, infective endocarditis 5- Empyema: accumulation of pus in thepleural cavity which is followed by adhesions 6- Atelectasis Empyema:involvement of pleural fluid by an abscess material **we will talk about chronic lung diseases next week, in TB. lectures. All slides are included ^^ ^^There are some key notes on acute pneumonias. The doctor bring them from the book and he put them in the slides. 20 P a g e

22 Key notes on acute pneumonias: S. pneumoniae (the pneumococcus) is the most common cause of community-acquired acute pneumonia, and the distribution of inflammation is usually lobar. Morphologically, lobar pneumonias evolve through four stages: congestion, red hepatization, gray hepatization, and resolution. Other common causes of acute pneumonias in the community include H. influenzae and M. catarrhalis (both associated with acute exacerbations of COPD), S. aureus (usually secondary to viral respiratory infections), K. pneumoniae (observed in patients who are chronic alcoholics), P. aeruginosa (seen in persons with cystic fibrosis, in burn victims, and in patients with neutropenia), and L. pneumophila, seen particularly in organ transplant recipients. *In contrast with acute pneumonias, atypical pneumonias are characterized by respiratory distress out of proportion to the clinical and radiologic signs, and by inflammation that is predominantly confined to alveolar septa, with generally clear alveoli. * The most common causes of atypical pneumonias include those caused by M.pneumoniae, viruses including influenza viruses types A and B, human metapneumovirus, C. pneumoniae, and C. burnetii (agent of Q fever). Edited by: Majd Abusharar. 21 P a g e