|
COMPLICATIONS IN PNEUMONIA Introduction Acute respiratory Distress-Syndrome (ARDS) Endocarditis Peri-/Myocarditis Severe generalized Bronchitis Sepsis with meningeal or encephalitic Irritation Symptoms Acute renal Injury and Exsiccosis Severe Icterus due to Liver-Involvement Pulmonary Hemorrhage Pulmonary Edema Lung-abscess Gangrene of the Lung Thromboembolic complications Pneumothorax Fibrosis of the Lungs Bronchiectasis Atelectasis COMPLICATIONS IN PNEUMONIA 1) Acute respiratory distress-syndrom 1) Pleurisy and pleural empyema 1) Endocarditis 1) Peri-/Myocarditis 1) Severe generalized bronchitis 1) Sepsis with meningitis 1) Acute renal failure with exsiccosis 2) Severe icterus due to liver-involvement 3) Pulmonary hemorrhage 4) Pulmonary edema 5) Abscess of the lung 6) Gangrene of the lung 7) Thromb-embolic complications (due to bed rest) 8) Pneumothorax 9) Fibrosis of the lungs 10) Bronchiectasia Introduction In this chapter we compiled orthodox and homeopathic information on the most common complications of pneumonia, which we found in the process of our literature-research. This information should help to understand the disease process and/or help find corresponding homeopathic remedies for a given state (e.g. prune-juice sputum as an important remedy-pointer in cases of gangrene of the lungs or lung-edema). Acute respiratory Distress-Syndrome (ARDS) ARDS is characterized by non-cardiogenic pulmonary edema, lung inflammation, hypoxemia, and decreased lung compliance. Unlike some disorders (e.g., coronary artery disease), ARDS, as its name suggests, is a syndrome, reflecting a constellation of clinical and physiologic observations thought to represent a common pathology. The pathogenesis of ARDS remains elusive and there is no gold standard diagnostic test. The heterogeneity of the clinical conditions associated with ARDS would be consistent with the possibility that ARDS is in fact a collection of different diseases that have not yet been separately identified. mur1,2016 ARDS was defined as a syndrome of acute onset, with bilateral opacities on chest radiography consistent with pulmonary edema, pulmonary artery occlusion pressure of 18 mm Hg or less (or absence of clinical evidence of left atrial hypertension), and hypoxemia as measured by the ratio of the arterial partial pressure of oxygen (arterial PO2) to the fraction of oxygen inspired (FIO2). Recognizing that there was a spectrum of severity of the disease, the consensus panel recommended that arterial PO2/FIO2 ratio = 300 would define an entity termed acute lung injury (ALI). ARDS was the most severe form of ALI and was diagnosed when arterial PO2/FIO2 = 200. The simplicity of the definition led to its general acceptance by clinicians and its incorporation into clinical research. At the same time, such a straightforward definition could not take into account the heterogeneity of the disease or the ambiguity of clinical practice. mur1,2016 The most common pulmonary disease leading to ARDS is pneumonia, especially aspiration pneumonia. The most common primary non-pulmonary conditions leading to ARDS are sepsis and severe trauma with shock from multiple transfusions. Less common causes include pulmonary contusion, fat emboli, near drowning, inhalation trauma, reperfusion edema after lung transplantation or pulmonary embolectomy, bypass surgery, and acute pancreatitis. kroe1,2014 The course of ARDS can be roughly divided into 3 phases: the exudative phase (1-2 days), the phase of hyaline membrane development (2-7 days), and the phase of interstitial inflammation or fibrosis (approximately from day 5-6). kroe1,2014 The alveolar-capillary barrier exhibits increased permeability, allowing for the leakage of protein-rich fluid into the air spaces. Alveolar filling leads to decreased respiratory system compliance as well as right-to-left shunting and profound hypoxemia. Although arterial PCO2 is generally within the normal range, dead space ventilation is significantly increased, as demonstrated by elevated minute ventilation. Pulmonary hypertension is also commonly observed in ARDS, and a number of mechanisms have been proposed including hypoxic vasoconstriction, intravascular fibrin deposition in the pulmonary capillaries, and compression of blood vessels by the positive pressure ventilation used to treat the disorder. mur1,2016 An important factor in the additional damage is ventilation and presumably the high inspiratory oxygen that is usually given to achieve 95% oxygen saturation. The high ventilatory pressures usually required for this purpose exacerbate leakage via stretch stress, which has been shown to worsen outcome. Studies with a reduction in ventilation volume from 12 to 6ml/kg body-weight have reduced morbidity by about 30%. kroe1,2014 Pleurisy and pleural empyema Ethiology mur1,2016 The underlying etiology of pleural infection is varied, with most cases being of community origin. Although this often results from a community-acquired pneumonia, a sizable proportion of cases show no evidence of consolidation on computed tomography (CT) imaging and are thought to have been acquired through hematologic spread or direct translocation from the oropharynx. The next largest group are hospital-acquired pleural infections, which are often the result of prolonged hospital admissions for other initial reasons, or complications following surgery or invasive procedures. Pleural infections and other pleural complications are common after lung transplantation. Other potential causes include direct (transdiaphragmatic) spread of abdominal sepsis, blunt or penetrating chest trauma, esophageal perforation, or rupture of a peripheral lung abscess into the pleural space. [Pleural effusion is a pathological accumulation of fluid in the pleural cavity that may occur as a symptom of primary pleural disease or, more commonly, secondary to pulmonary or extrapulmonary disease. Various pathogentic mechanisms are involved. Pleural effusion may occur in the presence of decreased oncotic pressure (e.g., hypoalbuminemia), increased pulmonary capillary pressure (e.g., heart failure), increased pleural leaflet permeability (e.g., pneumonia), and lymphatic obstruction (e.g., pleural malignancy) or reduced negative intrapleural pressure (e.g., atelectasis). Transudates are caused in 40 - 46% by heart, liver and kidney diseases. Exudative effusions on the other hand are mainly due to microbial (40 - 45%), malignant (20 - 30%) and thromboembolic causes (10 - 18%).] kroe1,2014 [If the protein concentration is less than 30g/l, the sample is a transudate. A predominance of neutrophils (above 50%) indicates bacterial pneumonia. A predominance of lymphocytes is typical of tuberculosis and malignant disease, but is also seen in other causes of chronic pleurisy. A mycobacterial culture is positive in about 30% of all tuberculosis patients.] ebm1,2015 Homeopathic additions: pew1,1904 Pleurisy is present in a large majority of cases and is inevitable when the pneumonic inflammation involves the lung surface. It usually appears early in the disease with quite copious exudation, peculiarly rich in fibrin. Other cases appear later during the course of the disease by extension of inflammation; these show less exudation. In pneumonia pleurisy can also develop on the opposite side of the affected by the pneumonia. In such a case with effusion care should be taken not to mistake it for a double pneumonia. Pathology mur1,2016 The evolution of a pleural infection can be divided into three stages, which may overlap with each other. The first, exudative stage is characterized by the rapid outpouring of sterile pleural fluid into the pleural space. Some of this comes from the interstitial spaces of the lung and some from the parietal pleura because of increased permeability. The pleural fluid will have a low white blood cell count and lactate dehydrogenase (LDH) level, together with a normal glucose level and pH. At this stage chest tube drainage is rarely required, and antibiotics alone should suffice. The second, fibropurulent stage evolves if bacteria invade the sterile exudative effusion. During this stage there is an accumulation of leukocytes, bacteria, and cell debris together with increased amounts of pleural fluid. Fibrin is then deposited over the visceral and parietal pleura, and there is a tendency at this stage for loculations to form within the pleural fluid, which may limit effective drainage of the effusion with a chest tube. The pleural fluid pH and glucose level will be lower, and the LDH level will rise, often dramatically. The final organization stage is characterized by aggressive fibroblast growth over the pleural surfaces to form an inelastic membrane called the "pleural peel." This is often extensive and reduces lung functionality considerably. The pleural fluid is often thick, consisting of pus and cellular debris. Primary empyema instead arises by direct translocation from the oropharynx or by hematogenous spread. In this circumstance, bacteria invade the pleural space as the initial insult leading directly to the fibropurulent stage. Classification Ed. The classification of pleurisy can be based on local (e.g., diaphragmatic pleurisy), temporal (e.g., acute or chronic pleurisy), etiological (e.g., tuberculous pleurisy), by its malignancy (e.g., malignant pleurisy) and according to the exudate (serous, fibrous, purulent). Since in homeopathic therapy the characteristics of symptoms and clinical signs are essential for the choice of the homeopathic remedy, the mentioned classification and its descriptions are layed out in the following. Symptoms bwax,1902 The symptoms usually depend on the type of effusion. Depending on the stage and cause of pleurisy, the effusion and thus the picture varies. Ed. 1. Dry Pleurisy Synonyms: Acute, plastic pleurisy, Pleuritis sicca, Fibrinous pleurisy Pain in the side is usually the first and most constant symptom. Accompanying or even preceding the pain there is a chill or chilliness; in some cases this is not marked. The pain in well developed cases is sharp and piercing, beginning at about the middle of inspiration and ceasing with the beginning of expiration. In some cases, especially in pleurisy of the apex and that accompanying pneumonia, the pain may be constant. The location of the pain will vary according to the portion of the pleura involved. It is usually felt in the axillary region, or below the nipple, but when the inflammation is at the apex of the lung it will be felt at the top of the shoulder or under the upper portion of the scapula. When the diaphragm is involved (diaphragmatic pleurisy Ed.), the pain is felt low in the back or in the abdomen, and is increased by pressure over the insertion of the diaphragm at the tenth rib. The pain is made worse by coughing and deep breathing. The patient assumes a position that protects the side most during motion. The face has a look of anxiety. The temperature is not high, usually from 100°F/37,8°C to 102°F/38,9°C; it may decline to normal after a few days and remain there during the course of the disease. The pulse is quickened, small, and may be irregular. [The characteristic pulse of pleurisy is small and tense, though it may be soft; heart-rate at 90 to 120/min. gccx,1902] The cough is dry, hacking and painful. There is but little or no expectoration, and the patient resists coughing. The respiration is slightly increased in frequency and is jerky. [There is some dyspnea, determined by the shallow respiration. gccx,1902] After three or four days the pain subsides leaving a feeling or soreness. The disease has a tendency to recur, or it may become chronic. Physical Signs Inspection. The patient is usually found in a position that restricts the movements of the diseased side. The respirations are increased in frequency and shallow. There is a limited movement of the affected side while the movement of the affected side while the movements of the sound side are increased. Palpation: Occasionally a friction fremitus is to be felt upon the affected side where deep pressure gives tenderness or pain. This is most marked at the tenth rib in cases of diaphragmatic pleurisy. Percussion: This does not give any information apart from the tenderness. Auscultation: This gives definite sign of this form of pleurisy - the friction sounds, which may be grazing, rubbing, or grating in character. They are heard both during inspiration and expiration, but most marked during the former. They may be increased by slight pressure with the stethoscope. The vesicular murmur is diminished on the affected side, owing to the restrained movements of the parts. Auxiliary Diagnostics Ed. In addition to symptoms analysis and clinical examination, the common imaging techniques such as ultrasound and x-ray are used for diagnosis, as well as laboratory examination of blood and exudate. 2. Sero-Fibrinous Pleurisy Synonyms: Pleurisy with effusion [Intensity: The pain varies greatly in severity. It may be only a feeling of soreness, later becoming acute. Or, from the onset it may be sharp and lancinating. Location: Usually the pain is referred to a spot outside the mammillary-line, in the fifth or sixth interspace. It may occur in other regions - beneath the sternum, under the clavicle, in the spinous fossa, or in the abdomen. gccx,1902] This is made worse by coughing, and deep breathing. In some cases there is no pain. Dyspnea is present in all cases when the effusion develops rapidly, while in those cases where it has appeared slowly there may be no dyspnea present even when the lung is completely compressed, except upon exertion. The patient usually takes a position upon the back, inclining slightly to the affected side. The temperature may not be above 102°F/38,9°C, and in some cases fever is absent. The pulse is quickened but not rapid. [Pulse: It is rapid; in quantity it is usually small and compressible; due tot pressure on the great vessels. Sometimes it is tense. Urine: Scanty and high-colored; when absorption begins, there is a great increase in quantity, with excess of chlorides. Gastro-intestinal: Anorexia; coated tongue; constipation. Rarely, nausea and vomiting. gccx,1902] Physical signs These vary with the amount of effusion present. With easy access to modern hospital- and intensive care nowadays pleuritic effusions are usually smaller until therapeutic amelioration sets in. Inspection: The patient seeks a position that will not interfere with action of the healthy lung, there are indications of cyanosis, and in some cases anemia and emaciation. The affected side may show enlargement and the lower intercostal spaces are wider than normal, but there is seldom any bulging and the respirations are increased in frequency. Dyspnea, while present all the time is increased upon exertion. The respiratory movement are restricted upon the side involved and correspondingly increased upon the healthy side. The apex beat of the heart is displaced to the opposite side from the effusion. Palpation: This shows the affected side to be enlarged and its movements restricted. The intercostal spaces are wider than normal, and in some cases they are filled out. Occasionally a sense of fluctuation is obtained by placing a finger upon an intercostal space and making gentle percussion upon the opposite side of the chest. The vocal fremitus is absent except along the lines of pleural adhesion, or when conducted from the sound side, and in the case of children, when it may remain for some time. The pulse is small, of low tension, rapid and often irregular. Percussion: This shows flatness over the effusion. The flatness may be found all over the affected side except in the upper portion of the interscapular region, where there is dullness due to the presence of the compressed lung. At times a vesicular-tympanitic note is obtained in the supraclavicular and suprascapular regions, the result of a vesicular emphysema. When the effusion is upon the left side it displaces the spleen downward and obscures the tympanitic note from the stomach. The liver dullness may extend as low as the umbilicus, while the area of cardiac dullness is also displaced. [Displaced Organs: Displacement of the heart, spleen and liver may be detected if the amount of effusion is great. gccx,1902] Skoda's Sign: When the upper limit of the fluid is at the third rib, in the infraclavicular space there is a tympanitic, or vesicular-tympanitic note, called Skoda's sign. It is from the compressed lung. It can be elicited behind, but is most evident in front. Williams' tracheal tone: Just below the inner end of the clavicle strong percussion elicits a high-pitched tympanitic note, which changes with opening and closing the mouth. It is from the trachea and large bronchi, the vibrations being transmitted through the compressed lung.) Auscultation: The vocal and respiratory sounds are absent over the effusion and are only feebly heard over the compressed lung in the interscapular region. At times, in cases of pronounced serous effusion, a whisper resonance can be detected; this is not present when the effusion is purulent. By auscultation the heart may be located when it is impossible to detect it by inspection or palpation. A systolic murmur may be heard over the heart which disappears with the effusion. Differential Diagnosis Ed.
Intercostal neuralgia - We use this term as a collective clinical term for various clinical condition of different etiology like fractures of ribs, pain after cured pleurisy, prolonged pain after thoracic surgery and many orthopedic conditions from simple blockage of vertebral joints, rib blockages to rheumatic diseases. 3. Empyema Ed. Synonyms: Purulent pleurisy, fibro-purulent pleurisy Empyema represents either primary suppuration or secondary colonization of the serous effusion in the pleural cavity and is always a very serious condition. The symptoms depend on the dimension of the empyema and differ from serous-fibrinous pleurisy mainly by a more or less pronounced septic state. [Empyema and/or pericarditis are seen in 5% to 30% of patients with group A streptococcal pneumonia; other complications include pneumothorax, mediastinitis, and bronchopleural fistula formation. The only classic nonsuppurative complication that follows S. pyogenes pneumonia is glomerulonephritis.] mur1,2016 In subacute or chronic forms night sweats, emaciation, anorexia, prostration, dyspnea are striking features of the disease, even if surgical interference is not resorted to, evacuation of the inflammatory pus may take place spontaneously: through the lungs (broncho-pleural fistula), chest-wall (Empyema necessitatis), or other structures. Therapeutic specifics mur1,2016 Surgical techniques such as video-assisted thoracic surgery have become widely available and can be offered to most patients if less invasive approaches are unsuccessful. As for empyemas caused by other pathogens [Ed. than group A streptococcus or S. pyogenes], drainage of empyema fluid is an important component of therapy. A complicated parapneumonic effusion is either located by ultrasonography or has a glucose level below 40 mg/dL or a pH below 7.2. ... Patients with pleural infection, particularly those with empyema who have had a delayed presentation, suffer the protracted catabolic consequences of chronic infection. A low albumin level has been shown to be a marker of poor outcome in one large published series. Addressing the patient's nutritional status at presentation is often overlooked and should be an early priority alongside tube drainage and the prescribing of suitable antibiotics. Early nutritional assessment should be seen as mandatory. Abnormal signs, symptoms, or blood test results in the context of a suggestive radiograph should lead to confirmation of the presence of an effusion and early sampling of the fluid. However, in a small retrospective series, Skouras and colleagues suggested that parapneumonic effusions less than 2 cm in thickness on chest CT scan can be treated with antibiotics without sampling because they are unlikely to become complicated or require intervention. Such patients would still require close monitoring and appropriate antibiotic therapy. Patients are usually referred for surgical intervention after initial medical treatment failed or if they presented late with highly organized empyemas that demonstrate significant pleural thickening and loculation. Practice varies, with some centers having an extremely low threshold for early surgery. The point at which medical management is deemed to have "failed" is necessarily ill defined, but one important indicator would be signs of ongoing sepsis despite attempted chest tube drainage and adequate antibiotic therapy. Another important consideration is the risk for long-term respiratory embarrassment without the removal of the fibrin and loculated fluid. The mortality of S. aureus CAP is generally higher than most etiologies, with the mortality in methicillin-sensitive strains about 30%. S. aureus CAP following influenza has a reported mortality of greater than 60%, even if not methicillin-resistant. [Therapy depends on the severity and type of effusion. Of course, in addition to the most individually appropriate homeopathic remedy and adequate nutrition, antibiosis and drainage may also be necessary.] Ed. Historical remarks on drainage mur1,2016 Open thoracic drainage remained the standard treatment for pleural infection until the influenza pandemic of 1919; however, there was a 70% mortality rate associated with this treatment. In 1918 the U.S. Army Empyema Commission was formed to address the problem. They noted that dogs with empyema died more often if treated with early open drainage rather than delayed intervention, and the commission recommended using the closed-tube drainage techniques described by Hewitt and Bulau. The commission's summary recommendations were: adequate pus drainage with a closed tube, avoidance of early open drainage, obliteration of the pleural space, and proper nutritional support. Endocarditis Endocarditis was - according to Paige pew1,1904 - a frequent complication in the USA in 19th century. Nowadays it is a rare complication in populations with good nutrition and sanitary surroundings. Risk factors for its occurrence are previously existing valvular disease or drug addiction. It is of malignant type and was formerly very often due to infection with pneumococcus [Ed. nowadays various infectious agents have to be taken into account!] and usually occurs in the left heart. Its discovery is difficult, as the physical signs are usually negative. It may be suspected with more or less certainty if embolism occurs, if sepsis appears, or meningitis is present. [If the endocardium becomes involved the pulse becomes irregular and the heart sounds become vague and obscure. The rhythm is disturbed. These are dangerous symptoms.] milx,1915 Peri-/Myocarditis In the 19th century pericarditis was a frequent, acute and serious complication of pneumonia in the USA, especially found in young people. The exudate is mostly fibrinous. There may be no local symptoms, owing to the preponderance of the pneumonia itself, but pain, rapid respiration and a feeble, accelerated pulse indicate the necessity of a careful investigation of the precordial region. [If pleurisy is close to the heart, distinction between the two diseases on auscultation can be difficult. glt2] Pulsus paradoxus can also occur in context with pericarditis. This is a sudden decrease of pulse-rate and blood-pressure on inhalation (>10mmHg) due to pericardial effusion. glt1,Dahmer,1988 [With an appropriate antibiotic (especially in cases with Streptococcus pneumoniae Ed.), a clinical response is usually expected within 24 to 48 hours. The onset of suppurative complications, such as purulent pericarditis, meningitis, endocarditis, arthritis, and cellulitis after initiation of therapy is uncommon in the modern era. The exception is empyema, which appears to be increased due to serotype replacement in the vaccinated populations by serotypes more often associated with empyema. Pneumococcal pneumonia remains a cause of septic shock and ARDS. Local or metastatic infectious complications also contribute to treatment failure. Metastatic infections such as endocarditis, arthritis, pericarditis, meningitis, or peritonitis can contribute to treatment failure and are more common in bacteremic pneumonia.] mur1,2016 Editors: In how far non-diagnosed endo- and/or myocarditis causes long-lasting weakness, dyspnea, and similar symptoms after pneumonia and/or severe respiratory infections (such as Long-COVID) seems an important question to us. If this is the case, certain homeopathic remedies with correspondence to these diseases may be valuable for curing these conditions. Severe generalized Bronchitis Generalized bronchitis may also arise in combination with lobar pneumonia, evidenced by the character of the cough, breathing and rales which are bilateral [also wheezing and slimy sputum might be present glt2]. This combination occurs especially with pneumonia following influenza and is a severe complication. [Resolution is delayed, emaciation and profound exhaustion are final signs.] glt2,2023 Sepsis with meningeal or encephalitic Irritation Symptoms [Meningitis ... usually appears during the height of the pneumonia, but may develop earlier or later. Its diagnosis during life is difficult, owing to the fact that in such cases it usually affects the convexity of the brain. It may be suspected in profound types of pneumonia, with delirium or coma and eye symptoms, paralysis, and bladder and bowel incontinence. [In certain cases it develops into Typhoid pneumonia (cp. Repertory), by which we mean the occurrence of symptoms peculiar to typhoid fever like low muttering delirium, sordes, etc.] dicx,1893 Hyperesthesia, increase of reflexes, irregular pulse, delirium increases, tonic-clonic spasms occur, and finally coma sets in. glt1,2023 In the 18th and 19th centuries cerebral and meningeal involvement during inflammations was often associated with high fever, headache, redness of eyes and face, intolerance of light and sound, watchfulness and delirium (Cp. Dunglison R., Dictionary of Medical Science, Blanchard and Lea, Philadelphia, 1860) The repertory rubric "Cerebral Pneumonia" refers to cerebral and/or meningeal symptoms during pneumonia. For further reference see the glossary and different sections in this book. Acute renal Injury and Exsiccosis Acute renal injury (former term - acute renal failure) according to the KDIGO (Kidney Disease: Improving Global Outcomes) criteria - is defined by increase of serum-creatinin within 48 hours and decrease of glomerular filtration rate (GFR) and/or reduction of urine for more than 6 hours. 19 In pneumonia it is mainly the pre-renal subtype. Acute renal failure in the course of pneumonia can have various reasons. The main reasons in this context are: the septic condition, exsiccosis, over-hydration and use of nephro-toxic drugs (e.g. NSAR's, Antibiotics like Penicilline, Beta-Lactamics, Vancomycin, etc.). The clinical signs and symptoms in acute kidney injury can be very mild despite the severity of the disease. Therefore, further examinations are necessary in case of suspicion. In addition, nausea, loss of appetite, renal sensitivity, oliguria, anuria, hypovolemia and hypervolemia may occur. If a patient shows signs of renal injury this indicates that the ambulant (homeopathic) treatment needs to show beneficial results quickly in order not to risk the patient's life. Otherwise the diseased needs comprehensive intensive care in a hospital. Correct assessment and management of fluid balance is a very important and difficult task - especially in intensive care - and is often neglected. This mistake can lead to a variety of avoidable complications during treatment! Especially patients on intensive care with pneumonia or other pulmonary issues often develop problems due to too much fluid supply. The following shows that the importance of kidney and liquid balance in the treatment of pneumonia was already obvious at the beginning of the 19th century. [The toxins and waste products of the inflammation should be eliminated as soon as possible. The kidneys are the best organs for eliminating these toxines and waste products so the utmost care should be taken to keep the kidneys in good condition. Kidney related symptoms are as important as lung symptoms and should be given equal rank.] ry2,1923 Editors: Also see the sections for urinary organs and urine in the repertory. Exsiccosis The symptoms of exsiccosis are thirst, oliguria (< 400ml/24h in adults), lack of perspiration, dry mucous membranes, increasing confusion, standing skin folds, prolonged recapilarization time and reduced blood pressure. It often occurs in infants and old people. This happens primarily if a patient has too little thirst (esp. with high fever) sometimes in combination with a pathological altered state of consciousness (e.g. delirum, unconsciousness, dementia, etc.). Therefore sufficient fluid supply is important for course and outcome of treatment during pneumonia. Thus lack of thirst is a very important symptom for assessment of homeopathic therapy. [The extent of dehydration is critical to treatment: in infants: mild 5%, moderate 10%, severe 15%; in children: mild 4%, moderate 8%, severe 12%, in adults: mild 3%, moderate 6%, severe 9%. Dry mucous membranes and oliguria are indications of mild dehydration. Weight loss can help estimate dehydration, as it largely corresponds to fluid loss in an acute illness. In combination with a cool periphery, reduced skin turgor and prolonged capillary refill time (> 2 seconds) are indications of moderate dehydration. The above symptoms, together with reduced blood pressure, deep, wheezing breathing and reduced general condition are signs of severe dehydration.] ebm1,2015 Together with pneumonia even moderate dehydration is a serious condition and should therefore be closely monitored. Hospitalization may be considered. Ed. Severe Icterus due to Liver-Involvement In homeopathic and general medical descriptions of the 18th and 19th centuries this liver-involvement received the name Bilious pneumonia (cp. Repertory). Signs like congestion and enlargement of the liver, and jaundice (conjunctivae, skin, other locations) during pneumonia pointed to this certain form. gccx,1902 Further symptoms could be diarrhea, pain in the abdomen, esp. in the region of the liver, or bile possibly present in the urine. See the clinical rubric "bilious pneumonia" and specific symptoms in the repertory and the Materia medica. Pulmonary Hemorrhage Pulmonary hemorrhage, also referred to as massive hemoptysis, is a potentially life-threatening condition involving bleeding from the pulmonary or bronchial vasculature. Therefore, it is of critical importance to provide rapid evaluation, stabilization, and definitive care of the patient. This involves first determining whether the bleed etiology is of gastrointestinal or pulmonary origin. Inspection of the upper gastrointestinal tract can localize the bleeding. Hematemesis is easily recognized by the black discoloration of the blood due to gastric acid. Intubation can protect the airway and preserve oxygenation and ventilation of the remaining functional lung. Modern bleeding therapy depends on the location and severity of the bleeding. It includes positioning (on the side of the bleeding), anti-fibrinolytic therapy by tranexamic acid, but also surgical interventions. In peripheral hemorrhage, bronchial artery embolization is the first-line treatment. If unsuccessful, surgical excision of the pulmonary area may be considered. In the case of bleeding from the central airways, bronchoscopy can localize and stop the bleeding. Most important causes for pulmonary hemorrhage are: Pneumonia/lung abscess, bronchiectasis, acute bronchitis, Tuberculosis (active and sequelae) and lung cancer. Symptoms: The onset of pulmonary hemorrhage is characterized by a cough productive of blood and worsening of oxygenation leading to cyanosis. Diagnostics: A Blood-cell count with differential should be drawn to evaluate hemoglobin and hematocrit and assess for thrombocytopenia. BMP should be drawn to evaluate for uremia as well as blood type and crossmatch and coagulation panel. A frontal chest radiograph should be obtained in an attempt to find a unilateral source. CXR can determine the site of bleeding 45 to 65% of the time and can determine the cause in 25 to 35%. If the patient is stable, CT can be considered to delineate source and etiology. CT may be more sensitive than bronchoscopy, and some sources consider it the first line in the evaluation. (Source: StatPearls - Pulmonary Hemorrhage - Brian Shee, Fatima Anjun, 7/2022) See the rubric in the repertory in chapter Chest. Ed. Pulmonary Edema Pulmonary edema as a complication of infectious lung disease results from damage to the capillary endothelium. Fluid initially enters the interstitium and leads to interstitial edema if the lymphatic vessels are overloaded. If the edema pressure becomes too high, the result is alveolar edema [which is seldom in pneumonia without heart disease Ed.]. In addition to a diffusion disturbance, the constriction of the vessels and the resulting increase in flow resistance also lead to a distribution disturbance of ventilation and perfusion. vau1,2015 On auscultation interstitial pulmonary edema sometimes can be heard as wheezing breathing sounds - in comparison to the coarse crackles or foamy sputum resulting from alveolar edema. The main reason for alveolar pulmonary edema during pneumonia is acute and/or chronic insufficiency either of the heart, the liver or the kidneys, or also from (iatrogenic) overload with fluids. Ed. [In alveolar pulmonary edema - in addition to the deterioration of lung function we can observe symptoms like coarse crackles [similar to the coarse crackles from pneumonic infiltration Ed.] ; watery, foamy sputum; quickly increasing dyspnea, cyanosis, and the patient feels the need to sit. Tracheal rales, especially combined with the inability to expectorate, usually portend death and indicate pulmonary edema. In cases of edema of lungs, sputum can be like prune-juice or brown like chocolate and foamy. glt2 Take care: In miliary tuberculosis we also find rusty sputum but without fibrin.] glt1,glt2,2023 Lung-abscess Murrey mur1,2016: Lung abscesses are pus-containing necrotic lesions of the lung parenchyma that result from aspiration of bacteria-laden secretions and show an air-fluid level. Lung abscesses are distinct from, and may follow, necrotizing pneumonia, in which multiple small cavities develop in contiguous areas of the lung. Lung abscesses must be distinguished from septic pulmonary emboli, which are often multiple and bilateral, involve the lower lobes, and are secondary to an endovascular infection. Unlike most other respiratory infections that are caused by single pathogens, lung abscesses are caused by mixed populations of bacteria. Secondary lung abscesses develop from congenital lung abnormalities, obstructing neoplasms, foreign bodies, and bronchiectasis. Lung abscess may also complicate pulmonary infarction, primary lung cancer (central carcinoma with necrosis), metastatic malignancies, and the necrotic conglomerate lesions of silicosis and coal miners' pneumoconiosis. Lesions in diseases such as granulomatosis with polyangitis (formerly termed Wegener granulomatosis) and rheumatoid arthritis with rheumatoid nodules may also mimic lung abscess. The clinical manifestations of lung abscesses are distinct from those of CAP, because they are usually prolonged in time (2 weeks to 3 months or more) and include fever, night sweats, cough with foul-smelling sputum, fatigue, weight loss, and sometimes hemoptysis. The typical appearance of a lung abscess on a chest radiograph is a thick-walled cavity with an air-fluid level. A contrast-enhanced CT is occasionally necessary to differentiate lung abscess from other conditions, and bronchoscopy may be needed to distinguish lung abscess from endobronchial carcinoma. mur1,2016 Indication for drainage: If the cavity is large (>8 cm), or if the abscess is due to pyogenic bacteria such as P. aeruginosa or S. aureus. CT-guided percutaneous transthoracic tube drainage or endoscopic drainage are alternatives to surgical resection; the reported success rates with both of these procedures are high, although no prospective controlled trials have been reported. Complications of CT-guided tube drainage include pneumothorax, pyopneumothorax, and bronchopleural fistula. After drainage, patients show clinical improvement usually in 48 hours. Persistent fever can also be seen if there is a secondary pleural empyema that requires drainage. mur1,2016 Diagnostical specifics: A pronounced rise of temperature to 102° or 104°F/38,9-40°C after defervescence (after 8th day) indicates that the disease has invaded a new lobe, or the occurrence of pleurisy, empyema, gangrene or abscess. pew1,1904 Take care: In pneumonia in infants with formation of abscesses due to Staphylococcus there also might be distension of the abdomen, hardly any peristalsis (sometimes leading to ileus) or atelectasis due to excessive sputum. On auscultation we find gurgling sounds if a lung abscess has developed. glt1,2023 Cases secondary to existing cardiac or renal disease are usually rapid and severe, with tendency to pulmonary edema, abscess or gangrene. In inebriates the symptoms are often masked by the cerebral manifestations; these cases usually have a low range of temperature and the prognosis is unfavorable. pew1,1904 We find gurgling sounds [Ed. on auscultation] if there is formation of lungs abscess. A recurrent rise of temperature after the 8th day is often a sign of formation of lung-abscess. gccx,1902 Gangrene of the Lung Pulmonary gangrene is a rare complication of severe pulmonary infection in which a pulmonary segment or lobe is sloughed. It is part of a spectrum of disease which includes necrotizing pneumonia and development of pulmonary abscess, processes in which lung tissue is devitalized. In the pre-antibiotic era, the term pulmonary gangrene was sometimes used to refer to multiple lung abscesses or necrotizing pneumonia. However, in more recent times, it has been used to describe sloughing of a large amount of lung tissue such as a segment or a lobe. The primary feature that sets pulmonary gangrene apart from necrotizing pneumonia and pulmonary abscess is the extent of necrosis and the fact that thrombosis of large vessels plays a prominent role in the pathogenesis. Pulmonary gangrene is usually "moist gangrene" associated with bacteria. Most frequently anaerobes are involved. Of course other microorganisms can also cause abscesses and necrosis. Ed. Mixed aerobic and anaerobic infection is usually a complication of macro-aspiration of oropharyngeal contents. mur1,2016 Anaerobic infections present as four different syndromes: chemical pneumonitis, aspiration pneumonia, anaerobic pleuropneumonia, or primary anaerobic empyema. mur1,2016 Anaerobic pleuropneumonia is characterized by necrosis and suppuration of lung parenchyma. Early in the course, imaging may demonstrate dense segmental opacification with multiple small lucent areas of lung necrosis (<2 cm in diameter), usually without air-fluid levels. In the absence of appropriate treatment, these lesions may evolve into a primary lung abscess and empyema. Patients commonly present with fatigue, low-grade fever, weight loss, and productive cough for several weeks after an episode of loss of consciousness. Approximately half describe putrid sputum, and some may have hemoptysis. Patients appear chronically ill and toxic, with temperatures up to 39° C/102,3°F. In some patients, a single lung abscess greater than 2 cm in diameter is detected in a dependent lung segment on radiography. The abscess may be multi-locular; occasionally, multiple abscesses are located in different lung segments. mur1,2016 Clinical Course: Uncomplicated aspiration pneumonia generally responds promptly to appropriate antibiotics. Fever resolves within a few days, and the chest radiograph normalizes within 3 weeks. Fever resolves more slowly in anaerobic pleuro-pulmonary infection. Closure of abscess cavities and resorption of empyema collections may require months. Fatality rates are low in adequately treated patients, except those with necrotizing pneumonia, in which mortality approaches 20%. Chronic lung abscess has been complicated by brain abscess, other metastatic abscess, secondary amyloidosis, life-threatening hemoptysis, bronchopleural fistula or empyema necessitans (rupture through the chest wall), but these complications are currently rare. mur1,2016 [A pronounced rise of temperature to 102° or 104°F/38,9-40°C after defervescence indicates that the disease has invaded a new lobe, or the occurrence of pleurisy, empyema, gangrene or abscess. Offensive expectoration or if "prune juice" in character, shows deterioration of blood and tissues, or possibly gangrene.] pew1,1904 Lung abscess and gangrene are often found simultaneously. The intense fetid odor and the characteristic stratification of the sputum are the strongest indications of this condition. Sometimes it is asymptomatic and is only found in the process of necropsy. osl1,1909 See also "Lung-Abscess" as well as the clinical rubric "gangrene of the lungs", and the specific rubrics for the above symptoms. Ed. Thromboembolic complications [Pulmonal embolism (PE) is the third most frequent cardiovascular syndrome with a global incidence of 39-115 per 100.000 population with an acute mortality rate of 34%. This sums up to about 300.000 deaths annually in the USA, for example. The strongest risk factors are age above 80 years, fracture of a lower limb, hospitalization for heart failure or atrial fibrillation, hip or knee replacement, major trauma, myocardial infarction, previous venous thromboembolism. Oestrogen-containing oral contraceptive agents are associated with an elevated risk, and contraceptive use is the most frequent risk factor in women of reproductive age. More specifically, combined oral contraceptives (containing both an oestrogen and a progestogen) are associated with an approximately two- to six-fold increase in risk over baseline. (Konstantinides S. et al, ESC Guidelines, European Heart journal, Volume 41/4, 1/2020, Page 543-603)] Kroegel 2014: Clinical symptoms associated with pulmonary embolism range from minor or barely perceptible discomfort to cardiorespiratory failure with sudden death, depending on the location of the thromboembolic event. Clinical symptoms Clinical symptoms are highly variable, and unremarkable physical examination findings do not rule out pulmonary embolism. A characteristic sign is sudden onset of respiratory thoracic pain caused by pleural involvement. Usually, this leads to a "respiratory blockade," which is perceived by the patient as an inability to take a deep breath or to breathe deeply. Other nonspecific symptoms such as restlessness, anxiety or trepidation, sweating, dyspnea, tachypnea, tachycardia, or tachyarrhythmia occur in varying intensity and combination. If the embolism is pronounced, signs of venous pressure elevation (prominent jugular veins, demonstrable hepato-jugular reflux, or hepatic pulsation) are found. In the early phase, auscultation remains unremarkable. However, as the disease progresses, peripheral localization allows auscultation of dry and moist accessory sounds that are due to alveolar exudate in the affected lung areas. Searing respiratory pain as a manifestation of pleurisy sicca may interfere with respiratory maneuvers during auscultation. An accentuated pulmonary valve closure sound may be heard above the heart. A pulmonary infarct may lead to secondary infarct pneumonia, pulmonary abscess, cavernous sinus, pneumothorax and hemothorax. Annotations by the Editors PE can also be a complication of pneumonia or vice versa. Definitive diagnosis includes laboratory diagnostics as well as instrumental measurements such as spiral CT, scintigraphy, ultrasound, and pulmonary artery angiography. Ed. Certain homeopathic remedies (like Am-c.) have shown a curative action on formation of blood-clots in the heart (also in the case of risk of pulmonary infarction). We could not find any clear clinical description of symptoms indicating this disease process, neither could we find valuable Materia medica or repertory-rubrics. Ed. Pneumothorax EBM1 2015: In case of pneumothorax, air accumulates in the potential space between the chest wall and lung parenchyma, decreasing the transmission of lower frequency sound vibrations of vocal fremitus. A spontaneous pneumothorax must be recognized and treated immediately. Consider spontaneous pneumothorax in case of acute chest pain and dyspnea (or increasing dyspnea) or worsening of these parameters in patients with chronic obstructive pulmonary disease. Chest pain and dyspnea are the main symptoms. Sudden onset of symptoms, which worsen on breathing and exertion, pain radiating to the ipsilateral shoulder, and coughing are further classical features. Attenuated breathing sounds, impaired thoracic mobility, and a hypersonoric percussion sound are also typical signs. (A small pneumothorax may be clinically unremarkable). Tachycardia, cyanosis, and hypotension occur in tension pneumothorax. In some patients, subcutaneous emphysema (crackling when pressure is applied to the skin) is found. A chest x-ray or sonography is required to confirm the diagnosis. A small pneumothorax can be difficult to find. An expiratory x-ray may be helpful. A large emphysematic bubble may look similar to a pneumothorax. Conservative treatment (follow-up with chest x-ray every 1-3 days) is possible for spontaneous pneumothorax if the following conditions are met: The patient is otherwise healthy. The patient has no dyspnea, and the air-filled space occupies less than half of the pleural cavity (maximum width is less than 3 cm) and does not increase in size on follow-up observation. Pneumothorax should decrease in size within 3-4 days and disappear in 2 weeks at the latest. Oxygen treatment may accelerate the resorption of air from the pleural cavity. If conservative treatment is not possible, active treatments such as aspiration or pleural drainage are the methods of choice. Take care - Pulsus paradoxus can also indicate pneumothorax. glt1,2023 Fibrosis of the Lungs Interstitial lung disease encompasses a broad spectrum of acute or chronic conditions associated with an inflammatory response and/or fibrosis of the lung parenchyma. The interstitium, endothelium, epithelium, alveolar spaces, and bronchioles may be involved. There are well over 100 different entities within this heterogeneous group of diseases. Differentiation requires laboratory findings, pulmonary function testing, HRCT, bronchoscopy with broncho-alveolar lavage (BAL), and possibly transbronchial biopsy in addition to medical history and clinical symptoms. kroe1,2014 Symptoms in patients with ILD (interstitial lung disease) are present for months to years and progress at varying rates. Several interstitial reactions are acute (days to several weeks). These are often confused with atypical pneumonias because they cause diffuse radiographic opacities and may be associated with fever. Included are acute interstitial pneumonia (AIP; Hamman- Rich syndrome), acute eosinophilic pneumonia, some cases of hypersensitivity pneumonitis, occasionally drug-related ILDs, some cases of organizing pneumonia, the diffuse alveolar hemorrhage syndromes, and the acute immunologic pneumonias seen with connective tissue diseases. mur1,2016 Cryptogenic organized pneumonia (COP) mur1,2016 Organizing pneumonia (OP) can be cryptogenic (i.e., COP) or result from various forms of lung injuries (e.g., postinfectious, drug related, connective tissue disease related, posttransplant, hypersensitivity pneumonitis, radiation, or aspiration of particulate matter). COP is a specific clinical pathologic syndrome characterized by a "pneumonia-like" illness, with excessive proliferation of granulation tissue inside the alveolar spaces associated with chronic inflammation in the surrounding alveoli. The pathologic process may also involve the small airways (bronchiolitis obliterans with organizing pneumonia [BOOP]). There are no major differences in clinical features of COP and secondary OP. OP may also be seen accompanying other histopathologic patterns (e.g., UIP). The diagnosis of COP is reserved for isolated OP in patients without an identifiable associated disease. The term idiopathic BOOP historically encompassed COP but is no longer recommended for this idiopathic condition. The incidence of COP is similar in both men and women. The mean age at presentation is about 50 to 55 (range, 21 to 80). Patients with COP are frequently specific about the timing of their disease onset. This is because the disease onset is recent (usually < 2 months) and is often dramatic, with the development of a flulike illness characterized by cough, mild dyspnea, fever, malaise, fatigue, and weight loss. Physical examination usually discloses focal sparse crackles but may be almost normal. Finger clubbing is rare. Routine laboratory studies are nonspecific. A leukocytosis without increase in eosinophils is seen in approximately half the patients. The initial erythrocyte sedimentation rate is frequently elevated in patients with COP. [In cases where resolution is slow, a proliferation of the connective tissue of the alveoli takes place, with a fibroid overgrowth of the septa, resulting in a contraction of the lung tissue which is known as Secondary Fibrinous Pneumonia.] bwax,1902 Bronchiectasis Bronchiectasis is the irreversible dilatation of the bronchi. This widening of the bronchi leads to chronic putrid bronchitis with destruction of the peripheral airways, which may exacerbate intercurrently. kroe1,2014 Bronchiectasis can be both a cause and a complication of pneumonia, bronchitis, and pertussis. In addition to cough, dyspnea, and hemoptysis, also crackles occur as normal auscultation findings. Sometimes an expiratory wheeze can be detected. A peribronchial striation or honeycomb pattern may be seen on chest x-ray. High-resolution CT will either confirm or invalidate the suspicion. Clinical experience shows positive effect of physiotherapeutic treatments such as "positional airway drainage". ebm1,2015 On auscultation you can hear medium to coarse bubbly, moist sidetones in bronchiolo- or bronchiectasis. glt2,2023 Atelectasis Atelectasis is a complete or partial collapse of the entire lung or area (lobe) of the lung. It occurs when the tiny air sacs (alveoli) within the lung become deflated or possibly filled with alveolar fluid. Causes: Atelectasis is one of the most common breathing (respiratory) complications after surgery. It's also a possible complication of other respiratory problems, including pneumonia, lung tumors, chest injuries, fluid in the lung, cystic fibrosis and respiratory weakness. You may develop atelectasis if you inhale a foreign object. Atelectasis can make breathing difficult, particularly if you already have a lung disease. There may be no obvious signs or symptoms of atelectasis. Possible signs and symptoms may include difficulty of breathing, rapid, shallow breathing, wheezing and cough, possibly attenuation of percussion with absent breathing sounds. Treatment depends on the cause and severity of the collapse. ◄ THE PATHOGNOMONIC COURSE AND SYMPTOMS | ▲ | DIFFERENTIAL DIAGNOSIS OF PNEUMONIA ► |