Community-Acquired Pneumonia in Adults

Recommendations of an International Expert Commission

Introduction

Community-acquired pneumonia (CAP) is one of the most important infectious diseases worldwide. The high mortality risk (median approx. 8–12%) of all patients is strongly dependent on the age of the patient and existing concomitant diseases (range 0%–50%).

In integrative medicine there is a wealth of individual experience in reducing the use of antibiotics through applying the therapeutic concept of Anthroposophic Medicine presented here. Due to Anthroposophic Medicine’s more complex view of patients, there are possibilities which allow the focus on antimicrobial therapy to be evaluated differently than is currently the case in pneumonia guidelines. Anthroposophic Medicine takes more into account the importance of the microbiome and the organism’s immune response to the disease process.

In this approach also it is known that various healthcare problems (e.g., stemming from resistance and societal aging) in the treatment of pneumonia are still unsolved. For example, further research on the detection of high-risk patients requiring inpatient and intensified care is still underway. Likewise, knowledge about risk stratification of the correlation between pneumonia and pre-existing chronic concomitant diseases is constantly increasing. Nevertheless, the increasing prevalence of antibiotic-resistant bacterial pathogens means that problems with treatment can be expected to grow in the future. Steadily rising societal aging is also of great importance for the prognosis of community-acquired pneumonia, because the risks of a severe and life-threatening course increase steeply with increasing age (1). In addition, the presence of a disturbed immune response – e.g., immune defects, drug-induced immune suppression) as well as chronic concomitant diseases (diabetes mellitus (2), structural lung diseases (3), tumor diseases (4) – is of great importance for mortality. Conversely, younger patients with unrestricted organ function and no comorbidities have more favorable prognostic conditions (5).

The main clinical symptoms of pneumonia are: 

  • respiratory complaints such as coughing, dyspnea, breath-related thoracic pain
  • general symptoms (“malaise”) such as myalgia and arthralgia, cephalgia, palpitations, circulatory problems, diarrhea
  • neurological symptoms like disorientation (confusion)

In addition to clinical examination (including auscultation of the lungs), the main diagnostics used are imaging diagnostics (chest X-ray or thoracic sonography) to determine:

  • (inflammatory) infiltrates in the lung tissue, including their extension and localization, and laboratory chemical diagnostics and evaluation of biomarkers:
  • C-reactive protein (CRP),
  • Leucocytes
  • Procalcitonin (PCT)

It should be noted that diagnostics in primary care is often a major challenge. Differentiation between deep respiratory tract infections (bronchitis) and pneumonia is often difficult to impossible to determine in everyday care. Currently, CRP and PCT determinations and chest X-rays are recommended. However, CRP discriminates poorly between lower respiratory tract infections and pneumonia, and PCT and X-ray diagnostics are not widely available in ambulatory care.

Central to risk stratification as the starting point for all therapy considerations is a clinical evaluation of lethality and risk (6, 7). 

Over the last decades, risk assessment strategies for community-acquired adult pneumonia have been further specified and simplified. In particular, CRB-65, a clinical score that can be used to estimate the severity of CAP (see Section 1.a.), has been the basis for the decision on whether to recommend outpatient or inpatient treatment (1, 8, 9, 10, 11, 12, 13, 14). Healthy adults up to 65 years of age have a low mortality risk of 0.6%.  Patients with pre-existing conditions, on the other hand, are much more likely to suffer from lethal complications (15). A major risk factor is the patient’s age. Due to the expected increase in the proportion of elderly in the population (65–95 years), the expected proportion of community-acquired pneumonia with lethal outcome will increase (1). According to WHO estimates (2020), three to four million people worldwide currently die from community-acquired pneumonia every year. Epidemiologic data in this area are often based on estimates (16, 17, 18). According to the data on community-acquired pneumonia, countries like Germany, with 83 million inhabitants, show a frequency of 0.5 million cases per year, i.e., approx. 600 per 100,000 inhabitants. Of these, 50% were hospitalized with mortality rates of 0.6% in non-comorbid patients and 10% in elderly and/or comorbid patients (19). From this large variance in the fatal course of the disease, it is clear that the real challenge in managing the disease is risk assessment and severity determination. This is defined in national and international guidelines according to the current state of knowledge in regional structures (20, 21, 22)

1. Severity assessment and therapy decision

a. Lethality and risk assessment

Identification of patients with a low risk of lethality (lethality assessment) can be easily achieved with CRB-65 scores, which have been evaluated in studies (15). The results show that a lethality of 0% is to be expected with a score of 0, a lethality of 6% with a score of 1–2, and a lethality of 23% with a score of 3–4 (11).

CRB-65

  1. Clouding of consciousness (C= confusion)
  2. Respiratory rate >/= 30/min (R = respiratory rate)
  3. Diastolic blood pressure </= 60 mmHg or systolic blood pressure < 90 mmHg (B = blood pressure)
  4. Age >/= 65 years (age in years)

While the CRB-65 allows reliable prediction for patients between 18 and 65 years of age, the fact that the index is not or has not been sufficiently evaluated in older patients must be considered as a limitation of this approach. Older patients therefore need further, greater attention than the age group of 18 to 65 years (23, 24, 25, 26). The most important evaluation criterion for this age group is mobility. The high-risk group consists of patients who are chronically bedridden (23). According to epidemiologic models, the age structure will couple with an increase in older ill patients, leading to an increase in vitally threatening pneumonia. The aging of society is expected to lead to a 50% increase in inpatient CAP and an increase in mortality of about 80% (i.e., from 10% to 18%) by 2050 (27).

Whether a higher probability of a severe to lethal course of this disease is to be expected (risk assessment) is currently determined by the organ dysfunctions present at diagnosis. Respiratory insufficiency and extrapulmonary organ dysfunction must be recognized and taken into account (15).

Patients who have a CRB-65 score of 0 and an oxygen saturation of >90% and no evidence of (relevant) comorbidities can and should be treated as outpatients. Despite the presence of inflammation of the pulmonary interstitium, a mortality rate of 0% is to be expected in this patient group as described above (1). For this group of patients we particularly recommend that the concept of anthroposophic therapy without antibiotics be considered (see Section 3).

For patients with organ dysfunction, more precise risk stratification should be undertaken (“sepsis bundle”) and adequate and calculated antimicrobial therapy should be started promptly (15).

Irrespective of the severity assessment, a differential diagnostic distinction from other diseases (such as pulmonary embolism, interstitial lung disease, lung carcinoma, aspiration, cardiac decompensation) should be made each time pneumonia is diagnosed.

b. Pathogens (risk stratification)

Currently, the authors of the guidelines for community-acquired pneumonia recommend an initial calculated antimicrobial therapy focused on the suspected pathogen, independent of any differentiated lethality and risk assessments and risk stratification to be performed. The therapy should be started within a maximum of 8 hours (for hospitalized patients). The probability that a bacterial pathogen will be present is classified as significantly higher (60–100%) than with primary viral pneumonia (0–40%) (15, 28, 29, 30). Primary viral and then secondary bacterial pneumonia occur less frequently in outpatient care than in inpatient care: bacterial coinfection is described in outpatient care with a frequency of 10–15% and in inpatient care with about 25% (31). One study showed that mortality was significantly increased after primary viral and secondary bacterial pneumonia (28, 15). Approximately 40% of primary bacterial pneumonias are Streptococcus pneumoniae (most common pathogen). Gram-negative cocci, Mycoplasma pneumoniae, Hemophilus influenzae, Coxiella burnetii, Klebsiella pneumoniae are rarer, as are Pseudomonas aeruginosa, Escherichia coli and others. Guidelines provide recommendations on the choice of antimicrobial therapy in consideration of regional resistance profiles, the presence of comorbidities and the estimated severity of the pneumonia.

Comorbidities are assessed in the form of three-class risk stratification (15):

  • Mild pneumonia (CRB-65 = 0, normal or compensated oxygenation, oxygen saturation minimum 90%, no decompensated comorbidity)
  • Moderate pneumonia (neither mild nor severe)
  • Severe pneumonia (acute respiratory insufficiency and/or severe sepsis or septic shock and/or decompensated comorbidity).

These statements on pathogens are based on projections of the evaluation of health care research in evaluation practices and clinics, as documented in health care research networks such as CAPNETZ or by the Robert Koch Institute. Considerable fuzziness must be taken into account in such evaluation. With the COVID-19 pandemic, scientific attention to viral pneumonia and the associated methodological difficulties have been put into a completely new light in public, political and scientific evaluation. It is expected that the genesis of viral and possibly other microbial pathogens of community-acquired pneumonia will be reassessed in the future as a consequence of the COVID-19 pandemic.

An increasing problem is the growing number of resistant and multi-resistant pathogens (MRE). In pneumonia, these include in particular MRSA (methicillin-resistant Staphylococcus aureus), ESBL formers (extended spectrum ß-lactamase formers) and Pseudomonas aeruginosa. The procedure, escalation and de-escalation strategy and the duration of therapy should be controlled by antibiotic stewardship because of the resistance problem. Various country-specific programs and their review are underway. Recommendations on the type and timing of oxygen substitution, ventilation, supportive therapy and procedures for treatment failure and complications will also be redefined. From these measures it becomes clear that exclusive and probatory, calculated antibiotic therapy is increasingly being evaluated critically, also in modern infectiology. New therapeutic concepts are being discussed (see notes on this in Section 4). Our concept (Section 2) wants to make a contribution to this.

c. The “host” (individual immune competence)

The treatment of “the host” itself, i.e., the disease-transcending immunity of the individual patient, does not make sense today beyond risk assessment in the opinion of guideline authors. In particular, there is a lack of studies justifying the influence of medications on patient immunity.

Since the beginning of scientific infectiology, such evaluation of “the host” has been controversial. For example, in 1892, the physician Max von Pettenkofer wanted to prove to the scientific community and to Robert Koch that pathogens have little and the host has decisive importance in treating epidemics (the Hamburg cholera epidemic at that time) and infectious diseases, by means of a self-experiment involving the ingestion of a suspension of cholera bacteria (33). Pettenkofer survived that public self-experiment with mild general symptoms. However, scientific evaluation of the significance of pathogens did not change.

The situation was similar with infection prophylaxis (34). Great discoveries like those of Ignatz Semmelweis were ignored by leading physicians such as Rudolf Virchow, although Semmelweis (without any recognition during his lifetime) was able to prove through his observations in 1847 that the mortality rate of childbed fever at that time could be reduced from 30% to 2% if obstetricians disinfected their hands.

Rudolf Steiner, in his 1920 lectures to inspire a spiritual approach to medicine, also pointed to the possibility and potential reasonableness of doctors acting between merely accompanying the spontaneous course of an infectious disease, intervening medically and influencing the course of the disease (35). His proposals to intervene in the infection process and treat the disease with herbal and potentized medicines, as well as with physical therapies, emerged at a time when targeted antimicrobial therapy was not available and the mortality rate of pneumonia was about 30%. Nevertheless, his ideas open up a field of treatment that has been shown by numerous expert observations to be an effective way to treat community-acquired pneumonia, even though systematic prospective clinical studies on these recommendations have not yet been conducted.

Since the production of synthetic antibiotics, the treatment of pneumonia has focused almost exclusively on bacterial pathogen control.

In the last 20 years, the importance of the microbiome of the intestines and lungs and its relation to human immunocompetence has been discovered and further researched, which raises questions about previous assessments of using only an antimicrobial approach to therapy.

2. Principles of therapy with a focus on sustainability and integrative aspects

Our therapeutic principles take into account the person’s warmth organism, respiration, fluid organism, as well as their age and individual circumstances (e.g., weakened physical organization, pulmonary or other previous illnesses). 

a. Warmth: Warm drinks, external applications (compresses)

Insufficient warmth generation and distribution within the human organism weakens the person’s immune system and thus the ability to self-regulate. The compresses described below (see Section 3.a.) and suitable warm drinks (Section 3.d.) support the person’s warmth organization and enable positive regulating handling of their fever. Symptomatic fever reduction with antipyretics has an unfavorable effect on both the immune system and self-regulation (see 3.g. fever).

b. Respiration: Inhalations, mucus solutions, external applications, respiratory therapy, oxygen administration

Respiration is centrally affected in pneumonia and can be supported with compresses (see 3.a.), as well as with inhalations, mucus solutions and respiratory therapy. In severe cases, additional oxygen is administered nasally and in cases of respiratory insufficiency, the indication for mechanical ventilation must be weighed on the basis of the overall situation. Good experience exists in Anthroposophic Medicine with the inhalation of bitter substances, which support the immune system in the respiratory tract and also have a slight broncho-dilatory effect (see 3.b.) (36).

c. Cardiovascular: Medication, volume administration

In pneumonia, it is not only the rhythmic organ of the lungs but also the cardiovascular system as another part of the rhythmic system that is burdened by tachycardia in case of fever or inflammation-related hyperemia. Therefore, the cardiovascular system is always co-treated with anthroposophic medicines to balance the excessive inflammatory forces from the metabolism (see 3.g.).

d. Fluids: Sufficient fluid intake in case of fever, for mucus dissolution, and to stabilize the circulation.

Sufficient fluid intake is indicated in the acute inflammatory phase with fever, sweating and secretion formation, with danger of exsiccosis and associated clouding of consciousness and circulatory instability (see 3.d.).

e. Immune defense: Nutrition, microbiome

Nutrition, avoidance of noxious substances and careful handling of the microbiome contribute to supporting the immune system and self-regulation, in addition to adopting a regulating approach to fever. (see 3.e.).

f. Social and biographical aspects: Social and psychological stress situations can play a significant role in patients with pneumonia. In this sense, pneumonia can be a biographical turning point and it is worthwhile to address such situations with the patient in a relaxed manner (see 3.f.).

3. General recommendations for therapy

a. Warmth: To improve warmth regulation

Ginger thorax compress: 1 x daily for 3–5 days

in case of fever below 39°C (102.2°F), for patients with weak warmth formation, for those with pre-damaged lungs. The compress has a deep and long-lasting warming effect
For instructions, see: https://www.pflege-vademecum.de/ingwer.php   

Mustard thorax compress: 1 x daily for 1–5 days in case of hypoxemia and fever below 39°C (102.2°F) and if the person’s general condition is adequate, or for spastic respiration, also in cases of pleuritis. Mustard essential oils irritate the skin and quickly lead to hyperemia and warmth development / burning in the skin area, therefore only apply these compresses briefly (a few minutes).
For instructions, see: https://www.pflege-vademecum.de/senf-thorax-wickel.php

Thorax compress with yarrow tea or yarrow oil extract : 1 x daily

in the acute-subacute phase (from day 3) in cases of extensive infiltrates, interstitial pneumonia, in the stage of hepatization with abundant fluid accumulation in the lungs. This compress strengthens the structural forces for healing the inflammation after the first 3 days of illness.
For instructions, see: https://www.pflege-vademecum.de/sg-luw.php

Farmer’s cheese (quark) thorax compress (low-fat farmer’s cheese, warm!) 1 x daily for 3–5 days initially, with temperatures above 39°C (102.2°F), leave on the thorax until the curd crumbles. It has a calming effect.
For instructions, see: https://www.pflege-vademecum.de/qbw.php

Salt compresses or salt washes (saturated saline solution): 1 x daily after the fever has gone down.
CAUTION: All of these compresses also relieve the patient’s breathing. Use only if the person’s skin is intact. Pause for a day if there is reddening due to the ginger or mustard in the previous day’s compress.

b. Respiration:

Steam inhalation with chamomile flowers: to mobilize secretions

Optional

inhalations with NaCl 0.9% (2 ml) and Gentiana lutea 5% dil. WELEDA: 5–10 drops 1–3 x daily.

Respiratory therapy: to mobilize secretions and facilitate breathing.

Oxygen administration: for in-patients as needed.

c. Heart/Circulation

Cardiovascular support is very important in the anthroposophic therapy concept for pneumonia, e.g., for inflammation-related hyperemia, tachycardia in fever). Studies prove the cardiovascular stress reaction in community-acquired adult pneumonia (37, 38).

d. Fluid intake

Warm drinks with warming, expectorant substances such as lime blossom, elderflower, ribwort, fennel seed, thyme tea, with lemon and a little honey.

e. To support immune defense

Nutrition: Patients mostly experience inappetence in the acute phase of pneumonia; so easily digestible food (e.g., light porridge with millet flakes, not-too-thick oat gruel with little salt, light bouillon of fresh, non-flatulent vegetables, steamed carrots, boiled potatoes, rice, cooked apples). Refrain from raw foods (too hard to digest) and sweets.

Noxae: Abstain from smoking and alcohol.

Microbiome: If possible, avoid antibiotics in the anthroposophic therapy concept, taking into account your assessment of lethality and risk (see Section 1.a.). The microbiome can be supported by probiotics such as lactobacilli. If antibiotics were used, sauerkraut (also as juice) can be taken during convalescence to regenerate the microbiome. 

f. Biographical and social factors

Pneumonia often occurs in the first or last phase of life and has a high mortality rate especially at the end of life. However, it also often occurs in people who are in a decision-making phase in their lives, either in their families or at work. These patients then begin to reflect on where relief – from stress, conflicts – or other changes may be necessary. Seen in this light, pneumonia can be the trigger for a conscious biographical step in life or can be decisive, especially for elderly people at the end of life.

g. Medication

Basic therapy according to the principles of Anthroposophic Medicine to support the organism’s regulatory resources includes ferrum preparations, Pneumodoron® 1 and 2 (also available as Aconite/Bryonia and Phosphorus/Tartarus Stibiatus drops), and Cardiodoron® (also available as Onopordon comp. A). Ferrum preparations are used to regulate the iron process in respiration and support the immune system, Pneumodoron® 1 and 2 regulate excessive metabolic processes in the stage of attack with hyperemia in the pulmonary capillary area, and exudate formation (alveoli, pleura) and secretion formation in the bronchial area. Cardiodoron® supports the cardiovascular system.

For treatments without a calculated administration of antibiotics, the patient should be carefully monitored medically, clinically and with regard to the disease development as measured in biomarkers (e.g., CRP). Careful assessment of lethality and risk, as well as participatory therapy decisions are recommended with regard to the critical evaluation of guideline recommendations for the use of calculated antibiotic therapy. Treatment with anthroposophic medicines eliminates the risks and undesirable effects of antibiotics (e.g., disruption of the microbiome) and antipyretics. In case of insufficient response during therapy, calculated antimicrobial therapy is recommended.

In cases of severe pneumonia, or with multimorbid and/or immunosuppressed patients, the indication for antibiotic treatment is given at the outset, but supplemented with anthroposophic medicines to improve the course of the illness.

  • Pneumodoron® 1 dil. (Aconite/Bryonia drops) WELEDA: 20 drops p.o. 4 x/d for 7–14 days at 1 to 2 hour intervals alternately with
  • Pneumodoron® 2 dil. (Phosphorus/Tartarus Stibiatus drops) WELEDA: 10–20 drops p.o. 3–4 x/d for 7–14 days (after fever has gone down last dose not after 6 p.m.)
  • Ferrum metallicum praep. D8 amp. WELEDA: 1 ml i.v. or s.c. in the morning daily for at least 7 days

or

  • Ferrum phosphoricum D8 amp. WELEDA: 1 ml i.v. or s.c. in the morning daily for at least 7 days

or

  • Pulmo/Vivianit comp. amp. WALA: 1 ml i.v. or s.c. in the morning daily for at least 7 days (if injection not possible, then sublingual)
  • Cardiodoron® amp. or dil. WELEDA: 1 amp. s.c. 1–2 x/d or 10 drops 3 x/d

Composition of the German medicinal products mentioned: Pneumodoron® 1: Aconitum napellus (monkshood) dil. D2, Bryonia dil. D2. Pneumodoron® 2: Phosphorus dil. D4, Kalium stibyltartaricum (Tartarus stibiatus) dil. D2. Pulmo/Vivianit comp.: Bryonia cretica ferm 33b dil. D5, Pulmo bovis Gl dil. D16, Tartarus stibiatus dil. D7, Vivianit dil. D7. Cardiodoron®: Liquid extract from fresh cotton thistle flowers (Onopordum acanthium, flos recens), liquid extract from fresh henbane (Hyoscyamus niger, herba recens).

In case of pleurisy:

  • Bryonia/Stannum amp., pilules WALA: 1 ml. s.c. 1–2 x/d for 3–5 days, then 10 pil. 3 x/d p.o. for 10 days

To stabilize the patient’s circulation, in addition to Cardiodoron®:

  • Camphora D3 amp. WELEDA: 1 ml. s.c. 1–3 x/d (for chills, cold feeling)

or

  • Camphora D1 dil. WELEDA :10–15 drops p.o. 3 x/d up to 2 x/h

For fever:

As a rule, fever should not be lowered; if necessary, support the process with hot water bottles during the initial warming phase. Exceptions: e.g., comorbid patients, patients with heart failure, very old patients

  • Argentum metallicum praep. D30 amp. WELEDA: 1 ml. s.c. 1–3 x/d

or

  • Argentum metallicum praep. D30 trit. WELEDA: 1 saltspoon (~¼ tsp.) 1 x/d at night

together with

  • Carbo Betulae D30 amp. WELEDA: 1 ml. s.c. 1–2 x/d (also effective for breathing difficulties)

For fever and fever regulation: see also https://www.anthromedics.org/PRA-0815-EN  

In case of impending sepsis (only inpatients)

  • Quarz D12 amp. WELEDA: 1 ml. s.c. 1 x/d

together with

  • Lachesis D20 amp. WELEDA: 1 ml. s.c. 1 x/d

In case of imminent and existing multiple organ failure (only inpatients):

  • Stibium metallicum praep. D6 amp. WELEDA: 10 ml. i.v. as a perfusion over 24 hours

and

  • Carbo Betulae D30 amp. WELEDA: 1 ml. i.v. 1–2 x/d

h. Convalescence

An average of 4 weeks is expected before complete recovery of the patient’s general condition (the residual infiltrates are radiologically detectable for 4–6 weeks). Therefore, even after the acute phase of the disease has subsided, continued sick leave is indicated, depending on the severity of the clinical course, and follow-up treatment to heal the pneumonia (structuring and reorganization of the inflammatory processes).

Follow-up medication for 1 month:

  • Ferrum rosatum D3/Graphites D15 dil. WELEDA: 15 drops p.o. 2 x/d

as an alternative:

  • Roseneisen/Graphit (Rose Iron/Graphite) pilules WALA: 10–15 pil. p.o. 2 x/d

or

  • Prunuseisen pilules WALA: 10–15 pil. p.o. 2 x/d 

or

  • Prunuseisen amp. WALA: 1 ml. s.c. 1 x/d
  • Cardiodoron® dil. WELEDA: 10 drops 2–3 x/d to support circulation (if required)

After the acute inflammatory phase, the patient’s lungs and breathing can be strengthened by eurythmy therapy or therapeutic speech therapy, or singing or music therapy.

4. Adult pneumonia (CAP) from an anthroposophic perspective

General condition

The clinical course of community-acquired pneumonia is impressive because of the severe impairment of the patient’s general condition within a short time. In the view of Anthroposophic Medicine this assessment is more comprehensive and also takes into account the patient’s constitution, susceptibility to the pathogen, individual disposition, self-regulation and biographical situation.

Phases of the illness

The phases of illness and their various pathological processes are also reflected in the response and resilience of “the host” in the concept of Anthroposophic Medicine (39, 40). In the first phase of the disease, the hyperinflammatory reaction (41) associated with endothelial hyperpermeablility of the lung parenchyma (40, 42) forms the starting point for anthroposophic therapy. The substances Bryonia and Aconitum napellus in potentized form play a leading role here (see Section 3). These substances are used to modulate the inflammatory response and improve pulmonary barrier function. The person’s metabolic functions are no longer mastered and controlled by regulatory processes of the organism, which is expressed in disturbed warmth regulation, as well as a barrier disturbance in the lungs, i.e., the healthy relationship between aeration (ventilation) and blood circulation (perfusion).

A further aspect of the first phase is to support the interaction of the body with the air and fluid functions in the lungs. Therefore, for example, it is important to ensure that the patient is appropriately positioned: to determine whether the ratio of air (aeration) and fluids (edema, infiltrate) in consideration of the force of gravity (physical) is beneficial or is impeding the healing of the inflammation.

Oxygen substitution and respiration

In this first phase of the disease, the principle of “relieving the organism” must be decided upon. For example, whether a substitution by enriched oxygen in the inhalation air is to be understood as medication and up to which point in time autoregulation of the organism (tachypnea) would result in a more favorable course without this admixture, because autoregulation can then be activated more optimally. Various pathophysiological models are available. It is unclear at what point hypoxemia negatively influences the course of the disease and whether transient hypoxemia can even be beneficial for regulatory processes. When using machine ventilation, it is important to consider how mechanical stress can best be avoided. On the other hand, the time of providing relief must not be missed. This includes participatory decisions on the measures to be taken with the patient and, if necessary, the relatives. 

Second phase

In the further course of the disease, the patient’s cardiovascular stress response must be assessed in terms of blood thrombogenicity, myocardial demand (especially right heart strain), and the right-left shunt (ventilation-perfusion mismatch) caused by edema and pulmonary infiltration. The occurring induction of apoptosis processes and the strength of the humoral and lymphocytic immune response of the organism can lead to healing and subsidence of the inflammation, or lead to a prolonged course. Here the support of cardiovascular function and the immune system (guidance and interaction) is an important part of the therapy (Cardiodoron®, Carbo Betulae, Camphora, see Section 3).

The role of antibiotics

The potential of the pulmonary local antimicrobial effects of antibiotics should be weighed against the irritation of the intestinal lung axis of the microbiome by this very therapy, as this in turn influences the organism’s autochthonous immune response. The hyperthermia (fever) accompanying the inflammation should be used and guided therapeutically, but not suppressed. For this purpose, potentized iron and phosphorus preparations are used in Anthroposophic Medicine (see Section 3). They can also be used to therapeutically regulate the body’s own immune stimulation – through interferons, interleukins, colony stimulating factors and inflammatory processes by tumor necrosis factors, as well as the reactions of the organism described as a “cytokine storm” (43, 44). The sole eradication of pathogens with antibiotics, as well as additional substitution of catecholamines (in cases of severe disease progression), should be supplemented by supporting the organism’s regulatory forces. Another aspect of therapy is to treat ineffective or exhausting ventilation. Here, the associated mechanical stress (patient self-inflicted lung injury (P-SILI)) can not only be treated by appropriate ventilation techniques, it can also be treated protectively by strengthening the compliance and resilience of the tissue. External applications (see Section 3) and rhythmical massage therapy are used for this purpose in the concept Anthroposophic Medicine. This becomes particularly important during threatened hardening of the inflammation (consolidation, fibrosis) to support the elasticity and lightness of the organ as a physical expression of immanent forces of the lung parenchyma.

To summarize, we can state: The inner core of our understanding of pneumonia is less about the physiology and mechanics of breathing; it is about a “wound” in the alveolar parenchyma, with its metabolic functions (40).

The diffuse alveolar damage can be understood as a “wound” in the lung tissue, in which a healing effect can be considered, as in a skin wound. For skin wounds, the principles of “cleansing, protecting and allowing time for healing” apply. This can be seen in a similar way for “wounds” of pneumonic infiltration. The interaction between intestinal and lung microbiome should also be taken into account, with the aim of minimizing damage to the microbiome and strengthening it at an early stage. 

In the view Anthroposophic Medicine, community-acquired pneumonia is a disease that requires a more complex interpretation of the disintegration of the lung organ in the whole organism. Just as an external wound is the consequence of an injury, e.g., a fall, so too in pneumonia there may be an “inner fall” in the person’s social or biographical context at the root of it. The relationship between the person’s respiratory organization (with its central organ, the lung) and his or her mental/emotional biographical experience is often revealed in decision-making situations, with their concomitant barriers and coping capabilities.

Even in current research, infectiologists agree that therapy with antibiotics alone does not do justice to the complexity of the pathological reactions in pneumonia (40). In Anthrophosophic Medicine, the synthesizing function of combinations of medicines as described in Section 3 is used to modulate the inflammatory response and improve pulmonary barrier function.

Finally, the special position of the lungs in the functional context of the entire organism can be seen through the described levels of reflection in the course of the disease (inflammatory processes, dynamics in the course of the disease and psychological and biographical background). This can be classified as the source of all rhythm functions with their alignments to the outside world. In contrast to current research, we assume that the inflammation and the alveolar damage have manifested themselves in the respiratory organization as part of the rhythmic system (which includes all rhythmic processes in the organism, with their balancing functions) without having their actual cause there. Primarily, the inflamed lung should be seen as an injured, wounded organ that has become “vulnerable” and its disintegration should be evaluated as an imbalance of the resilience acting in the organism. Often this can be caused by too much “down” regulation, lack of care of forces of recovery and “devitalization” in the person’s lifestyle, which creates the breeding ground for an “inner wound”. Pathogens are more the consequence than the cause in this view.

Disproportionate dominance of all nervous and sensory processes has a devitalizing effect. These processes can be an important starting point for disease and for the person’s susceptibility to pathogens. Warmth processes may not have been sufficiently strong and rhythmically differentiated in the organism over a longer period of time. The cooling function of air has possibly spread too strongly to the whole organism and favored the “wounding” of the lungs.

In this understanding, the disease pneumonia occurs as a disturbance of a state of equilibrium in the entire organism. The lung as the central organ of the complex human respiratory organization can be understood as the site of this disorder. The incidence of “strangeness” in the organism is followed by an exuberant inflammatory response from the organism’s metabolic-vital (cytokine-reactive) pole as a counter-reaction – which can thus also be understood as an attempt at healing, even though it can be potentially life-threatening and overstraining. The restoration (restitutio) after dissolution of the pneumonic infiltrate requires the formative forces of the entire organism in order to rebuild the primarily rhythmic functional qualities of the lungs in the overall organismic structure.

5. Prevention

a. Movement

Sufficient and regular exercise improves lung respiration, whether through physical exercise such as walking and hiking or through eurythmy therapy exercises. Soul activity is also connected with a healthy impulse to move, which has a positive effect on respiration.

b. Air

Good air quality is an important prevention factor for inflammatory diseases of the airways and the lungs. During convalescence after pneumonia, large cities with high levels of air pollution should be avoided.

c. Infection/Prophylaxis

In addition to basic hygiene measures – keeping one’s distance, washing one’s hands – the fear of infection must be addressed. Evaluation of pneumococcal and influenza vaccination in high-risk patients – age, preexisting cardiovascular or pulmonary disease, immunosuppression – with only evidence B for these vaccinations.

Prophylactic medication: 

  • Meteoreisen/Phosphor/Quarz (Meteoric iron/phosphorus/quartz) amp./pil. WALA:
    1 ml. s.c. 1–3 x/d or 10 pil. p.o. 1 x/d in the morning during the autumn and winter months, or as needed in case of acute danger of catching a cold 1 ml. s.c. 1–2 x/d or 10 pil. p.o. 3 x/d.

Prophylactic medication is mainly indicated in patients at increased risk for respiratory infections with complications – e.g., pre-existing cardiovascular disease, pulmonary disease such as COPD, asthma, and immunosuppression.

A good basic treatment of the underlying disease is also important for these patients.

d. Noxae

 Abstain from smoking and alcohol.

e. Strengthen the lungs

Therapeutic speech and singing therapy can make an important contribution to strengthening the lungs.

f. Relapse prophylaxis

Relapse prophylaxis is especially important in the first four weeks, see Section 3.h.

1 Ewig S, Birkner N, Strauss R, Schaefer E, Pauletzki J, Bischoff H, Schraeder P, Welte T, Hoeffken G. New perspectives on community-acquired pneumonia in 388 406 patients. Results from a nationwide mandatory performance measurement programme in healthcare quality. Thorax 2009;64(12):1062-1069. DOI: http://dx.doi.org/10.1136/thx.2008.109785. [Crossref]

2 Di Yacovo S, Garcia-Vidal C, Viasus D, Adamuz J, Oriol I, Gili F, Vilarrasa N, García-Somoza MD, Dorca J, Carratalà J. Clinical features, etiology, and outcomes of community-acquired pneumonia in patients with diabetes mellitus. Medicine (Baltimore) 2013;92(1):42-50. DOI: https://doi.org/10.1097/MD.0b013e31827f602a. [Crossref]

3 Gómez-Junyent J, Garcia-Vidal C, Viasus D, Millat-Martínez P, Simonetti A, Santos MS, Ardanuy C, Dorca J, Carratalà J. Clinical features, etiology and outcomes of community-acquired pneumonia in patients with chronic obstructive pulmonary disease. PloS One 2014;9(8):e105854. DOI: https://doi.org/10.1371/journal.pone.0105854. [Crossref]

4 Belda J, Cavalcanti M, Ferrer M, Serra M, Puig de la Bellacasa J, Canalis E, Torres A. Bronchial colonization and postoperative respiratory infections in patients undergoing lung cancer surgery. Chest 2005;128(3):1571-1579. DOI: https://doi.org/10.1378/chest.128.3.1571. [Crossref]

5 Klapdor B, Ewig S, Pletz MW, Rohde G, Schütte H, Schaberg T, Welte T, CAPNETZ Study Group. Community-acquired pneumonia in younger patients is an entity on its own. European Respiratory Journal 2012;39(5):1156-1161. DOI: https://doi.org/10.1183/09031936.00110911. [Crossref]

6 Ewig S, Woodhead M, Torres A. Towards a sensible comprehension of severe community-acquired pneumonia. Intensive Care Medicine 2011;37(2):214-223. DOI: https://doi.org/10.1007/s00134-010-2077-0. [Crossref]

7 Kolditz M, Ewig S, Höffken G. Management-based risk prediction in community-acquired pneumonia by scores and biomarkers. European Respiratory Journal 2013;41(4):974-984. DOI: https://doi.org/10.1183/09031936.00104412. [Crossref]

8 Bauer T, Ewig S, Marre R, Suttorp N, Welte T, CAPNETZ Study Group. CRB‐65 predicts death from community‐acquired pneumonia. Journal of Internal Medicine 2006;260(1):93-101. DOI: https://doi.org/10.1111/j.1365-2796.2006.01657.x. [Crossref]

9 Loke YK, Kwok CS, Niruban A, Myint PK. Value of severity scales in predicting mortality from community-acquired pneumonia: systematic review and meta-analysis. Thorax 2010;65(10):884-890. DOI: https://doi.org/10.1136/thx.2009.134072. [Crossref]

10 Chalmers JD, Singanayagam A, Akram AR, Mandal P, Short PM, Choudhury G, Wood V, Hill AT. Severity assessment tools for predicting mortality in hospitalised patients with community-acquired pneumonia. Systematic review and meta-analysis. Thorax 2010;65(10):878-883. DOI: https://doi.org/10.1136/thx.2009.133280. [Crossref]

11 Chalmers JD, Mandal P, Singanayagam A, Akram AR, Choudhury G, Short PM, Hill AT. Severity assessment tools to guide ICU admission in community-acquired pneumonia: systematic review and meta-analysis. Intensive Care Medicine 2011;37(9):1409-1420. DOI: https://doi.org/10.1007/s00134-011-2261-x. [Crossref]

12 Salih W, Schembri S, Chalmers JD. Simplification of the IDSA/ATS criteria for severe CAP using meta-analysis and observational data. European Respiratory Journal 2014;43(3):842-851. DOI: https://doi.org/10.1183/09031936.00089513. [Crossref]

13 Lim W, van der Eerden M, Laing R, Boersma WG, Karalus N, Town GI, Lewis SA, Macfarlane JT. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax 2003;58(5):377-382. DOI: https://doi.org/10.1136/thorax.58.5.377. [Crossref]

14 Fine MJ, Auble TE, Yealy DM, Hanusa BH, Weissfeld LA, Singer DE, Coley CM, Marrie TJ, Kapoor WN. A prediction rule to identify low-risk patients with community-acquired pneumonia. New England Journal of Medicine 1997;336(4):243-250. DOI: https://doi.org/10.1056/NEJM199701233360402. [Crossref]

15 Ewig S, Höffken G, Kern W, et al. Behandlung von erwachsenen Patienten mit ambulant erworbener Pneumonie und Prävention – Update 2016. Pneumologie 2016;70(3):151-200. DOI: http://dx.doi.org/10.1055/s-0042-101873. [Crossref]

16 Welte T, Marre R, Suttorp N. Das Kompetenznetzwerk “Ambulant erworbene Pneumonie (CAPNETZ)”. Der Internist 2004;45(4):393-401.

17 Gentile A, Bardach A, Ciapponi A, Garcia-Marti S, Aruj P, Glujovsky D, Calcagno JI, Mazzoni A, Colindres RE. Epidemiology of community-acquired pneumonia in children of Latin America and the Caribbean: a systematic review and meta-analysis. International Journal of Infectious Diseases 2012;16(1):e5-e15. DOI: https://doi.org/10.1016/j.ijid.2011.09.013. [Crossref]

18 Singanayagam A, Chalmers J, Welte T. Epidemiology of CAP in Europe. Community-Acquired Pneumonia. European Respiratory Monographs 2014;63:1838.

19 Schaaf B, Azzaui H, Lorenz J, Schulze-Raestrup U. Epidemiologie der stationär behandelten ambulant erworbenen Pneumonien in Deutschland. Der Pneumologe 2015;12(2):101-109.

20 Ewig S, Höffken G, Kern W, Rohde G, Flick H, Krause R, Ott S, Bauer T, Dalhoff K, Gatermann S, Kolditz M, Krüger S, Lorenz J, Pletz M, de Roux A, Schaaf B, Schaberg T, Schütte H, Welte T. Management of adult community-acquired pneumonia and prevention-update 2016. Pneumologie 2016;70(3):151-200. DOI: https://doi.org/10.1055/s-0042-101873. [Crossref]

21 Höffken G, Lorenz J, Kern W, Welte T, Bauer T, Dalhoff K, Dietrich E, Ewig S, Gastmeier P, Grabein B, Halle E, Kolditz M, Marre R, Sitter H. Epidemiologie, Diagnostik, antimikrobielle Therapie und Management von erwachsenen Patienten mit ambulant erworbenen unteren Atemwegsinfektionen sowie ambulant erworbener Pneumonie – Update 2009. Pneumologie 2009;63(10):e1-e68. DOI: https://doi.org/10.1055/s-0029-1215037. [Crossref]

22 Metlay JP, Waterer GW, Long AC, Anzueto A, Brozek J, Crothers K, Cooley LA, Dean NC, Fine MJ, Flanders SA, Griffin MR, Metersky ML, Musher DM, Restrepo MI, Whitney CG. Diagnosis and treatment of adults with community-acquired pneumonia. An official clinical practice guideline of the American Thoracic Society and Infectious Diseases Society of America. American Journal of Respiratory and Critical Care Medicine 2019;200(7):e45-e67. DOI: https://doi.org/10.1164/rccm.201908-1581ST. [Crossref]

23 Ewig S, Bauer T, Richter K, Szenscenyi J, Heller G, Strauss R, Welte T. Prediction of in-hospital death from community-acquired pneumonia by varying CRB-age groups. European Respiratory Journal 2013;41(4):917-922. DOI: https://doi.org/10.1183/09031936.00065212. [Crossref]

24 Torres OH, Muñoz J, Ruiz D, Ris J, Gich I, Coma E, Gurguí M, Vázquez G. Outcome predictors of pneumonia in elderly patients: importance of functional assessment. Journal of the American Geriatrics Society 2004;52(10):1603-1609. DOI: https://doi.org/10.1111/j.1532-5415.2004.52492.x. [Crossref]

25 Naito T, Suda T, Yasuda K, Yamada T, Todate A, Tsuchiya T, Sato J, Chida K, Nakamura H. A validation and potential modification of the pneumonia severity index in elderly patients with community‐acquired pneumonia. Journal of the American Geriatrics Society 2006;54(8):1212-1219. DOI: https://doi.org/10.1111/j.1532-5415.2006.00825.x. [Crossref]

26 Murcia J, Llorens P, Sánchez-Payá J, Reus S, Boix V, Merino E, Laghzaoui F, Portilla J. Functional status determined by Barthel Index predicts community acquired pneumonia mortality in general population. Journal of Infection 2010;61(6):458-464. DOI: https://doi.org/10.1016/j.jinf.2010.08.006. [Crossref]

27 Schaaf B, Azzaui H, Lorenz J, Schulze-Raestrup U. Epidemiology of stationary treated community acquired pneumonia in Germany. What can be expected in the next 50 years? What are the consequences for outpatient medicine? Der Pneumologe 2015;12(2):101-108.

28 von Baum H, Schweiger B, Welte T, Marre R, Suttorp N, Pletz MWR, Ewig S, CAPNETZ Study Group. How deadly is seasonal influenza-associated pneumonia? The German competence network for community-acquired pneumonia. European Respiratory Journal 2011;37(5):1151-1157. DOI: https://doi.org/10.1183/09031936.00037410. [Crossref]

29 Rodrigo C, Leonardi-Bee J, Nguyen-Van-Tam JS, Lim WS. Effect of corticosteroid therapy on influenza-related mortality: a systematic review and meta-analysis. Journal of Infectious Diseases 2015;212(2):183-194. DOI: https://doi.org/10.1093/infdis/jiu645. [Crossref]

30 World Health Organization. WHO guidelines for pharmacological management of pandemic (H1N1) 2009 influenza and other influenza viruses. 2010. Available at  https://www.who.int/csr/resources/publications/swineflu/h1n1_use_antivirals_20090820/en/ (01.02.2021)

31 MacIntyre CR, Chughtai AA, Barnes M, Ridda I, Seale H, Toms R, Heywood A. The role of pneumonia and secondary bacterial infection in fatal and serious outcomes of pandemic influenza a (H1N1) pdm09. BMC Infectious Diseases 2018;18(1):637. DOI: https://doi.org/10.1186/s12879-018-3548-0. [Crossref]

32 Murray J. Die historische Entwicklung der Tuberkulose seit Robert Kochs Entdeckung des Tuberkelbazillus 1882. Pneumologie 2007;61(12):764-770. DOI: https://doi.org/10.1055/s-2007-993029. [Crossref]

33 Langbein K, Ehgartner B. Das Medizin Kartell. Die sieben Todsünden der Gesundheitsindustrie. 2nd ed. Munich: Piper; 2002.

34 Gastmeier P. 300 Jahre Infektionsprävention an der Charité. Deutsche Medizinische Wochenschrift 2010;135(22):1137-1140. DOI: https://doi.org/10.1055/s-0030-1255138. [Crossref]

35 Steiner R. Geisteswissenschaft und Medizin. GA 312. 8th ed. Basel: Rudolf-Steiner-Verlag; 2020. Englisch translation: Steiner R. Introducing anthroposophical medicine. Great Barrington: Steiner Books; 2011.

36 Lee RJ, Cohen NA: bitter taste bodyguards. Scientific American 2016;314(2):38-43. DOI: https://doi.org/10.1038/scientificamerican0216-38. [Crossref]

37 Menéndez R, Méndez R, Aldás I, Reyes S, Gonzalez-Jimenez P, España PP, Almirall J, Alonso R, Suescun M, Martinez-Dolz L, Torres A. Community-acquired pneumonia patients at risk for early and long-term cardiovascular events are identified by cardiac biomarkers. Chest 2019;156(6):1080-1091. DOI: https://doi.org/10.1016/j.chest.2019.06.040. [Crossref]

38 Eurich DT, Marrie TJ, Minhas-Sandhu JK, Majumdar SR. Ten-year mortality after community-acquired pneumonia. A prospective cohort. American Journal of Respiratory and Critical Care Medicine 2015;192(5):597-604. DOI: https://doi.org/10.1164/rccm.201501-0140OC. [Crossref]

39 Medina E. Murine model of pneumococcal pneumonia. In: Proetzel G, Wiles MV (eds.) Mouse Models for Drug Discovery. Springer; 2010:405-410.

40 Müller-Redetzky H, Lienau J, Suttorp N, Witzenrath M. Therapeutic strategies in pneumonia: going beyond antibiotics. European Respiratory Review 2015;24(137):516-524. DOI: https://doi.org/10.1183/16000617.0034-2015. [Crossref]

41 Brands X, Haak BW, Klarenbeek AM, Otto NA, Faber DR, Lutter R, Scicluna BP, Wiersinga WJ, van der Poll T. Concurrent immune suppression and hyperinflammation in patients with community-acquired pneumonia. Frontiers in Immunology 2020;11:796. DOI: https://doi.org/10.3389/fimmu.2020.00796. [Crossref]

42 Witzenrath M, Gutbier B, Hocke AC, Schmeck B, Hippenstiel S, Berger K, Mitchell TJ, de los Toyos JR, Rosseau S, Suttorp N, Schütte H. Role of pneumolysin for the development of acute lung injury in pneumococcal pneumonia. Critical Care Medicine 2006;34(7):1947-1954. DOI: https://doi.org/10.1097/01.CCM.0000220496.48295.A9. [Crossref]

43 Channappanavar R, Perlman S. Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology. Seminars in Immunopathology 2017;39:529–539. DOI: https://doi.org/10.1007/s00281-017-0629-x. [Crossref]

44 Damjanovic D, Lai R, Jeyanathan M, Hogaboam CM, Xing Z. Marked improvement of severe lung immunopathology by influenza-associated pneumococcal superinfection requires the control of both bacterial replication and host immune responses. American Journal of Pathology 2013;183(3):868-880. DOI: https://doi.org/10.1016/j.ajpath.2013.05.016. [Crossref]


Research news

Art therapy & anxiety: In her doctoral thesis published 2020, Annemarie Abbing investigated the effectiveness of art therapy in the treatment of anxiety. Outcomes of a randomised controlled trial (n=59) showed preliminary evidence of the effectiveness of art therapy: Three months of anthroposophic art therapy led to a significant reduction in the severity of anxiety symptoms in the women compared to waiting list treatment. The therapy also improved quality of life and various aspects of self-regulation. The second part of this PhD research focused on case report methodology and the development of tools for research within this field. The doctoral thesis is available at 
https://scholarlypublications.universiteitleiden.nl/handle/1887/83276.


Further information on Anthroposophic Medicine