Pneumonia is an infection that affects the air sacs in one or both lungs. The air sacs may fill with fluid or pus (purulent material), causing cough with phlegm or pus, fever, chills, and difficulty breathing. A variety of organisms, including bacteria, viruses and fungi, can cause pneumonia. It can affect anyone regardless of age or sex but people with compromised immunity like new-born babies, AIDS patients and old age people are more prone to this disease. In some cases, it can happen as a secondary infection and can be fatal. Proper diagnosis and treatment are very important in restoring the respiratory health.
Signs and symptoms
- Chest pain while breathing or coughing
- Confusion or changes in mental awareness (especially in older people)
- Cough (mostly productive)
- Fever, sweating and shaking chills
- Lower than normal body temperature (in people with weak immune systems)
- Nausea, vomiting or diarrhoea
- Shortness of breath
- Bacteria – The most common cause of bacterial pneumonia is Streptococcus pneumoniae.
- Bacteria-like organisms – Mycoplasma pneumoniae also can cause pneumonia
- Fungi – This type of pneumonia is most common in people with chronic health problems or weakened immune systems, and in people who have inhaled large doses of the organisms. The fungi that cause it can be found in soil or bird droppings and vary depending upon geographic location.
- Viruses, including COVID-19 – Some of the viruses that cause colds and the flu can cause pneumonia. Viruses are the most common cause of pneumonia in children younger than 5 years. Viral pneumonia is usually mild. But in some cases, it can become very serious. Coronavirus 2019 (COVID-19) may cause pneumonia, which can become severe.
Any infectious organisms that reach the alveoli are likely to be highly virulent, as they have already evaded the host’s physical defence mechanisms. Consequently, they may overwhelm the macrophages, resulting in production of a fibrin-rich exudate that fills the infected and neighbouring alveolar spaces, causing them to stick together, rendering them airless. The inflammatory response also results in a proliferation of neutrophils. This can damage lung tissue, leading to fibrosis and pulmonary oedema, which also impairs lung expansion.
The inflammatory response can also lead to the development of a pleural effusion which is thought to complicate up to 40% of cases of pneumonia. These changes result in reduced gaseous exchange. As a result, vital organs become oxygen deprived and the respiratory effort required with each breath will be increased as a result of the disturbance in normal physiology. Respiratory and heart rate will increase in response to falling oxygen and rising carbon dioxide levels.
Blood tests – to identify the type of organism causing the infection. However, precise identification isn’t always possible.
Pulse oximetry to assess the oxygen levels
Sputum test to identify the causative organism
Pleural fluid culture
Antibiotics – in bacterial pneumonia
Antipyretics to reduce fever and analgesics to reduce pain. These include drugs such as aspirin, ibuprofen (Advil, Motrin IB, others) and acetaminophen (Tylenol, others).
Most people with pneumonia improve after three to five days of antibiotic treatment, but a mild cough and fatigue can last longer, up to a month. Patients who required treatment in a hospital may take longer to see improvement. Pneumonia can also be fatal.
- Bacteria in the bloodstream (bacteraemia) can spread the infection to other organs, potentially causing organ failure.
- Difficulty breathing.
- Fluid accumulation around the lungs (pleural effusion).
- Lung abscess.
Disease & Ayurveda
There is not a single disease name describing the exact condition of pneumonia. All the breathing difficulties are included under the name Swaasa in Ayurveda. But in pneumonia, the fever and infectious condition show more relation with the signs & symptoms elaborated under Kapha-Vaatha jwara where breathing problems are also a symptom.
Causative factors for the vitiation of three doshas separately or together
Aama(undigested & toxic metablic waste in GIT and channels in the body)
Aalasya – fatigue
Arati – restlessness
Gaatragauravam-Heaviness of body
Aasyavairasyam-Bad taste in the mouth
Aruchi – Loss of taste sensation
Jrmbha – Excess yawning
Saasraakulakshata – reddish, and dull looking eyes
Angamarda – Bodyache
Avipaaka – Indigestion
Alpapraanata – lack of vital force
Bahunidrata – Excess sleep
Romaharsha – horripulation
Vinamanam – hunching of the back
Pindikodweshtanam – pain in the calf muscles
Hitopadeseshu akshanti-lack of interest in good advices
Amla-patu-ooshane preeti-craving for amla-lavana and katu
Dwesha in swaadushu bhakshya and baala-aversion to sweet & kids
Bhrisam thrit-excess thirst
Animittata: iccha & dwesha in sabda, agni, seta, vaata, ambu, chaaya & ushna – likeness and aversion without any reason to sound, fire, cold, wind, water, shade and heat
Due to causative factors, the vitiated doshas individually or together enter the aamasaya, join with aama and by closing the channels expels out the agni from its normal site. The vitiated doshas along with this redirected agni, travels throughout the body and generates fever. There will be absence of sweat due to the closed channels in the body.
Taapahaani – Body temperature less than normal
Aruchi – loss of taste sensation
Parva-siroruk – Pain in joints & head
Peenasa – Running nose
Swasa – Breathing difficulty
Kaasa – Cough
Vibandha – Constipation
Seeta – Chills
Jaadya – Lethargy/lack of movements
Timira – Vision problems
Bhrama-tandra – Giddiness, fainting etc.
8 types of Jwara are
Saadhya when developed in physically and mentally strong persons, without any other complications
Ayurveda treatment of Kapha-Vaata jwara emphasises on removing the obstruction in channes, caused by metabolic waste and bringing back Agni into normal state giving special attention to respiratory system. By this, the normal metabolism will boost the immunity & positive health and the disease will be cured. Along with this principle, measures are taken for symptomatic relief also.
No sodhana therapies are done in a person with fever, unless in emergency.
Once the fever is subsided, Vamana or virechana can be done to remove the metabolic waste in the gastro-intestinal tract if needed. This should be done in a patient with good physical & mental strength only.
Commonly used medicines
No home remedy is proven to cure pneumonia.
- To be avoided
Heavy meals and difficult to digest foods – cause indigestion.
Junk foods- cause disturbance in digestion and reduces the bioavailability of the medicine
Carbonated drinks – makes the stomach more acidic and disturbed digestion
Refrigerated and frozen foods – causes weak and sluggish digestion by weakening Agni (digestive fire)
Milk and milk products – increase kapha, cause obstruction in channels and respiratory disorders.
Curd – causes vidaaha and thereby many other diseases
- To be added
Light meals and easily digestible foods
Green gram, soups, honey
Freshly cooked and warm food processed with cumin seeds, ginger, black pepper, ajwain etc
Protect yourself from cold climate.
Better to avoid exposure to excessive sunlight wind rain or dust.
Maintain a regular food and sleep schedule.
Avoid holding or forcing the urges like urine, faeces, cough, sneeze etc.
Avoid sedentary lifestyle. Be active.
Regular stretching and mild cardio exercises are advised. Also, specific yogacharya including naadisuddhi pranayama, bhujangaasana, pavanamuktasana is recommended.
Regular exercise helps improve bioavailability of the medicine and food ingested and leads to positive health.
Yoga can maintain harmony within the body and with the surrounding system.
Simple exercises for lungs and heart health
All the exercises and physical exertions must be decided and done under the supervision of a medical expert only.
To our knowledge, no previous study has systematically examined pneumonia-related and pneumonia-unrelated mortality. This study was performed to identify the cause(s) of death and to compare the timing and risk factors associated with pneumonia-related and pneumonia-unrelated mortality.
Methods For all deaths within 90 days of presentation, a synopsis of all events preceding death was independently reviewed by 2 members of a 5-member review panel (C.M.C., D.E.S., T.J.M., W.N.K., and M.J.F.). The underlying and immediate causes of death and whether pneumonia had a major, a minor, or no apparent role in the death were determined using consensus. Death was defined as pneumonia related if pneumonia was the underlying or immediate cause of death or played a major role in the cause of death. Competing-risk Cox proportional hazards regression models were used to identify baseline characteristics associated with mortality.
Results Patients (944 outpatients and 1343 inpatients) with clinical and radiographic evidence of pneumonia were enrolled, and 208 (9%) died by 90 days. The most frequent immediate causes of death were respiratory failure (38%), cardiac conditions (13%), and infectious conditions (11%); the most frequent underlying causes of death were neurological conditions (29%), malignancies (24%), and cardiac conditions (14%). Mortality was pneumonia related in 110 (53%) of the 208 deaths. Pneumonia-related deaths were 7.7 times more likely to occur within 30 days of presentation compared with pneumonia-unrelated deaths. Factors independently associated with pneumonia-related mortality were hypothermia, altered mental status, elevated serum urea nitrogen level, chronic liver disease, leukopenia, and hypoxemia. Factors independently associated with pneumonia-unrelated mortality were dementia, immunosuppression, active cancer, systolic hypotension, male sex, and multilobar pulmonary infiltrates. Increasing age and evidence of aspiration were independent predictors of both types of mortality.
Conclusions For patients with community-acquired pneumonia, only half of all deaths are attributable to their acute illness. Differences in the timing of death and risk factors for mortality suggest that future studies of community-acquired pneumonia should differentiate all-cause and pneumonia-related mortality
An official American Thoracic Society research statement: noninfectious lung injury after hematopoietic stem cell transplantation: idiopathic pneumonia syndrome
Angela Panoskaltsis-Mortari, Matthias Griese, David K Madtes, John A Belperio, Imad Y Haddad, Rodney J Folz, Kenneth R Cooke
American journal of respiratory and critical care medicine 183 (9), 1262-1279, 2011
Rationale: Acute lung dysfunction of noninfectious etiology, known as idiopathic pneumonia syndrome (IPS), is a severe complication following hematopoietic stem cell transplantation (HSCT). Several mouse models have been recently developed to determine the underlying causes of IPS. A cohesive interpretation of experimental data and their relationship to the findings of clinical research studies in humans is needed to better understand the basis for current and future clinical trials for the prevention/treatment of IPS.
Objectives: Our goal was to perform a comprehensive review of the preclinical (i.e., murine models) and clinical research on IPS.
Methods: An ATS committee performed PubMed and OVID searches for published, peer-reviewed articles using the keywords “idiopathic pneumonia syndrome” or “lung injury” or “pulmonary complications” AND “bone marrow transplant” or “hematopoietic stem cell transplant.” No specific inclusion or exclusion criteria were determined a priori for this review.
Measurements and Main Results: Experimental models that reproduce the various patterns of lung injury observed after HSCT have identified that both soluble and cellular inflammatory mediators contribute to the inflammation engendered during the development of IPS. To date, 10 preclinical murine models of the IPS spectrum have been established using various donor and host strain combinations used to study graft-versus-host disease (GVHD). This, as well as the demonstrated T cell dependency of IPS development in these models, supports the concept that the lung is a target of immune-mediated attack after HSCT. The most developed therapeutic strategy for IPS involves blocking TNF signaling with etanercept, which is currently being evaluated in clinical trials.
Conclusions: IPS remains a frequently fatal complication that limits the broader use of allogeneic HSCT as a successful treatment modality. Faced with the clinical syndrome of IPS, one can categorize the disease entity with the appropriate tools, although cases of unclassifiable IPS will remain. Significant research efforts have resulted in a paradigm shift away from identifying noninfectious lung injury after HSCT solely as an idiopathic clinical syndrome and toward understanding IPS as a process involving aspects of both the adaptive and the innate immune response. Importantly, new laboratory insights are currently being translated to the clinic and will likely prove important to the development of future strategies to prevent or treat this serious disorder.
Tocilizumab for the treatment of severe COVID-19 pneumonia with hyperinflammatory syndrome and acute respiratory failure: a single center study of 100 patients in Brescia, Italy
Paola Toniati, Simone Piva, Marco Cattalini, Emirena Garrafa, Francesca Regola, Francesco Castelli, Franco Franceschini, Emanuele Focà, Laura Andreoli, Nicola Latronico, Brescia International Research, HUB Training
Autoimmunity reviews, 102568, 2020
A hyperinflammatory syndrome (HIS) may cause a life-threatening acute respiratory distress syndrome (ARDS) in patients with COVID-19 pneumonia.
A prospective series of 100 consecutive patients admitted to the Spedali Civili University Hospital in Brescia (Italy) between March 9th and March 20th with confirmed COVID-19 pneumonia and ARDS requiring ventilatory support was analyzed to determine whether intravenous administration of tocilizumab (TCZ), a monoclonal antibody that targets the interleukin 6 receptor, was associated with improved outcome. Tocilizumab was administered at a dosage of 8 mg/kg by two consecutive intravenous infusions 12 h apart. A third infusion was optional based on clinical response.
The outcome measure was an improvement in ARDS assessed by means of the Brescia COVID Respiratory Severity Score (BCRSS 0 to 8, with higher scores indicating higher severity) at 24–72 h and 10 days after tocilizumab administration.
Out of 100 treated patients (88 M, 12 F; median age: 62 years), 43 received TCZ in the intensive care unit (ICU), while 57 in the general ward as no ICU beds were available. Of these 57 patients, 37 (65%) improved and suspended noninvasive ventilation (NIV) (median BCRSS: 1 [IQR 0–2]), 7 (12%) patients remained stable in NIV, and 13 (23%) patients worsened (10 died, 3 were admitted to ICU). Of the 43 patients treated in ICU, 32 (74%) improved (17 of them were taken off the ventilator and were discharged to the ward), 1 (2%) remained stable (BCRSS: 5) and 10 (24%) died (all of them had BCRSS≥7 before TCZ). Overall at 10 days, the respiratory condition was improved or stabilized in 77 (77%) patients, of whom 61 showed a significant clearing of diffuse bilateral opacities on chest x-ray and 15 were discharged from the hospital. Respiratory condition worsened in 23 (23%) patients, of whom 20 (20%) died.
All the patients presented with lymphopenia and high levels of C-reactive protein (CRP), fibrinogen, ferritin and interleukin 6 (IL-6) indicating a HIS. During the 10-day follow-up, three cases of severe adverse events were recorded: two patients developed septic shock and died, one had gastrointestinal perforation requiring urgent surgery and was alive at day 10.
In conclusion, our series showed that COVID-19 pneumonia with ARDS was characterized by HIS. The response to TCZ was rapid, sustained, and associated with significant clinical improvement
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Dr. Rajesh Nair, the co-founder and chief consultant of Ayurvedaforall.Com, is a graduate of prestigious Vaidyaratnam Ayurveda College (affiliated with the University of Calicut), Kerala, India. Additionally, he holds a Postgraduate Diploma in Yoga Therapy from Annamalai University.
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