Herold Example Ba

 

 

Legal Disclaimer  All diagnostic diagnostic and therapeuti therapeutic c procedures in the field field of science and medicine medicine are continuously continuously evolving evolving:: Therefore the herein presented medical evidence is state of the technical and scientific art at the time of the editorial deadline deadli ne for tthe he respective edition of the book.  All details provi provided ded herein related to a particular therapeutic mode mode of administration and dosing of drugs are screened employing utmost measures of accuracy and precision. Unless explicitly specified otherwise, all drug administration and dosing regimens presented herein are for healthy adults with normal renal and hepatic function. Liability Liabil ity cannot be assum assumed ed for any type of dosing and administration regimen presented herein. Each reader is advised to carefully consult the respective market authorization holders directions for use of the recommended drugs, medical devices and other means of therapy and diagnosis. This applies in particular also to market authorization holders summaries of product characteristics for pharmaceutical products. Despite all care, there t here may be translation errors. The reader is advised to carefully check information related to the indication for use, contraindications, dosing recommendations, side effects and interactions with other medications!  All modes of medi medication cation use and administration are at the consumers risk. The author and his team cannot be held responsible for any damage caused by wrong therapy or diagnosis. Please refer to, i.e: www.leitlinien.de or  www.guide  www .guideline.gov  line.gov   The trade name name of a trade name registered produ product ct does not provid provide e the legal privilege privilege to employ employ the trade name as a free trade mark even if it is not specificall specifically y marked as s uch. Drugs which are sold as generics are referred to throughout the book by their generic name and not necessarily by a particular brand name. Remark: 10 code 1.3may has have beenbeen employed for the index. Since was used,ICD different codeversion numbers assigned to indexed items! in the current edition ICD 10 code version 2.0 No part of the book – neither in part or in toto – may be reproduced in any form format at (print, c opy, opy, microfilm, microfilm, electronic storage, storage, use and/or distribution by any electronic format including the internet) in the absence of an explicit written permission by the editor. Be careful about reading health books. You may die of a misprint. (Mark Twain)

7

 

 

Abbreviations  AAA  AB  ACE  ADB  ADH  AET  AF  AG  AIDS  AIHA  AN  ANA

Abdominal aortic aneurism Antibodies Angiotensin converting enzyme Anti-Desoxyribonucleotidase B Antidiuretic hormone Aetiology Atrial fibrillation Antigen Acqu Acquire ire d Immunodeficiency Syndrome Syndrome Autoimmune haemolytic anaemia Autonomic neuropath neuropathy y Anti nuclear antibodies

FUO GBM GFR GI GN HBV HCT HI HIT HIV HLT HPV

Fever of unknown origin Glomerular basement membrane Glomerular filtration rate Gastrointestinal Glomerulonephritis Hepatitis B Virus Haematocrit Histology Heparin induced thrombocytopenia Human Immunodeficiency Virus Half life time Human Papilloma Virus

 ANCA  ANP  A.O.  APC  APS  APPROX  ARDS  ARF  ASAP  ASD  ASL  AT  AT  ATP  AXR BMI BMT BNP BP BU BW C CA CA. CDC CH CHD CI CK CL CMV CNP CNS CO CON COPD COX CRP CSE CSF CT CU CVI CVP CXR

Anti neutrophile cytoplasmatic antibodies Atrial natriuretic peptide And others Activated Protein C Antiphospholip Antiphospholipid id syndrome Approximately Adult respiratory distress syndrome Acute renal failure As soon as possible Atrial septum defect Antistreptolysin Antithrombin Antithrombin Adenosine Triphosphate Abdominal X-ray Body Mass Index Bone marrow transplant brain natriuretic peptide Blood pressure Bread unit Body weight Celsius Carcinoma Circa Centres for disease control Carbohydrate Coronary heart disease Contraindications Creatine Kinase Clinical picture Cytomegaly Virus Type C natriuretic peptide Central Nervous System Complications Contagiousness Chronic obstructive pulmonary pulmonary disease Cyclooxygenase C-reactive protein Cholesterol Synthesis Enzyme Cerebrospinal Fluid Computer tomography Carbohydrate unit Chronic venous insufficiency Central venous pressure Chest X-ray

HSV HUS HX IA IBS ICA ICD ICF ICP ICU IFAT IG IHA I.M. INC IND INR ISF ITP IU I.V. IVF LAB LAS LDH LDL LDV LMWH LOC M MDS MI MI MIO MM MOA MRI MW NK (cells) NSAID OAC OAD OCC OCC PA

Herpes Simplex Virus Haemolytic uraemic syndrome History Interaction Irritable bowel syndrome Internal carotid artery Implantable Cardioverter - Defibrillator Intracellular fluid Intracranial pressure Intensive care unit Indirect immunofluorescence antigen test Immunoglobulin Indirect Haemagglutinin test Intramuscular Incidence Indication International normalised ratio Interstitial fluid Idiopathic thrombocytopenia International units units Intravenous Intravascular fluid Laboratory tests Lymphadenopathy Lymphadenopathy syndrome Lactate Dehydrogenase Low density lipoprotein Lymphocyte doubling time Low molecular weight Heparin Localisation Male Myelodysplastic syndrome Mentzer index Myocardial infarction Million Multiple myeloma Mode of action Magnet resonance imaging Molecular weight Natural killer (cells) Non steroidal anti-inflammatory drug Oral anticoagulation Occlusive atherosclerotic disease Occasionally Occurrence Pulmonary artery

DD DEF DHD DHS DI DIC DNA DSA DVT EBV ECF ECG EEG EF EHEC ELISA EN ENT EP ESP ESR ET

Differential diagnosis Definition Dengue haemorrhagic fever Dengue haemorrhagic shock Diagnosis Disseminated intravascular coagulation Deoxyribonucleic acid Digital subtraction angiography Deep vein thrombosis Epstein Barr Virus Extracellular fluid Electrocardiogram Electroencephalogram Effects Enterohaemorrhagic Enterohaemorrhagic E. coli Enzyme linked immunosorbent assay Enteral nutrition Ear Nose & Throat Epidemiology Especially Erythrocyte Sedimentation Rate Etiology

PAT PAT PCR PE PEP PET PFO PG PI PID PMC PN PNH POSS PPC PPH PPSB PRG PRO PTCA PTH

Pathogen Pathology Polymerase chain reaction Pulmonary embolism Post exposure prophylaxis Positron emission tomography Persistent foramen ovale Pathogenesis Protease inhibitor Pelvic inflammatory disease Pseudomembranous Enterocolitis Parenteral nutrition Paroxysmal nocturnal haemoglobinuria Possibly Phenprocoumon Pathophysiology Prothrombin proconvertin Stuart-Prower factor antihaemophilic factor B Prognosis Prophylaxis Percutaneous transluminal coronary angioplasty Parathyroid hormone

EU F FFP

European Union Female Fresh Frozen Plasma

PTS PTT RA

Post Thrombotic Thrombotic Prothrombin timeSyndrome Rheumatoid arthritis

8

 

 

RES RF RNA RS RV SC SE SIADH SK SLE ST STD SU SYM SYN

Reticular Endothelial Syncythium Rheumatoid factor Ribonucleic acid Raynaud’s Syndrome right ventricular Subcutaneous Side effects Syndrome of inadequate ADH secretion Streptokinase Systemic lupus erythematosus Stage Sexually transmitted disease Sulfonyl urea Symptoms Synonym

TH THR TIA TOA TPHA TPN TSH TURP UFH URTI US UTI UV VUR VV

Therapy Total hip replacement Transitory ischaemic attack Thrombangiitis obliterans Treponema Pallidum Haemagglutinin Haemagglutinin Total parenteral nutrition Thyroid stimulation hormone Transurethral resection of the prostate Unfractioned Heparin Upper Respiratory Tract Infection Ultrasound Urinary tract infection Ultraviolet Vesico-ureteric-renal reflux Varicose veins

TAA TEA TEE

Thoracic aortic aneurism Thrombendarteriectomy Transoesophageal echocardiography

VZV WHO Y

Varicella Zoster Virus World health organisation Year

Find more medical abbreviations at   Find more general abbreviations at 

www.medizinische-abkuerzungen.de www.acronymdb.com www.chemie.fu-berlin.de/cgi-bin/acronym 

9

 

 

3. Lung volume reduction surgery: In selected patients with upper lobe-predominant emphysema, an approx. 20% reduction in emphysematic lung tissue leads to improved pulmonary function (evidence grade B). Bullectomy: removal of singular large emphysema vesicles 4. Bronchoscopic placement of small oneway vents, by which the air is evacuated from overinflated lung segments. Thus, emphysema-free emphysema-free s segm egments ents c can an expand. expand. The effect e ffect is similar to the one reached by lung volum volume e reduction surgery. In clinical testing t esting (Ve (Vent-study). nt-study). 5. Lung transplantatio transplantation: n: s see ee chapt. respiratory respiratory in insufficiency sufficiency Prg:   Critically dependent Prg: dependent upon early stage optim optimized ized therapy implementation. implementation. W ithout sm smoking oking cessation the disease disease progression cannot be influenced: average life expectancy for smokers s mokers is 48 years, for non-smokers non-smokers 67 years. y ears. With a FEV1 value of < 1 l, life expectancy is significantly reduced and the patient is occupationally disabled. Respiratory insufficiency insufficien cy and cor pulmonale are the most frequent causes of death.

BRONCHIAL ASTHMA

[J45.9] 

Internet info: www.atemwegsliga.de; www.leitlinien.de; www.ginasthma.com Def.:   Def.:

International consensus report on diagnosis diagnosis and therapy of asthma: Bronchial asthma is a chronic, inflammatory disorder of the airways. Inflammation in predisposed individuals leads to dyspnoea attacks due to the narrowing of the airways (bronchial obstruction). The airway obstruction is either spontaneous or reversible by treatment. Due to the inflammation the airways are more sensitive to a large number of irritants (bronchial hyper-rea hyper-reactivity). ctivity). German Airways Society: bronchial asthma is an inflammatory disorder of the airways characterized by bronchial hyper-reactivity hyper-reactivit y and variable, partially reversible airway obstruction.

Ep.:   Prevalen Ep.: Prevalence: ce: approx. 5% of adults and up to 10% of children; trend towards worldwide worldwide in increase crease in preval prevalence; ence; m : f = 2 : 1. The highest prevalence is found in Scotland and New Zealand; the lowest in Eastern Europe and Asia. Allergic asthma usually starts in childhood, non-allergic non-allergic asthma in contrast begins not until middle age (> 40 years of age). Frequency distribution among the individual types of asthma: 30% of adult asthmatics suffer e exclusiv xclusively ely from extrinsic asthma and another 30% exclusivel exclusively y from intrinsic int rinsic asthma. asthma. The rest suffers from a combination of both. Asthma caused by infection is the most frequently observed type for ages > 45 years. Allergic asthma is predominantly seen in infants and juveniles. Aet.:   A) Allerg Aet.: Allergic ic asthm asthma a (ex (extrinsic trinsic as asthma) thma) [J45.0] [J45.0] 1. cau c aused sed by environme environmental ntal allergens (s (see ee below) 2. caused by occupational allergens: occupational asthma ( 5%, occupational disease No. 4301 ; occupational illness No. 1315, if caused by isocyanates) B) Non-allergic asthma (intrinsic asthma) [J45.1] 1. Asthma due to respiratory infection 2. Asthma caused by analgesics: asthma induced by ASA and NSAID: pseudoallerg pseudoallergic ic reaction (PAR) to ASA and mostly (90%) also to NSAID 3. Asthma caused by chemi c hemical cal irritation or toxic toxic s substan ubstances ces (if work-related: occupational occupational disease No. 4302) 4. Asthma/coughing disorder due to gastrooesophageal reflux C) Mixed types consisting of A and B [J45.8] Genetic factors:  Atopic disea diseases ses (bronchi (bronchial al asthma, allergic rhiniti rhinitis s and neurodermitis) neurodermitis) have a preval prevalence ence of 30% and are characterized by a polygeni polygenically cally inherited predisposition for overshooting overshooting IgE formation (type I reaction). Only part of the carriers contract the disease. If both parents suffer from allergic asthma, their offspring will have have a risk of illness in 60 - 80% of cases (it is half that t hat number if only one parent is affected). Nearly 1/4 of patients suffering from pollen rhinitis develop pollen asthma after > 10 years (disease progresses into new stage ). People with the gene ORMDL3 have an increased risk of contracting asthma. 50% of the population of the island Tristan da Cunha suffer from asthma due to familial inheritance. The mutated gene CC16 (mutation variant 38 A) seems to play an important role in influencing the predilection to asthma. Pg.:   Genetic predisp Pg.: predisposition osition + exog exogenous enous triggers (allergens, inf infections) ections) lead to bronchi bronchial al inflamm inflammation. ation. This results in bronchial hyperreactivity and potentially in bronchial asthma. In conclusion, the disease is characterized by three features: 1. Bronchial inflammation: Of inflammation: Of primary primary importance in tthe he pathogenesis of asthma are inflammatory reactions of the bronchial mucosa caused by allergens or infections. Mast cells, T-lymphocytes, eosinophilic granulocytes and inflammatory mediators participate in this process.

289

 

 

2. Bronchial hyper-reactivity:  hyper-reactivity:   All asthmatics exhibit unspecific bronchial hyper-reactivity (= hyperreactive bronchial system) at disease onset and throughout the course of the disease. According to the methacholine provocation test 15% of the adult population e exhib xhibit it airway hypersensitivity. hypersensitivity. However, only 5% suffer from manifest bronchial asthma. 3. Endobronchial obstruction with limited airflow, due to: - Bronchospasm - Mucosal oedema and inflammatory mucosal infiltration - Hypersecretion of viscous mucus (Dyscrinia)  (Dyscrinia)  - Remodeling of airway walls  walls   Pathogenesis of allergic asthma: The IgE-mediated immediate immediate ttype ype reaction (type I) is critically involved. involved. By interacting with specific allergens, allergens, IgE triggers mast cell degranulation and the release of mediator substances such as histamine, ECF-A (eosinophil chemotactic factor of anaphylaxis), leukotriene and bradykinin. These mediating substances cause endobronchial endobronch ial obstructi obstruction on (see  (see above). In addition addition to the IgE-media IgE-mediated ted immediate asthmatic reaction that occurs after allergen inhalation, a IIgE-m gE-mediated ediated late reaction can occur after 6 – 12 hours. Some patients experience both types of reactions (dual reactions).  At the beginning beginning of the disease allergic asthma asthma is usually usually triggered by one single allergen. allergen. Over the years, however, the number of allergens causing asthmatic attacks frequently increases, so that allergen avoidance prophylaxis becomes more and more difficult.  Pathogenesis of pseudoallergic reaction (PAR) in case of ASA/ NSAID-intolerance: The activity of leukotriene C4 synthase is increased in eosinophilic granulocytes and mast cells of patients suffering from ASA/ NSAID-induced asthma. This may explain the effectiveness of leukotriene antagonists. The PAR activates the same mediator systems as do allergic reactions, but differs from allergic reactions in the following points: tr iggering age agent. nt. • The PARs are not specific to the triggering • They already occur after first-time first-time administration (no sensitisation, not IgE-medi IgE-mediated). ated). • They are not acquired but genetically determined.



Intolerance acetylsalicylic and nonsteroidal anti-inflammatory drugs (NSAID) is observed in approx. 10%towards of patients with non-allergic non-allacid ergic(ASA) asthma (but rrarely arely in children and in allergic asthma). Frequently, there is also an intolerance towards other compounds, such as sulfite (e.g. in wine), tyramine (cheese) and glutamate, among others. Triggering cause of an acute asthmatic attack: • Exposure to antigen, inhalative irritants • Respiratory viral infections • Asthma-triggering drugs (ASA, beta-blockers, parasympathomimetics) • Physical exertion (exercise-induced asthma) • Cold air • Inadequate therapy Cl.:   Cl.:

Asthmatic symptoms can be limited limited to specif specific ic seasons seasons (seasonal (seasonal asthma due to seasonal allergen exposure, e. g pollen allergy), can be without s season-spe eason-specific cific correlation or can c an occur y ear-round (perenni (perennial al asthma). t o upper airway  Cardinal symptom: dyspnoea attacks with expiratory stridor (DD: inspiratory stridor due to obstruction)  Chronic cough as asthma equivalent (cough-variant asthma)  Patient sitting upright during an attack, dyspnoic, using the accessory respiratory muscles: prolonged exhalation. In case of patients’ exhaustion possibly respiratory alternans = alternation of thoracic and abdominal breathing.  Tachycardia; possibly paradoxical pulse due to inspiratory fall in blood pressure > 10 mm Hg.  Ausc.: dry rales: rhonchi, rumbling, cooing. In severe cases of spasticity with ac acute ute pulmon pulmonary ary emphysema or marked emphysema there may be hardly any audible sound ("silent chest").  Perc.: Hypersonorous percussive sound, phrenoptosis  Lab.: •  Eosinophilia and ECP (= eosinophilic cationic protein) prot ein) in blood and sputum    • In allergic asthma, pot. total and specific IgE   • In non-allergic asthma caused by infection, pot. leukocytosis and ESR/CRP   infection-related asthma pot. greenishgreenish-yellowish yellowish coloured) coloured)  Sputum: scant, viscous, glassy (in infection-related  ECG: sinus tachycardia, a sign of right heart overload: p pulmonale, clockwise rotation of the heart along its axis when compared to a previous ECG, pot. right bundle-branch block, pot. S I/Q III type or S I/S II/SIII type  X-ray: Thorax: hyperinflated (markedly x-ray transparent) lung with low-lying diaphragm and narrow heart silhouette  Pufu: - FEV1, PEF = peak expiratory flow rate and decreased MEF50 - Peak-flowPeak-flow- (PEF) measurem measurement ent important ffor or patient self-assessment self-assessment.. Circadian Circadian PEF-variability PEF-variability with fluctuations of >20% are typical of asthma bronchiale in need of treatment. Airway obstruction is more severe in the early morning hours 290

 

 

- Broncholysis (= reversibility test) with: • inhalative bronch bronchodilators odilators (e.g. 400 µg Salbutamol) • inhalative glucocorticoids for 4 weeks.  A FEV1-increase FEV1-increase of >200 ml re resp. sp. of 1 15% 5% compare compared d to the iinitial nitial va value lue is typi typical cal of asthm asthma a needing needing treatment treatment . - Due to trapped intrathoracic air and a shift of the mean respiratory level towards inspiration, pronounced obstruction obstructi on charact characterized erized by a vital capacity decrease and a concurrent residual volume increase. - Increased respiratory resistance (Raw): at a resistance value of 0, 45 kPa/l/s and above, the asthmatic experiences experie nces dyspnoea. Drop of the RAR ≥ 1kp in the reversibility test. - In exercise-induced asthma drop of FEV1 ( ≥ 15%) and increase of RAR under ergometric strain

Note:  Since bronchial asthma is an episodic disease, pulmonary function may be normal during attack-free intervals. For detection within this interval, the hyperreactive bronchial system can be identified by positive provocation test (see below). Arterial blood gas analysis (mm Hg) during asthmatic attack: 3 attack:  3 stages  stages  Stage

pO2 pO n   < 50

 I 

Hyperventilation Partial respir respiratory atory insufficiency respirat ory insufficiency III  Global respiratory

II 

Co.:   Co.:

pCO pCO2

pH  

resp. alkalosis n   resp. acidosis (+ metabol. metabol. ac acidosi idosis) s)

 

n > 45

1. Status asthmaticus [J46] = life-threatening asthmatic attacks resistant to β2-adrenergics 2. Obstructive pulmonary emphysema 3. Pulmonary hypertonia with cor pulmonale 4. Respiratory insufficiency:

Severity degrees of chronic bronchial asthma (German asthma (German Airway Society, 2005): Severity degree 1.

Intermittent

Daytime symptoms ≤ 1 x / week

Nighttime symptoms  

≤ 2 x / month

 

FEV1 or PEF (% of required value) ≥ 80 %

PEF-Variability < 20 %

2. Persistent, Persist ent, mild

< 1 x / day

> 2 x / month

≥ 80 %

20-30%

3.

Persistent, moderate

daily

> 1 x / week

> 60% to < 80%

20-30%

4.

Persistent, severe

cons constant tant

frequently

≤ 60 %

> 30%

Severity levels of acute asthmatic attack in adults: 1. Mild and moderate attack with indication to immediate medical consultation and intensification of therapy: - PEF > 50% of desired or best value - normal speaking - breath frequency < 25/min - heart frequency < 110/ min 2. Acute attack with indication to hospitalisation accompanied by doctor on emergency call: - PEF < 50 of desired or best value - speech dyspnoea - breath frequency ≥ 25/min - heart frequency ≥ 110/min 3. Life-threatening asthmatic attack with indication to survey and treatment in intensive care unit: - PEF < 33% of the desired or best value or PEF 20% • Methacholine (MCH) provocation test: If normal FEV1 and resistance values are seen in a patient suspected to suffer from asthma, it is recommended recommen ded to perform a provocation test for identifying a hyperreactive hyperreactive bronchial system: The test result is positive when, after inhalation of bronchospastic agents (e.g. methacholine), the resistance doubles and the FEV1 drops by 20% at least. PC 20 = provocation concentration (PD 20 = provocation dose), which causes the FEV1 to drop by 20% at least. For methacholine, a PC of 20 ≤  8 mg/ml (or a PD of < 0.30 mg MCH) is regarded as proof that the bronchial system is hyperreactive. B) Diagnosis of manifest bronchial asthma: history + clinic + examination of pulmonary function by broncholysis test C) Allergy diagno diagnostics: stics: 1. Allergy history(occupational/re history(occupational/recreational creational history) 2. Avoidance Avoidance test (e.g. free of symptoms during vacation) and re-exposure test (e.g. recurrence of symptoms at the work place place)) 3. Skin t ests: tests: Prick test, intracutaneous test for detection of an IgE-mediated imme immediate diate type reaction (type I) • Ubiquitous allergen screening: - If pollen allergy is suspected, identification of the main pollen types : . Pollen of the hazelnut, alder, ash and birch tree in spring pollinosis Grass and grain pollen in early summer pollinosis Mugworth and celery in late summer pollinosis (celery-mugworth-spice syndrome) - House dust mites, molds, animal hair and -epithelia - Occupation Occupational al allergens: flour and baking produc products, ts, dust originating from food or feed st stuff, uff, plant allergens, wood and cork dust, latex allergens, animal antigens, hairdresser’s hairdresser’s products, cosmetics, are frequently occurring allergens. Asthma due to isocyanate = occupational disease No. 1315 • Confirmation test with suspected allergens Skin tests are only performed during symptom-free intervals. Depending on their duration of effectiveness, oral corticosteroids, antihistamines and mast cell stabilizers must be discontinued 1 - 4 weeks prior to the test. The evaluation of the test results (weal diameter) occurs after 15 - 20 minutes. The solvent serves as the negative control (0), histamine as the positive control (+++). For the unlike possibility of an anaphylactic reaction keep emergency medication in readiness.

P ay att attention ention to:  a positive outcome of the skin test is not sufficient proof for the allergen’s pathogenetic role. Only a provocation test result that is positive for the suspected allergen is final proof (see below).

292

 

 

4. Immunological diagnostics: • Determination of total IgE: elevated total IgE levels indicate polysensibilisation, in monosensibilisation the values are usually normal. Total IgE is only of limited diagnostic value, since elevated values are also seen in 1/3 of patients with non-allergic asthma. • Determination of specifi specific c IgE antibodies: provides proof that a suspected s uspected allergen has induced induc ed IgE antibody formation (method: e.g. RAST = radioallergosorbent test) • Pot. histamine release test from basophilic granulocytes (not a routine test): Suspected allergens are added in vitro to a leukocyte suspension followed by the measurement of histamine release. 5. Inhalativ I nhalative e allergen provocation ttest: est: In uncertain cases, exposure of target organ mucosa to suspected allergen and evaluation if mild allergy symptoms can be elicited or if an obstruction is measurable (= positive result is regarded as proof). The test is not free of risks (emergency drugs available and resuscitation readiness) and late reactions may occur after 6 - 8 hours (patient should be monitored over this time period). Two days prior to the test discontinue drugs that exert an effect on the bronchial system. 6. Diagnosis of occupational asthma: • Exposure-re Exposure-related lated incr increase ease in bronchial obstruction obstruct ion (peak flow recording during dur ing leisure and work time activities) •Identification of suspected allergen via occupational history (contact company doctor), skin testing and determination of specific IgE antibodies • Provocation test positive Th.:   Th.:

 Causal:

Only possible to a limited degree • Allergic asthma: allergen avoidance or alternatively hyposensitisation (see below) • Non-allergic asthma: Avoidance and rigorous respiratory infection therapy; restoration from existing sinusitis; treatment of underlying gastrooesophageal gastrooesophageal reflux • In case of analgesics intolerance, no application of ASA or NSAID deactivation in order to treat an often simultaneou simultaneous s polyposis nasi (oral application of ASA , repetitiv repetitive e • Adaptive in rising doses).  Medicinal

therapy: •  Anti-infl  Anti-inflammatory ammatory perm permanent anent med medication ication for long- term co control ntrol (“Controller”) Bronchodilators dilators = medi medication cation as needed (“Reliever”) • Broncho Inhalative therapy is preferable whenever possible. 4 stage therapy (German Airway Society, 2005):

Stage 1 Stage 2

“As needed” medication Short-act Short-acting ing beta2 mimetics Short-act Short-acting ing beta2 mimetics

Long-term medication None Low dose of inhalation corticosteroids cortic osteroids (ICS)

Sta Stage 3

Short hort-a -act ctiing bet eta2 a2 mimet etic ics s

Low to med ediu ium m dose dose of ICS ICS plu lus s in inh hala lati tiv ve long-acting beta2 mimetics, ( pot. also in firm combination)  Additional  Additi onal options options - ICS in higher doses

- Montelukast - Retarded theophylline Stage 4 Short-act Short-acting ing beta2 mimetics Same as in stage 3, however, inhalation corticosteroids in high dosage plus oral corticosteroids Note: The medicaments involved in the stage therapy plan can be applied also by pregnant women. 2 variations: 1. “Step down”- principle: orient therapy initially by a higher stage than the current one, application of combination therapies in order to achieve a faster alleviation of symptoms. Gradually reduce medicaments and doses. 2. “Step up”- principle: initial therapy according to the current stage and gradual rise of doses or combination therapy until the best possible symptom control is reached. Every patient should receive a written therapy plan and asthma education. Treatment objective is not to maximize monotherapy effectiveness, but to optimize treatment by combination therapy. The staged therapy diagram can only serve as orientation help for selecting effective therapeutic treatment. In case of acute deterioration, there has to be a quick move upwards in the diagram to the next higher stages. After im improvement provement of symptoms, the reduction in therapy should occ occur ur slowly slowly and cautiously. cautiously. Patient education and patient self-measurement by simple peak flow meter are an integral part of therapy optimisation. 293

 

 

The patient obtains the target value by determining the personal optimum value = highest peak flow value measured while symptom-free. All recorded data is based on the personal optimum value   “traffic light” diagram: Green: Peak flow value 80 - 100% of persona personall optimum valu value: e: symptom-free Yellow: Peak flow va value lue 60 - 80% of personal optimum value: increasing severity of symptoms  urgent need for action according to the staged therapy diagram, application of short-acting short -acting betamimetics betamimetics Red: Peak flow va value lue < 60 %: use em emergency ergency drugs and consult doctors immediately immediately (life (life-threatening -threatening situation) 4 questions to be addressed in “st “steroid-resi eroid-resistant“ stant“ asthma: 1. Does the patient take tthe he required medicine (compliance)? (compliance)? 2. Are there unrecognized trigger mechanisms (allergens, beta-blockers, ASA intolerance, etc.)? 3. Is bronchial asthma diagnosis correct? 4. Do we deal with a steroid-nonresponder? A) Glucocorti Glucocorticosteroids costeroids (CS): D Drugs rugs with the stronges strongestt anti-inflammator anti-inflammatory y effect: Effect(s):

• Anti-inflammatory, anti-allergic and immunosuppressive • Beta-perm Beta-permissive issive effect on bronchi: In status asthmaticus asthmaticus the effectiveness of bronchodilators bronchodilators is temporarily diminished due to poor beta-receptor responsiveness. CS restore beta-receptor sensitivity.



 Topic application as inhalative glucocorticosteroids (ICS) as aerosol inhaler or turbohaler: Evidence degree  A ICS are well-tolerated and are the most effective anti-inflammatorydrugs. Therefore, they are the most reliable component component of anti-asthmatic therapy. ICS are effective only after 1 week and therefore not suited for the treat treatment ment of acute asthma attacks. In acute asthma attacks CS are always administered parenterally (in combination with bronchodilators) In most patients in need of temporary oral CS, substitution by IICS CS is successful. Equivalent doses of inhalation glucocorticosteroids in µg/d (1 mg = 1000 µg): Drug

Low dose

Beclometasone (BDP) Beclomethasone-HFA Budenoside (Pulmicort®) Budenoside Turbohaler ® Ciclesonide (Alvesco® )1)  Flunisolide (Inhacort®) Fluticasone (Flutide®) Mometasone (Asmanex ®)

≤ 500 ≤ 200 ≤ 400 ≤ 200 ≤ 80 ≤ 500 ≤ 250 ≤ 200

Moderate dose

High dose

 ⎞  ⎟  Up to ⎬  2 times the ⎟  low dose amount   ⎟   ⎠ 

 ⎞  ⎟  Up to ⎬  4 times the ⎟  low dose amount   ⎟   ⎠ 

BDP = beclometasonedipropionate – 1) Ciclesonide max. dose 160 µg / d HFA = hydrofluoroalkane The biologically active forms of Budesonide, Flunisolide and Fluticasone are already in existence at the time of application and are rapidly inactivated by the body’ body’s s circulatory circulatory system. Beclometasone Beclometas one and Ciclesonide are pro-drugs that need to be activated enzymatica enzymatically lly in in order to exert exert their full effect. SE:

Oral candid candidiasis; iasis; hoarseness hoarseness (rarely) A dail daily y dose of < 1 mg wil willl most likely not not cause systemic systemic SE. Doses of > 1 mg/d mg/d given to adults over a longer period of time must be e expected xpected to cause systemic systemic SE: suppression of the suprarenal cortex, osteoporosis, cataract formation; growth delay in infants is already observed at doses of > 0.5 mg/d.

Note  The consequences consequences of inadequately inadequately treated asthma are much more serious than the side effects effects of inhalative steroids ((in this case , for example, growth delay is stronger than with ICS). This applies also to pregnant women. Cl.: Lung TBC, mycosis, bacterial bacteri al airway infections

Inhalation guidelines: • At the same total dose, administration twice a day is as effective as inhalation four times a day. • Intrabronchial drug deposition is improved when inhalation aids (spacer) are used. •  Per aerosol dose, only a maximum of 30% of active drug reaches the airways, the remainder settles within the oropharynx. Oropharyngeal fungal infection can usually be prevented by using the spray before meals meals and by rinsing the mouth thereafter. • ICS therapy is not intermittent but consistent long-term base therapy. 294

 

 

• If spasticity is observed, successive administration of beta2-adrenergics followed by administration of ICS after initiation of broncholysis.

•  Combination preparations consisting of ICS and long-acting beta2-agonists may improve compliance ( 

indicated in stages III or IV).   Sytemic application: Evi Evidence dence degree A SE: Monitoring o off side effects is requ required ired for systemi systemic c therapy beneath the cu cushing shing thresho threshold ld dose of 7.5 7.5 mg prednisolone (-equivalent) (-equivalent) per day (see chapter CS): Indications for oral steroid therapy: - Asthma symptoms bec become ome more severe despite optimal dosage of bronchodilators bro nchodilators and inhalation steroids. - Increasing use of bronchodilators by patient. - Peak flow values decrease is < 60% of individual optimum value - Nighttime asthma attacks despite optimal therapy Dos: initially, depending on severity, 25 - 50 mg/d. Slow, step-wise reduction after clinical improvement. Indication for intrav intravenous enous CS therapy: For treatment of status asthmaticus i.v CS therapy is essential. Dos: Initially, ca.100 ca.1 00 mg prednisolone i.v.; when obstruct obstruction ion subsides, 50 mg every 4 h. Clinical improvement should be accompanied by further dose reduction and by switch over to oral treatment. While taking the clinical picture of the patient into account, daily reduction of the dose by 5mg. Usually Usually the total daily dose is administered in the morning. Nighttime asthma attacks are treated by administering in the evening 1/3 of the daily dose around 3 PM. If needed, the amount of CS to be administered can be split into 3 doses, which are then given at different times of the day (e.g. 7 AM, 3 PM and 11 PM). If the dose falls below 20 mg prednisolone/d, inhalation CS should be added as part of the treatment. At a dose below 10 mg prednisolone/d a switch over from oral to inhalation CS should carefully be attempted.

B) Bronchodi Bronchodilators lators:: The bronchial musculature possesses 4 types of receptors: bronchodilatation can only be achieved by beta2receptor stimulation. Stimulation of the remaining receptors (alpha-receptors – histaminergic receptors – cholinergic receptors) leads to bronchoconstri cholinergic bronchoconstriction. ction. The contraction state of the bronchial musculature is dependent upon the cAMP/cGMP (cyclic adenosine monophosphate/cyclic monophosphat e/cyclic guanosine monophosp monophosphate) hate) rat ratio. io. The larger the ratio, the th e slacker the bronchial musculature. β2-sympathomimetics (adenylcyclase stimulants) increase this ratio. Metered dose aerosol utilisation is the method of choice ( respirable size of particles 1-6 µ), since an effect is noticeable within one minute. Volumatic spacers ensure optimal substance dispersion. Dry powder- devices with inspiration-controlled valves improve the synchronisation of dose-release and inspiration. Only 10% of the dose of orally administered preparations are needed when administering by metered dose aerosol 1. Beta2-sympath Beta2-sympathomime omimetics tics (beta2-adrenergics, (beta2-adrenergics, bet beta2-agon a2-agonists): ists): Evidence Evidence degree A Effects: act primarily on bronchial β2-receptors; there are only minor cardiac effects (the heart muscle possesses primarily β1-receptors). Beta2-sympathomime Beta2-sympathomimetics tics are the most effective bronchodilators bronchodilators

• Rapid-acting beta2-sympathomimetics (=RABA): Duration of effectiveness: 4-6 hours Ind: for immediate asthma attack therapy - Fenoterol = Berotec ® - Salbutamol (generics) - Terbutaline = Bricanyl® 

• Long-acting beta2-sympathomimetics (long acting beta antagonists = LABA): Duration of effectiveness 8 -12 h Ind: use on and above stage 3 of the 4-stage diagram: prophylaxis of nighttime asthma attacks. Salmeterol is not suited for immediate therapy of asthma attacks! Formeterol has a faster effect. Not to be used as a monotherapeutic. Only for use in combination with ICS

Note: from stage 3 asthma on, base therapy consists of long-acting beta2-sympathomimetics beta2-sympathomimetics + inhalation corticosteroids! LABA and ICS-combination strengthen the bronchodilating effect. Salmeterol has a delayed effectiveness and is therefore not suited for immediate therapy . Formeterol has a more rapid effectiveness. Examples: Formoterol = Foradil ® or Oxis®  Salmeterol = Serevent® or A eromax eromax®  Combination preparations facilitate the application of ICS+ LABA, e.g. Salmeterol + Fluticasone (Viani ®), Formoterol + Budesonide (Symbicort® ); Formoterol+ Beclametasone (Foster ®).  SE:

related: tachycardia and palpitation, ventricular arrhythmias, blood pressure increase, induction •  Heart of angina pectoris in coronary heart disease.

295

 

 

• Tremo Tremor, r, restlessne restlessness, ss, sleep disorders disorders • Pot. hypokalemia at higher doses  According to the SMART study, mo mortality rtality rate was higher under administration of long acting betamimetics than under administration of inhalative steroids alone. LABA are indicated only from stage III onwards For mild asthma ( ST. I, II), only symptom-oriented doses of short-acting beta 2adrenergics are recomm recommended. ended. CI:

Coronary heart hyperthyroidism

disease,

hypertrophic

obstructive

cardiomyopathy,

tachyarrhythmias

and

Dos: beta2-adrenergics: renergics: are appli applicated cated for initial therapy in all therap therapy y stages. 2-4 strokes of a • Short-acting beta2-ad short-acting beta 2- adrenergic are administered; if needed, repeat the procedure after 10-15 minutes. Consider maximum dose/d .

• Long-acting beta2-adrenergics: 2 strokes in the morning and/or evening Long-acting beta2-adrenergics are also effective against nighttime asthma.

Note:  Warning signs of deterio deterioration ration are: drop of the peak-flow peak-flow-value -value >15% o off the individual best value, value, diminished ability to withstand strain, night-time asthmatic complaints, no improvement after 2 strokes of a short-acting betamimet betamimetic ic Reevaluation of the entire therapy plan and adjustment to a higher disease stage is required. 2. Parasympatholytics (anticholinergics): (anticholinergics): Evidence Evidence degree A ® • Long-acting :Tiotropium (Spiriva ): 1 puff per day • Short-acting :Ipratropium bromide (Atrovent®): 3 X 1-2 puffs per day  Anticholinergics are signif  Anticholinergics significantly icantly less less effective than beta2-sympathom beta2-sympathomimetics imetics . (In COPD, COPD, it is vice-versa). SE: Unlike atropine, both substances are absorbed poorly within the gastrointestinal tract. Thus, systemic atropine effects effect s (oral dryness, accommodation disturbances dis turbances)) occur rarely and are only mild. Oxitropium bromide is effective for approx. 6 h, thus making it suitable as a protectant against nighttime asthma. Parasympatholytics may be combined with β2-stimulators, in which case the β2-stimulator dose can be reduced, e.g. Berodual® metered dose aerosol (= Ipratropium bromide + Fenoterol). 3. Theophylline/-derivatives (Methylxanthine): Evidence degree A Effect(s):Broncholysis, mast cell protection, stimulation of the respiratory centre and the respiratory musculature, positive inotropic and chronotropic cardiac effect. In moderate-grade obstruction, theophylline acts less bronchodilatory than beta2-adrenergics. In severe obstruction its effect is additive to that of beta2adrenergics. Ind: Option of reserve on th therapy erapy stage III . As tthe he risk risk of cardiovascular m mortality ortality is increased under under administration of theophilline, it is a means of last choice both in long term therapy and in case of emergency. SE:

• Central nervous system: restlessness, sleep disorders, headache, muscle tremor, hyperventilation • Gastrointestinal system: heartburn, nausea, vomiting and diarrhoea tachycardial al arrhythmias • Heart related: tachycardia, extrasystoles and tachycardi • Other SE: Hypokalemia, allergic reactions occurring after i.v. application of ethylendiamine-containing preparations

Cl.:

Recent m myocardial yocardial infarction, tachyarrhythmia and hypertrophic obstructive obstructi ve cardiomyopathy

Theophyllines only have a narrow therapeutic window. The therapeutic range lies between 5 - 15 mg/l (plasma level). At higher levels SE become more frequent and severe (tachycardial arrhythmias, convulsions, deaths). Theophylline-clearance and/or plasma half-life period varies significantly among individuals. Primarily the liver metabolizes 90% of administered theophylline. The drug decomposing cytochrome P 450 enzyme enzym e system is influ influenced enced by various factors  increased elimination-half-life elimination-half-life period in patients > 60 years of age, febrile infections, liver damage, right heart insufficiency (cor pulmonale) as well as by oral intake of specific drugs (e.g.cimetidine, macrolide antibiotics, quinolones, allopurinol). These situations require a dose reduction. Caffeine also acts bronchodilatory and amplifies the effect and SE of theophylline. Consequence: since Consequence: s ince clearance clearance varies among individ individuals uals and ma may y also be altered by oral intake of additional additional drugs, it is recommended to monitor the therapy by measuring plasma levels (e.g. drug monitoring via test strip). This is especially recommended for the above mentioned situations  Appl.:  Usually, retard tablets are given orally (e.g. Bronchoretard ®); when given as drops the effect occurs more rapidly (e.g. Solosin®). Dos: Very slow incr increase ease in dosage; daily dosage 400 - 800 mg administ administered ered in 2 doses, preferably while monitoring the plasma level. Division of the daily dose into a 1/3 morning and 2/3 evening delivery or (in nighttime asthma) onetime dose in the evening.  Intraveno  I ntravenous us (e. (e.g. g. Solosin®) Only in hospital, not in outpatient emergency service. Dose: see below . 296

 

 

C) Leukotriene receptor antagonist (= LTRA) = anti-leukotrienes:  anti-leukotrienes:   Not all the patients benefit from leukotriene antagonist treatment. If after a period of 1 - 2 weeks no effect is observed, they will continue c ontinue to remain ineffective. Montelukast Monteluka st (Singul (Singulair  air ®) Ind: For prophylactic use only (beginning at stage III), Analgesic asthma; not appropriate for therapy of acute asthma attacks. Cl.: Pregnancy, Pregnancy , lactat lactation ion period and allergic reaction reactio n Dos: e.g. Monteluka Montelukast st (Singulair  (Singulair ®) 10 mg/d orally at nighttime Effect(s): Blocks the media mediators tors of inflam inflammation mation SE: Headache, abdominal discomfort, very rarely other SE (  producer’s indication)  D) Cromones : Cromones : Effects: Inhibition of mediator release from sensitized mast cells  Almost all studies studies of the la last st 20 years show no better better effect than placebo  placebo  Cromoglicine acid , Dinatriumchromoglicicum (DNCG) and Nedocromil E) Omalizumab Omalizumab (  ( Xolair ® )  Effects: Monoclonal IgE-ab with s.c. application SE : e.g. oversensitivity reactions up to anaphylaxis; headaches; CI are to br considered Ind.: last resort in therapy-resi therapy-resistant stant allergic allergic asthma; asthma; high costs of therap t herapy y Dos.: every 2-4 weeks a s.c. dose ( dose results from pre-therapeutic IgE and bw.)  F) Additional therapeutic measures:  Administration of antibiotics for treatment of airway infection: Selection of appropriate antibiotics: see c hapt. on COPD. Successful treatment of the infection restores the responsiveness of the bronchial beta-receptors to administered bronchodilators  Expectorants (also see chap. COPD): Ind: viscous bronchi bronchial al secretion (dyscrinia), stagnant secretion (mucostasis), which which is difficult to expectorate. - Secretoly Secretolytics: tics: ( Bromhexine, ambroxol) } - Mucolytics Mucolytics:: ( N- acetylcysteine) acetylcyst eine) } Benefit not proven



Note:  • The most effective secretolytic is the intake of copious amounts of fluid. Reduction of exsiccation and avoidance of overhydration.   Humidi Humidification fication of tthe he inhaled air facilitates expectoration. Water with an optional addition of sodium • chloride is sufficien s ufficient. t.   Antituss Antitussives, ives, e.g. codeine, are not ind indicat icated ed (except (except for nighttime irritating cough and sleep disorder).   Facilitat Facilitation ion of mucus ex expect pectoration oration by flutter mucus mucus clearing device (e.g. V VRP1-Desiti RP1-Desitin n®)





 Breathing training:  Avoidance  Avoi dance of pursed breathing and hyperventilation, hyperventilation, breathing with pointed lips (= preceding respiratory respiratory resistance = "pursed lip breathing")   prevention of expiratory bronchial collapse; learning of productive expectoration, facilitation of expectoration by performing tapping massage



 Therapy of possible gastrooesophageal reflux



 Psychosomatic therapy and suitable clim c limatotherapy atotherapy may be helpful helpful..

Therapy of severe asthma attacks: 

 Intensive care unit: monitoring monitoring of c ardiovascular ardiovascular and pulmonary function, water and electrolyte balance



 Maintain in seated position



 Sedation: Doctor or nursing staff must make an effort to calm down the patient. Tranquilizers (e.g. diazepam) should not be given due to their respiratory depressive effect. They are absolutely contraindicated in starting CO2retention as well as under ambulant conditions.



 Oxygen administration: Pulse oximetry-/blood gas analysis- controlled O 2 supply via nasal tube as needed (dependent on the degree of hypoxia, hypoxia, 2 - 4 l/min). At the same time pay attention to signs of respiratory respiratory depression and initiate, initiate, if needed, assisted/controlled artificial ventilati ventilation. on.



 I.v.  I. v. glucocorticosteroids are indispensable Dos: 50-100 mg of prednisolon (-equivalent) every 4 - 6 h i.v.



 Use of broncholytic broncholytics s with consideration of previous - Short-acting beta2-sympathomimetics are the therapy: most effective bronchodilators (3 x more effective than theophylline). Initial dosage: every 30 minutes 3 strokes, then increase dose interval to 2 - 4 h. 297

 

 

Pay attention to:   after previous self-overdosing of beta-adrenergics by patient, the further use of betaadrenergics is potentiall pot entially y dangerous (tachycardial arrhythmias, arrhythmias, hypokalemia, hypokalemia, amo among ng others others). ). Beta-adrenergic parenteral therapy only for heart-healthy patients and at heart frequencies < 130/min, e.g. reproterol (e.g. Bronchospasmin Bronchospasmin®) 1 amp. = 1 ml = 90 µg slowly i.v., additional drug is administered via infusion ( see manu manufacturer’s facturer’s specification). - Theophylline: Parenteral (i.v.) application only in hospital ( in ambulant emergency service, the German  Airway Society Society does not recom recommen mend d it because of possible S SE) E) Dos.: Initially 5mg/kg BW as short i.v. infusion. Maintenance dose 0.5 to 0.7 mg/kg BW/h. In case of preceding theophylline theophylline therapy first detect s serum erum concentration, concentration, then adjust the dose (careful: intoxication) - Magnesium sulfate ( 2, 000 mg in in 50 ml N NaCl aCl 0.9 % slowly via infusion). 

 Sufficient parenteral supply of liquid



 If infection-rel infection-related ated asthma is s suspe uspected, cted, administration of an antibiotic (see c chapt. hapt. COPD)



 Before indica indicating ting invasive ventilat ventilation, ion, non-invasive non-in vasive ventilatio ventilation n should by all means be attempted, if the th e aforementioned therapy measures have not led to improvement: with non-invasive ventilation, the rate of complications as well as the mortality rate are considerably lower than with invasive ventilation. Diaphragmatic muscle fatigue with paradoxical inspiratory retraction of the abdominal wall as well as an increasing disturbance of conciousness are indications for invasive ventilation. Ind.: for acute respiratory insufficiency with pO2 < 50 and pCO2 > 55 mm Hg, and for respiratory acidosis. To some extent, patients suffering from pre-existing chronic hypercapnia tolerate higher pCO 2  values. Artificial respiration is indicated when the following symptoms are observed: diaphragmatic muscle fatigue with paradoxical inspiratory retraction of the abdominal wall as well as a worsening reduced state of consciousness.



 Stress ulcer prophylaxis (with acid blockers)

In case of an asthma attack be aware of: of:    Antitussives,  Antitussiv es, beta-blockers beta-blockers (also in the form of eye drops!), ASA/NSAIDs ASA/NSAIDs (PAR!), sedatives (respiratory (respiratory depression!), parasympathomimetics (pilocarpine, carbachol), subclavian catheter (increased risk of pneumothorax). pneumo thorax). Avoid the use of digitalis medicines if possible; monitoring of blood levels if administration is necessary (danger of developing hypoxemia- and catecholamine-induced arrhythmias). In severe acute asthma attacks do not use dry powder inhalers.

Note: take every asthma attack seriously and immediately transfer patient to the hospital by medical emergency service (emergency physician present) Monitor patient on intensive medical care level No premature aggressive therapeutic measures (intubation and artificial respiration) unless all other possibilities have been exhausted. If the patient does not respond respond to the therapy, the following possible reasons have to be excluded: - insufficient adherence to therapeutic recommendations recommendations - wrong inhaler technique of the patient - Other illnesses: COPD? Central airway stenosis? Churg-Strauss-Syndrome? Vocal chord dysfunction? Anxiety state? Recurrent pulmonary embolisms? - Continuous exposure to harmful substances and allergens - Administration of ASA/NSAID despite ASA/NSAID-intolerance - Treatment with betablockers and other medicaments which can worsen/trigger asthma

Bronchial asthma prophylaxis 1. Protection of the t he hyperreactiv hyperreactive e bronchial system from irritating stimuli: • Allergen avoidance (if patient suffers from seasonal pollen allergy, vacation choice dependent on pollen season) • Quit smoking • Avoidance of cold air, fog, dust, (occupational) harmful inhalant substances • I Infection nfection prophylax prophylaxis is • Active immunisation against pneumococcae and influenza virus • Avoidance of exaggerated physical strain (danger of developing exercise-induced asthma) • Therapy of possible gastrooesophageal reflux  Avoidance measures for patients  Avoidance patients sufferin suffering g from house dust mite mite allergy: • No small domestic animals, indoor plants, carpets, upholstered furniture and other dust traps •  Mite-resistant beds and covers (mattresses, bed coverings and pillows) with synthetic fibre fillings, which are watervapor permeable. • Wearing of pajamas at nighttime (prevention of epithelial scale accumulation in the bed) • Maintain low relative humidity and room temperature  Daily vacuum cleaning with fine dust filter and frequent change of bed linens •• Examine dust for mite faeces (Acarex®-Test) and house clean-up with acaricide acaricides s (e.g. Acarosan® foam and powder) • Vacation in the high mountains or in areas with desert climate 298

 

 

2. Approx. Approx. 50% o f all cases of infantile asthma are avoidable through atopy prevention in infants: breast-feeding as long as possible, no pets and no exposure to passive smoke (see also chapt. food allergy) 3. If pollen allergy is diagnosed, e exam xamine ine for frequently occurring cross-allergy, cross-allergy, e.g. between birch pollen and raw pomaceous fruit (esp. apples) and carrots; between mugwort and celery/spices. (mugwort/celery/spices/syndrome) 4. Do not use medicines that may initiate an attack, e.g. - Acetylsalicylic acid or NSAID for PAR - Beta-receptor blockers 5. For life-threatening allergies (e.g. insect venom allergics) prescribe emergency kit + instruct to enable initial emergency treatment by patient/fam patient/family ily member. 6. Specific immune therapy (SIT): Syn: hyposensibilisation, desensibilisation Ind: Patient < 55 years of age, p period eriod of symptoms not not > 5 year years. s. Preferabl Preferably y monovalent monovalent allergy. allergy. Treatment Treatm ent principle: perfor perform m hyposensibilisi hyposensibilisisation sation during the asthma-free period. By subcutan subcutaneously eously administering small subclinical doses of inhalant allergen, which are increased during the course of therapy, an increased tolerance to the relevant allergen is to be achieved. Duration of hyposensibilisation: at least 3 years. SE: In 5 - 15% of cases mild mild local symptoms symptoms at the injection injection site, bronchospasm, bronchospasm, anaphylactic anaphylactic reactions (rare (rare); ); late reactions after 4 - 8 h are possible  the patient pat ient should rem remain ain at least ½ hours (better 2 hours) at the t he doctor’s office and should be educated about possible late reactions (bronchospasm) and their treatment by the patient. Cl.: Infections, a asthmatic sthmatic disorde disorder, r, consumin consuming g diseases, therapy therapy with beta-blockers (decrease (decrease in the the efficacy of therapies that use adrenaline to treat anaphylactic reactions); diseases which cause a necessary shock therapy with adrenaline to be an additional danger to the patient (e.g. coronary heart disease), immunologic immunologic diseases, disease s, pregnancy. Success rate: up to 70%, depending on age (outcome more favourable for young patients than for old patients, outcome more favourable for monovalent allergy than for polyvalent allergy) Prg:   Infant asthma: absence of complaints in later life in > 50% Prg: 50% of cases  Adult asthma: approx. approx. 20% of cases are cured cured,, improvem improvement ent in approx. 40% of cases  A rigorous, long-term therapy utilizing inhalan inhalantt glucocorticoids glucocorticoids can signif s ignificantly icantly im improve prove the prognosis. Germany Germany is presently still one of the countries with the highest bronchial asthma mortality rates (after England, Australia and New Zealand).

PNEUMONIA

[J18.9] 

Internet-Info: www.capnet.de  Def.:   Acute or chronic inf Def.: inflamma lammation tion of the alveol alveolar ar and/or interstitial interstitial space of the lung. Ep.:   In industrial countries it is the iinfectious Ep.: nfectious disease disease with the highest mortality mortality rate. Worldwide pneumonia pneumonia ranks third in statistics on causes of death. Incidence: 8 – 15/1,000/y Classification principles  A. Pathological Pathological classification:  By location of pneumonia: - Alveolar pneumonias (usually bacterial infections) - Interstitial I nterstitial pneum pneumonias onias (usually viral infections) 

 By size of the pneumoni pneumonic c area: - Lobar pneumonia - Lobular (focal) pneumonia

B. Aetiol Aetiologic ogic c classifi lassification: cation:  Infections: viruses, bacteria, fungi and parasites  Physical noxious stimuli (radiation, foreign body in bronchi)  Chemical noxious stimuli (e.g. irritating gases, aspiration of gastric juice or of oil)  Cardiovascular disorders (e.g. infarct pneumonia, congestive pneumonia) C. Clinical C linical classification: 1. Taking into account pre-existing illnesse illnesses: s: - Primary pneumonias: pneumonia occurrence in individuals with no pre-existing cardiopulmonary condition - Secondary pneumonias: resulting from some other pulmonary or cardiac disease, e.g.  Circulatory disorders (congestive pneumonia in patients with left heart insufficiency, infarct pneumonia after pulmonary embolism, hypostatic pneumonia in bedridden patients)   Bronchia Bronchiall changes (bronchial carcinoma, bronchial stenoses, e.g. c aused by foreign bodies, bronchiectases)  After aspiration of foreign material (aspiration pneumonia) pneumonia)   Bacterial superinf superinfection, ection, e.g. resulting from influenza infection 2. By course of disease: acute or chronic (DD: TBC, fungal infections) 299

 

 

Copyright © 2010 by Dr. Gerd Herold, Cologne, Germany. All rights reserved. Original German Textbook by Gerd Herold Translation by Ralf Brücker, Bettina Mues, Hedwig Möller, Sylvia Möller Project coordination by Björn Gemein Volume One: 432 pages in total, Royal (6” x 9”) Table of Contents: Evidence based medicine, Haematology, Cardiology, Pulmonology, Gastroenterology (part 1) ISBN 978-1-4467-6367-4 Price: € 23.50 Volume Two: 408 pages in total, Royal (6” x 9”) Table of Contents: Gastroenterology (part 2), Salt and water homeostasis, Nephrology, Rheumatology, Metabolic system disorders, Endocrinology, Angiology, Infectious Inf ectious diseases, …, Reference intervals ISBN: 978-1-4467-6368-1 Price: € 23.50 Digital Edition: 824 pages in total, DIN A4 Table of Contents: See Vol. 1 + 2 Available at Lulu.com, ID 9545211 Price: € 35.00 The e-book requires Adobe Digital Editions  For more information about Adobe Digital Editions visit http://www.adobe.com/products/digi http://www.adobe.com/products/digitaleditions/ taleditions/  http://blogs.adobe.com/digitalpublishing/supported lishing/supported-devices -devices For a list of supported devices visit http://blogs.adobe.com/digitalpub

For more information about the book visit http://www.herold-internal-medici http://www.herold-internal-medicine.com/ ne.com/ Adobe Digital Editions (incl. logo) and the Acrobat/PDF-logo are copyright © by Adobe Systems Inc. (www.adobe.com) The Lulu-logo is c opyright © by Lulu Enterprises Inc. (www.lulu.c (www.lulu.com) om)