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Abbreviations
AAA AB ACE ADB ADH AET AF AG AIDS AIHA AN ANA 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 DD DEF DHD DHS DI DIC DNA DSA DVT EBV ECF ECG EEG EF EHEC ELISA EN ENT EP ESP ESR ET EU F FFP Abdo minal aortic aneurism Antibodies Angiotensin converting enzyme Anti-Desoxyribonucleotidase B Antidiuretic hormone Aetiology Atrial fibrillation Antigen Acquired Immunodeficiency Syndrome Autoimmune hae molytic anaemia Autonomic neuropathy Anti nuclear antibodies Anti neutrophile cytoplasmatic antibodies Atrial natriuretic peptide And others Activated Protein C Antiphospholipid syndrome Approximately Adult respiratory distress syndro me Acute renal failure As soon as possible Atrial septum defect Antistreptolysin Antithrombin Antithrombin Adenosine Triphosphate Abdo minal 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 disease Cyclooxygenase C-reactive protein Cholesterol Synthesis Enzyme Cerebrospinal Fluid Computer tomography Carbohydrate unit Chronic venous insufficiency Central venous pressure Chest X-ray 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 E. coli Enzyme linked immunosorbent assay Enteral nutrition Ear Nose & Throat Epidemiology Especially Erythrocyte Sedimentation Rate Etiology European Union Female Fresh Frozen Plasma FUO GBM GFR GI GN HBV HCT HI HIT HIV HLT HPV 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 PAT PAT PCR PE PEP PET PFO PG PI PID PMC PN PNH POSS PPC PPH PPSB PRG PRO PTCA PTH PTS PTT RA Fever of unknown origin Glo merular basement membrane Glo merular filtration rate Gastrointestinal Glo merulonephritis Hepatitis B Virus Haematocrit Histology Heparin induced thrombocytopenia Human Immunodeficiency Virus Half life time Human Papillo ma Virus Herpes Simplex Virus Haemolytic uraemic syndro me 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 Intravenous Intravascular fluid Laboratory tests Lymphadenopathy syndrome Lactate Dehydrogenase Low density lipoprotein Lymphocyte doubling ti me 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 Pathogen Pathology Polymerase chain reaction Pulmonary embolism Post exposure prophylaxis Positron emission tomography Persistent foramen ovale Pathogenesis Protease inhibitor Pelvic infla mmatory disease Pseudome mbranous 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 Post Thrombotic Syndrome Prothrombin time Rheumatoid arthritis

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

Reticular Endothelial Syncythium Rheumatoid factor Ribonucleic acid Raynauds Syndrome right ventricular Subcutaneous Side effects Syndrome of inadequate ADH secretion Streptokinase Systemic lupus erythematosus Stage Sexually transmitted disease Sulfonyl urea Symptoms Synonym Thoracic aortic aneurism Thrombendarteriectomy Transoesophageal echocardiography

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

Therapy Total hip replacement Transitory ischaemic attack Thrombangiitis obliterans Treponema Pallidum Hae magglutinin 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 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

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 segments can expand. The effect is similar to the one reached by lung volume reduction surgery. In clinical testing (Vent-study). 5. Lung transplantation: see chapt. respiratory insufficiency Prg: Critically dependent upon early stage optimized therapy implementation. Without smoking cessation the disease progression cannot be influenced: average life expectancy for smokers is 48 years, for non-smokers 67 years. With a FEV1 value of < 1 l, life expectancy is significantly reduced and the patient is occupationally disabled. Respiratory insufficiency 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.: International consensus report on 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-reactivity). German Airways Society: bronchial asthma is an inflammatory disorder of the airways characterized by bronchial hyper-reactivity and variable, partially reversible airway obstruction. Prevalence: approx. 5% of adults and up to 10% of children; trend towards worldwide increase in prevalence; 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 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 exclusively from extrinsic asthma and another 30% exclusively from intrinsic 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) Allergic asthma (extrinsic asthma) [J45.0] 1. caused by environmental allergens (see 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: pseudoallergic reaction (PAR) to ASA and mostly (90%) also to NSAID 3. Asthma caused by chemical irritation or toxic substances (if work-related: 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 diseases (bronchial asthma, allergic rhinitis and neurodermitis) have a prevalence of 30% and are characterized by a polygenically inherited predisposition for 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 a risk of illness in 60 - 80% of cases (it is half that 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 predisposition + exogenous triggers (allergens, infections) lead to bronchial inflammation. This results in bronchial hyperreactivity and potentially in bronchial asthma. In conclusion, the disease is characterized by three features: 1. Bronchial inflammation: Of primary importance in the 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.

Ep.:

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2. Bronchial 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 exhibit airway 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) - Remodeling of airway walls Pathogenesis of allergic asthma: The IgE-mediated immediate type reaction (type I) is critically involved. By interacting with specific 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 obstruction (see above). In addition to the IgE-mediated immediate asthmatic reaction that occurs after allergen inhalation, a IgE-mediated late reaction can occur after 6 12 hours. Some patients experience both types of reactions (dual reactions). At the beginning of the disease allergic asthma is usually triggered by one single 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: The PARs are not specific to the triggering agent. They already occur after first-time administration (no sensitisation, not IgE-mediated). They are not acquired but genetically determined. Intolerance towards acetylsalicylic acid (ASA) and nonsteroidal anti-inflammatory drugs (NSAID) is observed in approx. 10% of patients with non-allergic asthma (but rarely 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.: Asthmatic symptoms can be limited to specific seasons (seasonal asthma due to seasonal allergen exposure, e. g pollen allergy), can be without season-specific correlation or can occur year-round (perennial asthma). Cardinal symptom: dyspnoea attacks with expiratory stridor (DD: inspiratory stridor due to upper airway 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 acute pulmonary 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) in blood and sputum In allergic asthma, pot. total and specific IgE In non-allergic asthma caused by infection, pot. leukocytosis and ESR/CRP Sputum: scant, viscous, glassy (in infection-related asthma pot. greenish-yellowish coloured) 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. SI/QIII type or SI/SII/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-flow- (PEF) measurement important for patient self-assessment. Circadian 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
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- Broncholysis (= reversibility test) with: inhalative bronchodilators (e.g. 400 g Salbutamol) inhalative glucocorticoids for 4 weeks. A FEV1-increase of >200 ml resp. of 15% compared to the initial value is typical of asthma needing treatment . - Due to trapped intrathoracic air and a shift of the mean respiratory level towards inspiration, pronounced obstruction characterized 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 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 stages Stage I Hyperventilation II Partial respiratory insufficiency III Global respiratory insufficiency Co.: pO2 n < 50 n > 45 n resp. acidosis (+ metabol. acidosis) pCO2 pH resp. alkalosis

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

Severity degrees of chronic bronchial asthma (German Airway Society, 2005): Severity degree 1. Intermittent 2. Persistent, mild Daytime symptoms 1 x / week < 1 x / day Nighttime symptoms 2 x / month > 2 x / month > 1 x / week frequently FEV1 or PEF (% of required value) 80 % 80 % > 60% to < 80% 60 % PEF-Variability < 20 % 20-30% 20-30% > 30%

3. Persistent, moderate daily 4. Persistent, severe constant

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 <100 l/min - SaO2 < 92% (PaO 2 < 8 kPa) - PaCO2 normal (4,6-6kPa) or raised - No breath sound (quiet lung) - Shallow breathing - Cyanosis - Bradycardia or arterial hypotension, arrhythmias - Exhaustion, confusion, somnolence or coma DD: A) Other diseases: Chronic obstructive bronchitis (COB): history Cardiac asthma = dyspnoea in patients with left heart insufficiency and pulmonary congestion (impending pulmonary oedema): wet rales, x-ray thorax: pulmonary congestion Dyspnoea resulting from recurrent pulmonary embolisms Pay attention to: since both diseases may additionally be accompanied by reflex bronchoconstriction, antiasthmatic therapy may lead to a partial improvement of symptoms; this, however, must not lead to the misdiagnosis of bronchial asthma.
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 Inspiratory stridor in extrathoracic airway obstruction: e.g. foreign body aspiration, glottic oedema Vocal cord dysfunction (VCD): Predominantly younger women are affected (partly in medical occupations, families). Paradoxical, intermittent closure of vocal cord with peracute and often threatening dyspnoea, usually inspiratory audible stridor,self-limiting (seconds/minutes), cause: gastrooesophageal reflux or mucus irritation due to post-nasal drip caused by sinusitis/rhinitis or psychosomatic factors. Frequently in combination with asthma. Cough attacks can generate VCD. During symptom-free intervals no pathological findings. Th.: patient education, learning of specific breathing techniques; asthma therapy is ineffective Tension pneumothorax (auscultation reveals difference between sides) Hyperventilation syndrome Bronchial asthma in carcinoid syndrome and Churg-Strauss syndrome Eosinophilic bronchitis: Chronic cough with sputum eosinophilia without bronchial hyperreactivity of indistinct genesis, good reaction to inhalative corticosteroids B) DD extrinsic (allergic) - intrinsic (non-allergic) asthma: Extrinsic asthma Atopic individual in the family Allergic rhinitis and/or conjunctivitis Hypersensitivity towards analgesics Specific i.s. IgE elevated Positive skin and/or provocation test Disease onset Di.: Very frequent Very frequent Yes Yes Predominantly in infancy Intrinsic asthma

Frequent Predominantly in adulthood

A) Diagnosing the hyperreactive bronchial system: Peak flow record documenting morning and evening measurements over a 4 week period: fluctuations of the peak flow value > 20% Methacholine (MCH) provocation test: If normal FEV1 and resistance values are seen in a patient suspected to suffer from asthma, it is recommended to perform a provocation test for identifying a 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 diagnostics: 1. Allergy history(occupational/recreational history) 2. Avoidance test (e.g. free of symptoms during vacation) and re-exposure test (e.g. recurrence of symptoms at the work place) 3. Skin tests: Prick test, intracutaneous test for detection of an IgE-mediated immediate 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 - Occupational allergens: flour and baking products, dust originating from food or feed stuff, plant allergens, wood and cork dust, latex allergens, animal antigens, hairdressers 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. Pay attention to: a positive outcome of the skin test is not sufficient proof for the allergens pathogenetic role. Only a provocation test result that is positive for the suspected allergen is final proof (see below).

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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 specific IgE antibodies: provides proof that a suspected allergen has induced 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. Inhalative allergen provocation test: 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-related increase in bronchial obstruction (peak flow recording during 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.: 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 reflux In case of analgesics intolerance, no application of ASA or NSAID Adaptive deactivation in order to treat an often simultaneous polyposis nasi (oral application of ASA , repetitive in rising doses). Medicinal therapy: Anti-inflammatory permanent medication for long- term control (Controller) Bronchodilators = medication as needed (Reliever) Inhalative therapy is preferable whenever possible. 4 stage therapy (German Airway Society, 2005): As needed medication Short-acting beta2 mimetics Short-acting beta2 mimetics Short-acting beta2 mimetics Long-term medication None Low dose of inhalation corticosteroids (ICS)

Stage 1 Stage 2 Stage 3

Low to medium dose of ICS plus inhalative long-acting beta2 mimetics, ( pot. also in firm combination) Additional options - ICS in higher doses - Montelukast - Retarded theophylline Stage 4 Short-acting 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 improvement of symptoms, the reduction in therapy should occur slowly and cautiously. Patient education and patient self-measurement by simple peak flow meter are an integral part of therapy optimisation.
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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 personal optimum value: symptom-free Yellow: Peak flow value 60 - 80% of personal optimum value: increasing severity of symptoms urgent need for action according to the staged therapy diagram, application of short-acting betamimetics Red: Peak flow value < 60 %: use emergency drugs and consult doctors immediately (life-threatening situation) 4 questions to be addressed in steroid-resistant asthma: 1. Does the patient take the required medicine (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) Glucocorticosteroids (CS): Drugs with the strongest anti-inflammatory effect: Effect(s): Anti-inflammatory, anti-allergic and immunosuppressive Beta-permissive effect on bronchi: In status asthmaticus the effectiveness of 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 of anti-asthmatic therapy. ICS are effective only after 1 week and therefore not suited for the treatment 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 ICS is successful. Equivalent doses of inhalation glucocorticosteroids in g/d (1 mg = 1000 g): Drug Beclometasone (BDP) Beclomethasone-HFA Budenoside (Pulmicort) Budenoside Turbohaler Ciclesonide (Alvesco )1) Flunisolide (Inhacort) Fluticasone (Flutide) Mometasone (Asmanex ) Low dose 500 200 400 200 80 500 250 200 Moderate dose Up to 2 times the low dose amount High dose Up to 4 times the low dose amount

BDP = beclometasonedipropionate 1) Ciclesonide max. dose 160 g / 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 bodys circulatory system. Beclometasone and Ciclesonide are pro-drugs that need to be activated enzymatically in order to exert their full effect. SE: Oral candidiasis; hoarseness (rarely) A daily dose of < 1 mg will most likely not cause systemic SE. Doses of > 1 mg/d given to adults over a longer period of time must be expected to cause 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 of inadequately treated asthma are much more serious than the side 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 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 and by rinsing the mouth thereafter. ICS therapy is not intermittent but consistent long-term base therapy.
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 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: Evidence degree A SE: Monitoring of side effects is required for systemic therapy beneath the cushing threshold dose of 7.5 mg prednisolone (-equivalent) per day (see chapter CS): Indications for oral steroid therapy: - Asthma symptoms become more severe despite optimal dosage of bronchodilators 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 intravenous CS therapy: For treatment of status asthmaticus i.v CS therapy is essential. Dos: Initially, ca.100 mg prednisolone i.v.; when obstruction 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 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) Bronchodilators: 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 bronchoconstriction. The contraction state of the bronchial musculature is dependent upon the cAMP/cGMP (cyclic adenosine monophosphate/cyclic guanosine monophosphate) ratio. The larger the ratio, the slacker the bronchial musculature. 2-sympathomimetics (adenylcyclase stimulants) increase this ratio. Metered dose aerosol utilisation is the method of choice ( respirable size of particles 1-6 ), 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-sympathomimetics (beta2-adrenergics, beta2-agonists): Evidence degree A Effects: act primarily on bronchial 2-receptors; there are only minor cardiac effects (the heart muscle possesses primarily 1-receptors). Beta2-sympathomimetics are the most effective 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 + 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 Aeromax Combination preparations facilitate the application of ICS+ LABA, e.g. Salmeterol + Fluticasone (Viani), Formoterol + Budesonide (Symbicort ); Formoterol+ Beclametasone (Foster ). SE: Heart related: tachycardia and palpitation, ventricular arrhythmias, blood pressure increase, induction of angina pectoris in coronary heart disease.

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 Tremor, restlessness, sleep disorders Pot. hypokalemia at higher doses According to the SMART study, mortality 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 recommended. CI: Coronary heart hyperthyroidism disease, hypertrophic obstructive cardiomyopathy, tachyarrhythmias and

Dos: Short-acting beta2-adrenergics: are applicated for initial therapy in all therapy stages. 2-4 strokes of a 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 deterioration are: drop of the peak-flow-value >15% of the individual best value, diminished ability to withstand strain, night-time asthmatic complaints, no improvement after 2 strokes of a short-acting betamimetic Reevaluation of the entire therapy plan and adjustment to a higher disease stage is required. 2. Parasympatholytics (anticholinergics): 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 significantly less effective than beta2-sympathomimetics . (In COPD, it is vice-versa). SE: Unlike atropine, both substances are absorbed poorly within the gastrointestinal tract. Thus, systemic atropine effects (oral dryness, accommodation disturbances) 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 2-stimulators, in which case the 2-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 therapy stage III . As the risk of cardiovascular mortality is increased 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 Heart related: tachycardia, extrasystoles and tachycardial arrhythmias Other SE: Hypokalemia, allergic reactions occurring after i.v. application of ethylendiamine-containing preparations Cl.: Recent myocardial infarction, tachyarrhythmia and hypertrophic obstructive 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 system is influenced by various factors increased 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 clearance varies among individuals and may also be altered by oral intake of 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 increase in dosage; daily dosage 400 - 800 mg administered 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. Intravenous (e.g. Solosin) Only in hospital, not in outpatient emergency service. Dose: see below .
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C) Leukotriene receptor antagonist (= LTRA) = 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 to remain ineffective. Montelukast (Singulair) Ind: For prophylactic use only (beginning at stage III), Analgesic asthma; not appropriate for therapy of acute asthma attacks. Cl.: Pregnancy, lactation period and allergic reaction Dos: e.g. Montelukast (Singulair) 10 mg/d orally at nighttime Effect(s): Blocks the mediators of inflammation SE: Headache, abdominal discomfort, very rarely other SE ( producers indication) D) Cromones : Effects: Inhibition of mediator release from sensitized mast cells Almost all studies of the last 20 years show no better effect than placebo Cromoglicine acid , Dinatriumchromoglicicum (DNCG) and Nedocromil E) 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-resistant allergic asthma; high costs of therapy 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 chapt. 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 bronchial secretion (dyscrinia), stagnant secretion (mucostasis), which is difficult to expectorate. - Secretolytics: ( Bromhexine, ambroxol) } - Mucolytics: ( N- acetylcysteine) } Benefit not proven Note: The most effective secretolytic is the intake of copious amounts of fluid. Reduction of exsiccation and avoidance of overhydration. Humidification of the inhaled air facilitates expectoration. Water with an optional addition of sodium chloride is sufficient. Antitussives, e.g. codeine, are not indicated (except for nighttime irritating cough and sleep disorder). Facilitation of mucus expectoration by flutter mucus clearing device (e.g. VRP1-Desitin) Breathing training: Avoidance of pursed breathing and hyperventilation, breathing with pointed lips (= preceding 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 climatotherapy may be helpful. Therapy of severe asthma attacks: Intensive care unit: monitoring of cardiovascular 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 O2 supply via nasal tube as needed (dependent on the degree of hypoxia, 2 - 4 l/min). At the same time pay attention to signs of respiratory depression and initiate, if needed, assisted/controlled artificial ventilation. I.v. glucocorticosteroids are indispensable Dos: 50-100 mg of prednisolon (-equivalent) every 4 - 6 h i.v. Use of broncholytics with consideration of previous therapy: - Short-acting beta2-sympathomimetics are the most effective bronchodilators (3 x more effective than theophylline). Initial dosage: every 30 minutes 3 strokes, then increase dose interval to 2 - 4 h.
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Pay attention to: after previous self-overdosing of beta-adrenergics by patient, the further use of betaadrenergics is potentially dangerous (tachycardial arrhythmias, hypokalemia, among others). Beta-adrenergic parenteral therapy only for heart-healthy patients and at heart frequencies < 130/min, e.g. reproterol (e.g. Bronchospasmin) 1 amp. = 1 ml = 90 g slowly i.v., additional drug is administered via infusion ( see manufacturers specification). - Theophylline: Parenteral (i.v.) application only in hospital ( in ambulant emergency service, the German Airway Society does not recommend it because of possible SE) 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 therapy first detect serum concentration, then adjust the dose (careful: intoxication) - Magnesium sulfate ( 2, 000 mg in 50 ml NaCl 0.9 % slowly via infusion). Sufficient parenteral supply of liquid If infection-related asthma is suspected, administration of an antibiotic (see chapt. COPD) Before indicating invasive ventilation, non-invasive ventilation should by all means be attempted, if the 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 pCO2 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: Antitussives, beta-blockers (also in the form of eye drops!), ASA/NSAIDs (PAR!), sedatives (respiratory depression!), parasympathomimetics (pilocarpine, carbachol), subclavian catheter (increased risk of pneumothorax). 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 to the therapy, the following possible reasons have to be excluded: - insufficient adherence to therapeutic 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 hyperreactive 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 Infection prophylaxis 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 suffering from house dust 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 acaricides (e.g. Acarosan foam and powder) Vacation in the high mountains or in areas with desert climate
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2. Approx. 50% of 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, examine for frequently occurring 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/family member. 6. Specific immune therapy (SIT): Syn: hyposensibilisation, desensibilisation Ind: Patient < 55 years of age, period of symptoms not > 5 years. Preferably monovalent allergy. Treatment principle: perform hyposensibilisisation during the asthma-free period. By subcutaneously 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 local symptoms at the injection site, bronchospasm, anaphylactic reactions (rare); late reactions after 4 - 8 h are possible the patient should remain at least hours (better 2 hours) at the doctors office and should be educated about possible late reactions (bronchospasm) and their treatment by the patient. Cl.: Infections, asthmatic disorder, consuming diseases, therapy with beta-blockers (decrease in 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 diseases, 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% of cases Adult asthma: approx. 20% of cases are cured, improvement in approx. 40% of cases A rigorous, long-term therapy utilizing inhalant glucocorticoids can significantly improve the prognosis. Germany is presently still one of the countries with the highest bronchial asthma mortality rates (after England, Australia and New Zealand).

P N E U M O N I A [J18.9]
Internet-Info: www.capnet.de Def.: Acute or chronic inflammation of the alveolar and/or interstitial space of the lung. Ep.: In industrial countries it is the infectious disease with the highest mortality rate. Worldwide pneumonia ranks third in statistics on causes of death. Incidence: 8 15/1,000/y A. Pathological classification: By location of pneumonia: - Alveolar pneumonias (usually bacterial infections) - Interstitial pneumonias (usually viral infections) By size of the pneumonic area: - Lobar pneumonia - Lobular (focal) pneumonia B. Aetiologic classification: 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 classification: 1. Taking into account pre-existing illnesses: - 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) Bronchial changes (bronchial carcinoma, bronchial stenoses, e.g. caused by foreign bodies, bronchiectases) After aspiration of foreign material (aspiration pneumonia) Bacterial superinfection, e.g. resulting from influenza infection 2. By course of disease: acute or chronic (DD: TBC, fungal infections)
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Classification principles

Copyright 2010 by Dr. Gerd Herold, Cologne, Germany. All rights reserved. Original German Textbook by Gerd Herold Translation by Ralf Brcker, Bettina Mues, Hedwig Mller, Sylvia Mller Project coordination by Bjrn 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 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
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