Medicine and Clinical Skills

Review Article


Abdulmohsen H. Al-Elq, MD

Department of Internal Medicine, College of Medicine, King Faisal University, Dammam, Saudi Arabia


الهدف  الرئيسي  من المناهج  الطبية هو تزويد  الخريجين بالمعلومات  والأخلاقيات اللازمة لمزاولة مهنة الطب في المستقبل .

  خلال العقد الأخير أصدر المجلس الطبي البريطاني عام 1993م تقريراً أطلق عليه " طبيب الغد " دعا فيه إلى تسويق التعليم عن طريق حل المشكلات الطبية بالإضافة إلى التقليل من محتويات المناهج  الطبية المعتمدة على حقائق ثابتة  فقد أدى ذلك إلى تغيير جذري في مناهج الطب والتمريض. وبالرغم من أن المناهج  الجديدة قد ركزت  على تدريس  وتعلم  المهارات  الطبية إلا أن هناك تساؤلاً عن مستويات ومدى فاعلية المهارات لدى خريجي الطب الجدد.

إن التغيرات التي استحدثت على طرق التدريس والتعلم مع التغيرات  الجذرية التي طرأت على تقديم الخدمات الصحية والنمو السريع للتقنية كلها وضعت تحديات على الطرق البدائية لتطوير المهارات  الطبية  مما أدى إلى ظهور المختبرات  الطبية  كاتجاه جديد في مجال التعليم الطبي لدى كثير من مدارس الطب والتمريض .

ومع شيوع مختبرات المهارات الطبية هناك أهمية لدراسة هذه الظاهرة وتعريف القارئ على استخداماتها مع الأخذ بعين الاعتبار أن هناك شحاً في المعلومات عن هذا الموضوع في السنوات الأخيرة. 

الكلمات المرجعية: مختبرات , مراكز , وحدات , المهارات , السريرية.


The main objective of the medical curriculum is to provide medical students withknowledge, skills and attitudes required for their practice. A decade ago, the UK Medical Council issued a report called “Tomorrow’s Doctors”1 which called for the reduction in the factual content of the medical course with the promotion of problem-based and self-dedicated learning. This report was the basis for a move toward an extensive reform of the medical and  nursing curricula. The new reformed curricula enhanced the integrated medical teaching and emphasized the teaching and learning of clinical skills. However, there were still concerns about the standards and appropriateness of the skills of new medical graduates.2

      The changes in the teaching and learning methods, the radical changes in the health care delivery and the rapid growth of technology challenged the traditional way of clinical skills development and led to the emergence of clinical skills laboratories (CSLs) in the medical education of many medical and nursing schools.  With the proliferation of the CSLs, it is important to evaluate and introduce the reader to their applications, bearing in mind the paucity of information on this subject particularly over the last couple of years. This article is based on literature review.

Key Words: Clinical, Skills, Laboratories, Centers, Units.


Correspondence to:

Dr. Abdulmohsen H. Al-Elq, Consultant Internist/Endocrinology, Assistant Professor, Department of Internal Medicine, King Fahd Hospital of the University, P.O. Box 40154, Al-Khobar 31952



Clinical skills laboratories are educational facilities that have the potential benefit for undergraduate and postgraduate medical students and medical staff. They provide a safe and protected environment in which the learner can practise clinical skills before using them in real clinical settings. These skills laboratories help to ensure that all students acquire the necessary techniques and are properly assessed before practising on real patients. In addition, they support the acquisition, maintenance and enhancement of the clinical skills of students in the healthcare profession.  The term 'clinical skills' involves history-taking, physical examination, clinical investigations, using diagnostic reasoning, ­­­­­­­­­­ procedural perfection, effective communication, team work and professionalism.3-5

      Medical schools and postgraduate centers have gone to considerable lengths to create educational facilities dedicated to the teaching of clinical skills. The first CSL was established in Maastrich, The Netherlands Limburg University 1976.6 Since then many medical schools and educational institutions have integrated CSLs into their curricula. Currently, CSLs are established in several innovative medical schools including the University of Leeds, Dundee, Dublin, Southampton, Liverpool, and the Imperial College.3,7-9 In the Arab world, the United Arab Emirates University was the first to establish CSL in 1988.10 At present, there are many universities in the region using CSLs as a teaching tool.

Table 1 Skills that can be taught and learned in the CSLs

·    Investigational skills

o   Test selection

o   Data Interpretation

·    Patient management

·    Resuscitation procedure and techniques

·    Clinical reasoning and critical appraisal

·    Teaching and learning methodology

·    Presentation skill

·    Communication skill

·    Information and communication technology

·    Prescribing skill

·    Documentation

·    Clinical and legal consideration

·    Health safety and manual handling

·    Attitudinal awareness and professionalism

·    Administrative, economic and organization skill

·    Leadership

·    Team work and interprofessional skills learning

      Most CSLs have core clinical skills that can be taught and learned. These include history taking with communication skills, physical examination and some technical and practical procedures. In general, the exact nature of the skill taught is usually determined by the local logistical and educational requirements. With advances in technology and the changes in teaching methodology, the list of skills that can be taught and learned in the CSLs has grown longer (Table 1).4 Because of the variety of these skills, it is important to define them and determine the level of competence required at each institution. For that reason, many CSLs involve curriculum development committees, undergraduate and postgraduate faculty members in the planning process.


In setting up a clinical skill facility, it is important to follow the modern educational theory in the development and delivery of the program. The development of communication skills is a crucial area of focus for CSLs.  In fact, a better name for those laboratories would be clinical and communication skills centers or units, because the proper application of clinical skills requires the integration of technical clinical skills and those of communication.11

      Educational strategies that can be adapted in CSLs include student-centered, integrated, problem-based and self-directed learning as well as multi-profession, community-oriented or outcome-based education.12 Moreover, a small group, a large group, real, standardized and simulated patients or role play may be part of the method of learning.  Audio and video recording is important particularly in the development of communication skills.4

      Clinical skills laboratories vary in location, shape and site depending on the availability of space and resources. Most CSLs are located in hospitals or medical schools. However, Dacre J, et al (1996) has suggested the use of satellite centers where the skills and communication centers can be linked to peripheral facilities and teaching situations in the primary care clinics, lecture theatres or even the community through information technology.13 Many centers have placed computers and information technology in or near the clinical skills facility.

      Clinical skills laboratories may consist of a large open space for seminars and several small side rooms for interviews. It may include a variety of clinical settings such as general practice consulting rooms, procedural skill rooms, accident and emergency cubicles, an Intensive Care Unit and a place for simulators. Storage areas and offices for teachers and support staff are important. It is also necessary that the available space is kept fluid for possible rearrangement to suit a particular lesson. In general, a clinical skills facility should provide a sense of a real clinical environment.

      Simulation is an important component of the clinical and communication skill centers. Simulators can be classified into four types (Table 2).14

1.   A part-time trainer:  training model which represents part of the body or structure that can be used alone or can be attached to simulated patients for simultaneous technical and communication skills development.15

2.   A computer-based system which can be in the form of: (a) multimedia program using audio and video systems; (b) interactive systems which provide the users with clinical variables that can be manipulated to provide feedback on the decisions and actions; (c) virtual reality that creates environments or objects such as computer-generated imaging that replicate kinaesthetic and tactile perception.

3.   Simulated patients and environments:  Simulated patients can be professional actors trained to present history and ­sometimes mimic physical signs or can be trained patients. Both can be used as standardized patients.16 Creation of simulated environment is common in CSLs.

4.   Integrated simulators. These simulators combine manikins with advanced computer controls that can be adjusted to provide various physiological parameter outputs.

Table 2: Simulator types

·    Part-time trainer

·    Computer-based system

o   Multimedia program

o   Interactive system

o   Virtual reality

·    Simulated patients and environments

·    Integrated simulators

      Adequate staffing is important for the success of CSLs. Both teaching and support staff should be selected carefully. Teaching staff can be full time, part time, and seasonal or peripatetic clinical skill teachers. The support staff usually includes administrators, patient coordinators, a secretary and technicians.4 Finally, depending on its setting, CSLs can be used for teaching and learning at both undergraduate and postgraduate levels. They can be used by different professions including medical students, nursing students, dentistry and applied medical science students.


A number of factors have led to the reduction in the number of patients available for students' training. They include: the recommended early student exposure to clinical skills, the growing number of students, the dramatic reduction of inpatient beds, shorter hospital stay and the shift of care to the ambulatory setting.1 Indications for hospital admission have changed, especially in urban areas as a result of advancement in the day care units. Consequently, patients admitted to hospitals are usually sicker and therefore, unsuitable for bedside clinical skills training. In addition, there is concern that bedside case presentation makes the patient uncomfortable.17 In fact, the estimated time allotted to bedside teaching as a component of medical training declined from 75% in the 1960s to 16% in 1978 and is even lower now.18,19

      The above changes have raised concerns of inadequacy in the performance skills of students because of their altered clinical experience and the reduction in their opportunities for acquiring clinical skills.2,20

      The increased demand and decreased number of the teaching staff resulting from financial constraints, the competing pressure, work load, administrative and research duties as well as an increase in the number of students and gender separation adopted by some medical schools in Muslim communities have urged the move towards the development of CSLs. The supervision of students and immediate feedback by the teaching staff have therefore become difficult. There is also the problem of legal action. Patients are now better informed, have greater expectations and will no longer accept the role of passive participants in bedside education. Patients reserve the right not to be involved with students.4 In addition to cultural issues, ethical issues are raised when genital, vaginal, rectal and breast examinations are to be done. These factors as well as the invasion of the medical field by computer technology has led to the increase in the number of CSLs and the use of simulation as an innovative teaching approach to medical education.


Clinical skills laboratories can be used for teamwork and multi-professional education.21 It provides the students with the access to learning opportunities in a safe and protected environment. Bridging the gap between the classroom and the clinical setting decreases students' anxiety.

      The new learning methods and educational strategies discussed above are difficult to employ in the traditional method using bedside teaching and are, therefore, best used in the CSLs. Students' communication skills and attitudes to their importance can be improved by integrating these skills into the overall clinical skills program.22 One of the most important advantages of CSLs is that by integrating them into the theoretical component of the curriculum, skills are learnt within their proper context.23 Computer assisted learning and information technology can be used to enhance the interaction between theory and practice.24 

      The use of simulators enable students to practise and make mistakes without the risk to the patients or themselves. Unlike patients, simulators have predictable behavior, experiences are reproducible and allow standardized experience. They are neither embarrassed or stressed, have no time restrictions and so can be used as required. They can be programmed to simulate selected findings, conditions, or complications and they can be used for training on the management of difficult situations.25 It has been shown that the single most important determinant of skills and knowledge retention is repeated practice,26 which is more feasible in CSLs. Studies have shown that students who graduated from innovative medical schools used more skills during clerkships than students who had followed traditional programs.7 Clinical skills laboratories encourage self-learning since both the medico-legal and ethical issues are not a concern and the use of manikins obviate institutional, individual, and cultural barriers. Students can practice genital, vaginal, rectal and breast examinations without embarassment. This gives them the practice they need and are, therefore, able to approach patients with greater confidence. Direct feedback on performance can be provided with the use of audio-visual aids,27 peer review and teachers' assessment with opportunities for reflection, evaluation and enhancement or modifications for further action on the part of the learners. The innovative medical institutions require fewer teaching staff who are not required to be full-time teachers. This provides greater flexibility and opportunity for research and staff development. The use of simulators reduces the time spent by students and faculty looking for enough suitable patients for teaching or learning.

      The CSLs provide the ideal environment for the assessment of skills acquisition. It has been shown that candidates successful at written examinations have variable practice experiences. In fact, skills cannot be assessed properly by written examinations and should not be tested in isolation. Objective structured clinical examination (OSCE), which can be carried out at the clinical skills learning facilities, is becoming a standard method of skills evaluation.

      Video recording and frequent feedback from teachers can also help in both formative and summative assessment. Computer-based simulation allows meticulous assessment of performance including a detailed analysis of movement and behavior and can be used as a method of measuring procedural psychomotor skills.28

      The use of CSLs has many advantages, but there are also drawbacks. Skills centers provide different contexts for learning, but cannot replicate reality. There is also the problem of the lack of expertise to maintain CSL centers. Since there are no medico-legal issues to be mindful of, students may ignore the learning of certain clinical skills. Furthermore, simulation instruments can be used to test a specific aspect of technical competence but may not provide a complete assessment of a holistic approach to the patient. The clinical skills facilities are costly. In one study, it was shown that the cost of setting up the main lab was $133,000, and had the mean annual budget of $11,000.29 Information technology resources and simulators need continuous maintenance and updates. The use of informatics resource in developing countries would be hampered by technical difficulties.


For many medical schools, the high cost of the facility and equipment and the need for continuous update and maintenance is a major barrier to the incorporation of CSLs in their curriculum. Many teaching staff who are strong believers of bedside clinical teaching may resist the change.19 In addition, planning skills centers involves a variety of stakeholders and users, some of whom may not be enthusiastic for change. Since CSLs are costly, it is important to ensure that the outcome is justifiable so that investors can be persuaded. Clinical skills laboratories should be designed to support the intended learning outcome and to form an integral part of the overall curriculum. The development of clinical skills should be integrated into the communication skills program and other parts of the curricula, to avoid reverting to formal method of education. To be successful, clinical skill units need to be flexible in design and schedule.  It needs to be within or near the medical schools. The environment and the clinical space should as far as possible mimic the conditions of real practice.30

      In conclusion, with the recent changes in the medical education and the fast pace of technological development, CSLs have become an important educational environment for the acquisition of clinical skills. Many clinical skills can be learned and taught in CSLs which also provide ideal environment for assessment. However, they should not replace, but rather complement bedside teaching.


1.     Education Committee of the General Medical Council. Tomorrow’ Doctors. Recommendations on Undergraduate Medical Education.  London, UK: General Medical Council; 1993.

2.     Remmen R, Scherpbier AJ, Derese A, Denekens J, Hermann I, van der Vleufen CPM et al.  Unsatisfactory basic skills performance by students in traditional medical curricula. Med Teach 1998; 20:579-582.

3.     Boulay CD, Medway C.  The clinical skills resource: a review of current practice.  Medical Education 1999; 33:185-191.

4.     Bradley P, Postlethwaite K.  Setting up a clinical skills learning facility.  Medical Education 2003; 37(Suppl.1):6-13.

5.     Sebiany AM.  New trends in medical education: The clinical skills laboratories.  Saudi Med J 2003; 24(10):1043-1047.

6.     Al-Yousuf NH.   The clinical skills laboratory as a learning tool for medical students and health professionals.  Saudi Med J 2004; 25(5):549-551.

7.     Bligh J, Bradley P.  One year’s experience with a clinical skills resource centre.  Medical Education 1999;33:114-20.

8.     Remmen R, Scherpbier A, Vleuten CV, Denekens J, Derese A, Hermann I, et al.  Effectiveness of basic clinical skills training programmes: a cross-sectional comparison of four medical schools.  Medical Education 2001;35:121-128.

9.     Morgan R.  Using clinical skills laboratories to promote theory-practice integration during first practice placement: an Irish perspective.  Journal of Clinical Nursing 2006;15:155-161.

10.   Das M, Townsend A, Hasan MY.  The views of senior students and young doctors of their training in a skills laboratory.  Medical Education 1998;32(2):143.

11.   Kneebone R, Kidd J, Nestel D, Asvall S, Paraskeva P, Darzi A.  An innovative model for teaching and learning clinical procedures.  Medical Education 2002;36:628-634.

12.   Dent JA, Ker JS, Angell-Preece HM, Preece PE.  Twelve tips for setting up an ambulatory care  (outpatient) teaching centre.  Med Teach 2001;23(4):345-350.

13.   Dacre J, Nicol M, Holroyed D, Ingram D. The development of a clinical skills centre. J. R. Coll. Physicians Lond. 1996; 30(4): 318-324

14.   Bradley P.  The history of simulation in medical education and possible future directions.  Medical Education 2006;40:254-262.

15.   Kneebone R, Nestel D.  Learning clinical skills – the place of simulation and feedback.  Clinical Teacher 2005;2(2):86.

16.   McGraw RC, O’Connor HM.  Standardized patients in the early acquisition of clinical skills.  Medical Education 1999;33:572-578.

17   .White LL.  Preparing for clinical just in time.  Nurse Educator 2006;31(2):57-60.

18.   Gale CP,  Gale RP.  Is bedside teaching in cardiology necessary for the undergraduate education of medical students? Medical Education 2006;40:11-13.

19.   M EL-Bagir KA.  What is happening to bedside clinical teaching?  Medical Education 2002;36:1185-1188.

20.   Carter R, Aitchison M, Mufti GR, Scott R.  Catheterisation: your urethra in their hands.  BMJ 1990;301(6757):905.

21.   Tucker K, Wakefield A, Boggis C, Lawson M, Roberts T, Gooch J.  Learning together: clinical skills teaching for medical and nursing students. Medical Education 2003;37:630-637.

22.   Willis SC, Jones A, O’Neill PA.  Can undergraduate education have an effect on the ways in which pre-registration house officers conceptualize communication? Med Educ 2003;37:603-8.

23.   O’Connor HM.  Training undergraduate medical students in procedural skills.  Emergency Medicine 2002;14:131-135.

24.   Schittek M, Mattheos N, Lyon HC, Attstrom R.  Computer assisted learning: A review.  Eur J Dent Educ 2001;5:93-100.

25.   Issenberg SB, McGaghie WC, Hart IR, Mayer JW, Felner JM, Petrusa ER, Waugh RA, et al.  Simulation technology for health care professional skills training and assessment.  JAMA 1999;282(9):861-866.

26.   Kneebone RL, Scott W, Darzi A, Horrocks M.  Simulation and clinical practice: strengthening the relationship.  Medical Education 2004;38:1095-1102.

27.   Paul S, Dawson KP, Lanphear JH, Cheema MY.  Video recording feedback: a feasible and effective approach to teaching history-taking and physical examination skills in undergraduate paediatric medicine.  Medical Education 1998;32:332-336.

28.   Datta V, Mandalia M, Mackay S, Chang A, Cheshire N, Darzi A.  Relationship between skill and outcome in the laboratory-based model.  Surgery 2002;131:318-23.

29.   Korndorffer Jr JR, Stefanidis D, Scott DJ.  Laparoscopic skills laboratories: current assessment and a call for resident training standards.  The American Journal of Surgery 2006;191:17-22.

30.   Kneebone RL, Kidd J, Nestel D, Barnet A, Lo B, King R, et al.  Blurring the boundaries: scenario-based simulation in a clinical setting.  Medical Education 2005;39:580-587. 


The Approach to A Patient

Review Article


Layla  A.M. Bashawri, MBBS, KFUF (CP), Mirghani A. Ahmed, PhD

Division of Hematology, King Fahd Hospital of the University, Al-Khobar, Saudi Arabia


إن التسلسل الطبيعي لإيقاف النزيف يتطلب تفاعل الصفائح الدموية وعوامل التخثر بالإضافة إلى الأوعية الدموية والأنسجة المساندة.

وإذا نظرنا إلى مشاكل النزف نجد أنها من الحالات السريرية الشائعة ومن أعراض هذه الحالات سهولة النزف عند الإصابة بالجروح . دراسة وتشخيص هذه الحالات تتطلب عملية تقييم شامل تتضمن الحصول على تاريخ مرضي كامل ومفصل وكشف طبي شامل وفحوصات مختبريه وغالباً ما يتم تشخيص العديد من الحالات مباشرة من التقييم ألسريري , أما في حالات أخرى فان التشخيص يكون صعبا وذلك  لعدم وجود علامات مرضيه ظاهره عند هؤلاء .

إن الكشف والفحص الدقيق يجب أن يخطط له بشكل منتظم لأنها بمثابة الخطوات الأولى للتشخيص والمعالجة طويلة المدى.

الكلمات المرجعية: اضطرابات النزيف، الفحص ألسريري، الفحوصات ألمختبريه .


Normal Hemostasis requires the interaction of platelets and the clotting cascade with normal blood vessels and supporting tissues. Bleeding problems and easy bruising are commonly encountered clinical problems. Assessment of these patients is a multistep evaluation process that involves a complete detailed history, thorough physical examination and relevant laboratory evaluation. Many disorders are usually relatively straight forward to diagnose, but in other disorders, patients may have "hidden" signs and symptoms making diagnosis more difficult. A meticulous approach must be used to plan the first steps of management.

Key Words: Bleeding disorder, clinical history, laboratory tests.



Hemostasis is the process by which bleeding is arrested after injury to blood vessels. It is a delicate multiphase process that involves interactions between the blood vessels, platelets and coagulation factors. A defect in any of these phases of coagulation can result in a bleeding problem which may be inherited or acquired.1-4 This process of coagulation is a combination of cellular and biochemical events that function together to keep blood in the fluid state within the vessels and prevent blood loss following injury by the formation of a stable blood clot. Blood clots are eventually dissolved by the fibrinolytic system, a complex but well regulated system dependent also on several other additional systems. Interaction of these systems include vessel wall constriction, platelet adhesion and aggregation, blood coagulation,  fibrinolytic system, kinin system, natural coagulation factor inhibitors i.e. mainly antithrombin III, Protein C, Protein S, and the complement system. Evidently, there is a delicate controlled balance between formation and dissolution of a blood clot during the haemostatic process (Figure 1). A disruption of this unique balance may cause bleeding or thrombosis.1-4

      The objectives of this review is to provide primary care physicians with a systematic diagnostic approach in dealing with patients suffering from bleeding disorders, and demonstrate the importance of routine laboratory screening procedures. 


Correspondence to:

Dr. Layla A.M. Bashawri, Associate Professor and Consultant Hematopathologist, Division of Hematology, King Fahd Hospital of the University, P.O. Box 2208, Al-Khobar 31952


Figure 1: Simplified diagram of the basic components of coagulation


Careful history taking is always important, as is known in clinical medicine, but never more important and critical than when a bleeding disorder is suspected. A good detailed comprehensive history is the best predictor of a bleeding problem.3,5-9 Questions should be asked to assess the type and sites of bleeding, whether it involves the skin (cutaneous) and mucous membranes i.e. petechiae, purpura (Figures 2a, 2b and 2c), bruises, epistaxis, gingival bleeding, menorrhagia and/or hematuria which would suggest a platelet and/or vascular abnormality. Bleeding into deep tissue, joints and muscles (Figure 3) suggest a coagulation factor defect. Questions on whether the bleeding is spontaneous or follows trauma must also be asked. Usually a history of easy bruising or bleeding excessively after injury suggests an inherited bleeding problem. Information on the duration must also be sought. This would indicate whether symptoms have been lifelong (since childhood) or of recent onset. There should be questions on any childhood history of epistaxis, umbilical stump bleeding, bleeding after circumcision, the answers to any of  which would suggest inherited bleeding disorders. Any history of blood transfusion or other blood components, as well as a comprehensive review of past medical and surgical history is very important. Information on all operations including tooth extractions are to be listed together with any abnormal bleeding during or after surgery or poor wound healing. Drug history is of extreme importance since a wide variety of drugs affect hemostasis.10,11 The discovery of isolated thrombocytopenia in a patient who is taking several medications is a challenging clinical problem. It is very important to distinguish between drug induced thrombocytopenia and idiopathic thrombocytopenic purpura (ITP)11,12 In ITP, all other causes of thrombocytopenia must be excluded. A very careful family history is critical; any family history of abnormal bleeding in both parents, maternal grandparents, aunts, uncles, and siblings as well as any history of consanguineous marriage (or among relatives) should be taken. A proper history is vital because the information gathered will ultimately guide the direction and extent of the laboratory evaluation and also help in determining how complications can be managed and prevented.3,5,8-10 A study has shown that a patient’s perception of his or her own bleeding may be understated or exaggerated. This study showed that 65% of women and 35%




Figures 2a and 2b shows scattered petechiae and purpura and figure 2c shows a large ecchymosis


Figure 3: Haemarthrosis seen in hemophilia

of men without a laboratory confirmed bleeding disorder responded to the questions as if they did have a bleeding disorder, while 38% of women and 54% of men who had documented Von Willebrand disease or a functional platelet disorder, answered as if they were  completely unaware of their bleeding disorder.13 Inherited bleeding disorders are found in a substantial number of women with menorrhagia during routine gynecological examination.14 This shows the importance of taking a detailed history. Questions with the four "W’s", who, when, where and what are crucial.10

Who: who is the patient, sex, age, race and family history?

When: when did the bleeding occur, i.e. onset of bleeding? Is it related to drug ingestion or any underlying disorder? Did it develop after surgery or trauma?

Where: sites of bleeding, skin, muscle etc.

What: description of the type of bleeding.

The history is followed by a careful thorough physical examination to assess the sites and severity of the bleeding and evaluate whether the bleeding is part of a systemic illness, a local anatomical defect or a haemostatic disorder. From the clinical assessment, one is able to assess whether: (1) the bleeding is the result of a local anatomic defect or part of a systemic defect in hemostasis, (2) the bleeding is due to a vascular defect, platelet abnormality or coagulation disorder, or (3) the haemostatic defect is inherited or acquired.

      Often a careful history and physical examination will make the documentation of the presence or absence of a haemostatic disorder possible with at least 90% accuracy. It should also enable the categorization of the type of defect, i.e. coagulation versus platelet defect, and the possibility or absence of a systemic illness. This should also enable the physician to determine whether this bleeding problem is hereditary or acquired.


Careful and thorough clinical assessment allows the adoption of a sensible plan for laboratory investigation. The use of these tests are never a substitute for clinical assessment, for there is evidence that screening tests are unhelpful in the prediction of a bleeding disorder especially when applied indiscriminately.3 For each phase of hemostasis, screening tests which help in distinguishing a platelet disorder from a coagulation defect are available. The tests include a complete blood count (CBC) to assess platelet count, the often ignored peripheral blood smear examination, prothrombin time (PT), activated partial thromboplastin time (APTT), a thrombin time and a bleeding time3 or platelet function analysis (PFA) (Table 1). PFA-100 is an instrument recently developed to assess the global platelet response. The PFA-100 is extremely sensitive to the presence of aspirin and may be used to monitor antiplatelet drug therapy. It is also used to screen patients for Von Willebrand disease as well as platelet function disorders.15-18

Table 1: Screening tests of hemostasis

Complete blood count (CBC)

Platelet count

Peripheral blood smear examination

Prothombin time (PT)

Activated partial thromboplastin time (APTT)

Bleeding time or PFA-100

Thrombin time

      These baseline screening tests should be ordered before appropriate specialized tests are suggested. This is to avoid the unstructured ordering of unnecessary laboratory procedures. The CBC will reveal abnormalities in platelet numbers and the blood film will show platelet morphology, exclude the possibility of a systemic illness and other hematological disorders. The intrinsic pathway of coagulation is assessed by APTT (normal value 25-38 seconds) so that any abnormalities are detected. Prothrombin time (normal value 10-14 seconds), assesses the extrinsic coagulation pathway and the generation of fibrin, detected by the thrombin time (normal value 15-19 seconds)3-6,9,10 Normal control ranges vary somewhat from laboratory to laboratory. Bleeding time (normal value 3-9 minutes) or PFA-100 detect a platelet function abnormality; however, it is very important to ensure that the patient is not taking any drugs, aspirin, for instance, which are known to affect platelet function resulting in prolonged bleeding time and impact on PFA-100 result. Although the bleeding time has been clinically utilized for almost a century and modified several times in attempts to improve reliability, it is the least reliable of the screening tests. There are disadvantages.  It is difficult to standardize and the results can be both poorly reproducible and insensitive to milder forms of platelet dysfunction. A definite advantage is that it is a simple test of natural haemostasis including the contribution of the vessel wall. It also avoids potential anticoagulation artifacts. However, the consensus is that the test does not necessarily correlate well with the bleeding risk, so an accurate clinical history is more valuable.19,20 A number of different in vitro methods have, therefore, been devised to measure such platelet function as PFA- 100. In PFA-100, platelet function is measured within whole blood exposed to conditions that attempt to simulate in vivo haemostasis.19

      The aim of the screeningtests is thus, to reveal broadly the source of problem, and accordingly request further investigations. It should be borne in mind that tests of hemostasis are not only numerous but also expensive. Specialized laboratory testing should only be directed by the initial clinical impression and results of baseline screening tests or else a lot of time, effort and money will be wasted.3,6 One should also be aware of conditions that may be associated with prolonged APTT but without a bleeding diathesis. Examples include deficiency of Factor XII, high molecular weight Kininogen, and Prekallekrein. Lupus anticoagulant can be a cause of a prolonged APTT without a bleeding disorder.19  

      Specialized investigations may include, for example, mixing studies in the case of abnormal PT or aPTT for further information on the nature of the defect; coagulation factor assays to confirm and assess the severity of the coagulation factor deficiency such as in Hemophilia A or B; platelet aggregation studies to confirm platelet qualitative defects and investigations for Von Willebrand disease. If all baseline-screening tests are normal then investigations for factor XIII deficiency and alpha 2-antiplasmin deficiency which are not detectable by the routine screening tests are warranted. Factor XIII deficiency may be diagnosed by a clot solubility test, and the alpha 2-antiplasmin activity can be measured by a chromogenic assay.3,7,8 It is also worth mentioning that some patients with a definite history of bleeding, have normal results for baseline screening tests. Further diagnostic evaluation for such patients are needed to consider mild hemophilia and Von Willebrand disease (VWD), for mild hemophiliacs may have a normal APTT. Therefore, repeated testing may often be needed to diagnose VWD, especially in mild cases because of the fluctuation of Von Willebrand factor in the plasma.1,3,5,21-23 This again demonstrates the importance of a complete history. If all investigations are found normal, the patient should be investigated for blood vessel wall abnormalities. A vessel wall defect can result in abnormal bleeding despite an otherwise normal coagulation system. Since there are no reliable clinical tests of vascular integrity, diagnosis depends on a high level of suspicion, when all laboratory tests are normal. Blood vessel disorders can be hereditary like hereditary hemorrhagic telangiectasia and Ehlers-Danlos Syndrome, or acquired like Henoch-Schonlein purpura, scurvy and Cushing’s syndrome8,9,23,24 Table 2 summarizes the interpretation of various screening tests.

Table 2: Interpretation of abnormalities of coagulation screening tests


Possible conditions

Prolonged PT

Factor VII deficiency, early oral

  anticoagulation therapy


Deficiency of Factors VIII, IX, XI,

  XII, and Prekallikrien, Von

  Willebrand disease, Lupus


Prolonged PT and


Deficiency of Factors V, X, II, oral

  anticoagulants, vitamin K

  deficiency, liver disease.

Prolonged PT,

  APPT and TT

Fibrinogen deficiency/disorder, liver

  disease, heparin.

Prolonged bleeding

  time or abnormal

  PFA result

Platelet function defect, Von

  Willebrand disease



Platelet Disorders

1. Thrombocytopenia

      A normal platelet count is 150 – 400 x 109/liter. Thrombocytopenia can result from a number of causes; a) congenital thrombocytopenia which is uncommon and typically presents with other features i.e. Wiscott-Aldrich syndrome accompanied by eczema and impaired immunity. b) Impaired bone marrow production i.e. aplastic anemia, megaloblastic anemia and bone marrow infiltration. c) Increased platelet destruction/ consumption. Examples include, immune-related conditions like autoimmune thrombocytopenia (ITP), systemic lupus erythematosis, drugs and non-immune conditions such as disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP) and hypersplenism (splenic sequestration).24

2.   Disorders of Platelet Function: (Where numbers are adequate but bleeding is due to abnormal platelet function) a) Inherited: eg. Glanzmanns thrombasthenia, Bernard Soulier syndrome and Von Willebrands disease. Inherited disorders of platelet function may sometimes be difficult to diagnose, so family studies are needed.25 b) Acquired: eg. aspirin ingestion, uraemia and in myeloproliferative disorders.26

Disorders of the Coagulation Cascade

1.   Inherited Bleeding Disorders

      Examples: Hemophilia A (Factor VIII deficiency), Hemophilia B (Factor IX deficiency), Von Willebrand disease and congenital fibrinogen deficiency.  Studies from the Kingdom have shown that the distribution of hereditary bleeding disorders (HBD) resemble what has been established in western countries, with the exception of an increase of platelet disorders mostly due to the increased rate of consanguinity in the Kingdom.27-29 The most common HBD in the Kingdom is hemophilia A, followed by VWD, then hemophilia B followed by qualitative platelet disorders most commonly Glanzmanns thrombasthenia.27-29

2.   Acquired Bleeding Disorders

      These include liver disease, vitamin K deficiency, DIC and anticoagulant therapy.3

Disorders of vessels and supporting tissues

The weakening of the supportive tissues and blood vessel abnormalities as occurs in the aging process or corticosteroid usage should not be overlooked.6-8


The approach to a patient with a bleeding disorder needs a comprehensive detailed history and thorough physical examination. There must be a logical systematic approach and a discriminate use of laboratory investigations to reach the diagnosis and assess severity. Particular emphasis should be placed on family and drug history. A simple approach to detect the cause is to look at the hemostatic system as three compartments, blood vessels, platelets and coagulation proteins.


1.     Handin RI, Lux SE., Stossel TP. In: Blood Principles and Practice of Hematology. J.B. Lippincott Company Philadelphia 1995. 949-72.

2.     Ogedegbe HO. An Overview of Hemostasis. Lab Med 2002;12(33):948-53.

3.     Bick RL Clinical assessment of patients with Hemorrhage. In: Disorders of Thrombosis and Hemostasis Clinical and Laboratory Practice. Lippincott William’s and Wilkins Philadelphia PA, USA, 2002, 3rd edition:1-37.

4.    Schiffman F.J. Hemostasis and Thrombosis In: Hematologic Pathophysiology. Lippincottts Pathophysiology series. Lippincott-Raven Publishers, Philadelphia and New York, 1998:161-223.

5.     Liu MC, Kessler CM. A systematic Approach to the bleeding patient. In: Consultative Hemostasis and thrombosis. 2002 W.B. Saunders Company USA:27-39.

6.     Goodnight SH, Hathway WE. Evaluation of Bleeding Tendency in the Outpatient Child and Adult In: Disorders of Hemostasis and Thrombosis A Clinical Guide. Second edition 2001. The Mc Graw-Hill Companies;52-60.

7.     Beatty C. The Patient with Easy Bruising and Bleeding. Medicine 1995;23(12):514-71.

8.     Colman RW, Marder VJ, Clowes AW, George JN, Goldhaber SZ. Clinical approach to the bleeding patient: In Hemostasis and Thrombosis: Basic Principles and Clinical Practice. Fifth edition 2006, Lippincott Williams and Wilkins , USA:1147-58.

9.     Kujovich J. Approach to a Bleeding Patient. Lab. Med 2001; 32(5): 250-6.

10.   Hillman RS, Ault KA. Clinical Approach to Bleeding Disorders. In: Hematology in Clinical Practice. McGraw Hill Medical Publishing  Division 3rd edition 2002:308-15.

11.   George JN, Raskob GE, Shah SR, Rizvi MA, Hamilton SA, Osborne S., Vondracek BA, Vondracek T. Drug-Induced Thrombocytopenia: A Systemic Review of  Published Case Reports. Ann Intern Med. 1998;129:886-90.

12. Pedersen-Bjergaard U, Andersen M, Hansen PB. Drug-Induced Thrombocytopenia: Clinical data on 309 cases and the effect of corticosteroid therapy. Eur J Clin Pharmacol 1997; 52:183-9. 

13.     Wahlberg T, Blomback M, Hall P, Axelsson G. Applications of indicators, Predictors and Diagnostic Indices in Coagulation Disorders. Evaluation of a self-administered questionnaire with binary questions. Methods Inf Med 1980; 19:194-200.

14. Kadir RA, Economides DL, Sabin CA, Owens D, Lee CA. Frequency of Inherited Bleeding Disorders in Women with menorrhagia. The Lancet  1998;351:485-9.

15.   Mammen EF, Comp PC, Gosselin R, et al. PFA-100 system: a new method for assessment of platelet dysfunction. Semin Thromb Hemost. 1998;24:195-202.

16.   Carcao MD, Blanchette VS, Dean JA, He L, Kern MA, Stain AM, et al. The platelet function analyzer (PFA- 100): A novel in Vitro system for evaluation of primary hemostasis in children. Br J Haematol  1998; 101:70-3.

17. Kottke-Marchant K, Powers JB, Brooke L, Kundu S, Christie DJ. The effect of antiplatelet drugs, heparin and preanalytical variables on platelet function detected by the platelet function analyzer (PFA- 100). Clin Appl Thromb Hemost 1999;5:1-10.

18. Kundu SK, Heilmann EJ, Sio R, Garcia C, Davidson RM, Ostgaard RA. Description of an in Vitro platelet function analyzer – PFA- 100. Semin Thromb Hemost 1995;21:106-12.

19. Kitchen S, Makris M. Laboratory tests of hemostasis. In: Practical Hemostasis and Thrombosis, Blackwell Publishing Ltd 1st edition 2005;8-17.

20. Lind SE. The bleeding time does not predict surgical bleeding. Blood 1991;77(12):2547-52.

21. Kouides PA. Females with Von Willebrand disease: 72 years as the silent majority. Hemophilia 1998; 4: 665-76.

22. Nichols WC, Ginsburg D. Von Willebrand disease. Medicine 1997;76 1-20.

23.   Triplett DA. Coagulation and Bleeding Disorders: Review and Update. Clin Chem 2000; 46 (8B):1260-9.

24.   George JN. Platelets. Lancet 2000; 355: 1531-9.

25.   Colman RW, Koneti RaO A, Rubin RN. Platelet Bleeding Disorder in a 30 Year Old Female. Mechanisms of Congenital Platelet Function Defects. Am J Hematol 1993;44: 139-44.

26. George JN, Shattil SJ. The clinical importance of acquired abnormalities of platelet function. N Engl J Med 1991;324:27-39.

27.   Al Fawaz IM, Gader AMA., Bahakim HM, Al Mohareb F, AlMomen AK, Harakati MS. Hereditary Bleeding Disorders in Riyadh, Saudi Arabia. Ann Saudi Med 1996;16(3): 257-61.

28.   Ahmed MAM, Al-Sohaibani MO, AlMohaya SA, Sumer T, AlSheikh EH, Knox-Macaulay H. Inherited bleeding disorders in the Eastern province of Saudi Arabia. Acta Haemat 1988; 79:202-6.

29.   Bashawri L, Qatary A, Fawaz N, Al-Attas R, Ahmed M. Glanzmann’s Thrombasthenia. Bahrain Med Bull 2005; 27(3):123-8.


Thunderstorm associated

Review Article


Abdullah M. Al-Rubaish, MD

Department of Internal Medicine, College of Medicine, King Faisal University, Dammam, Saudi Arabia


ترتبط نوبات الربو الحادة ببعض المسببات كملوثات الهواء والأحوال الجوية كالعواصف وتشير الدلائل إلى أن حالات الربو المرتبطة بالعواصف تشكل مجموعة خاصة من المصابين و أن أوبئة من هذا النوع تم رصدها ولكن ليس في المملكة العربية السعودية.

السبب المباشر لهذه المراجعة لأدبيات هذا النوع من الربو كان الوباء الذي وقع في نوفمبر من العام 2002م بالمنطقة الشرقية بالمملكة العربية السعودية حيث تمت معالجة أغلب الحالات في مستشفى الملك فهد الجامعي بالخبر بفعالية وكذلك المستشفيات المجاورة.

وترتبط ثلاثة عوامل بحالات الربو الناتجة عن العواصف : الملوثات البيولوجية أو الكيميائية أو الأحوال الجوية. وتضم الملوثات البيولوجية المحمولة بهواء العواصف التي تتسبب في إحداث حالات الربو.

وتشمل الملوثات الكيميائية الغازات المنبعثة من المحميات الزراعية، المعادن الثقيلة، الأوزون، وثاني أكسيد النيتروجين، وثاني أكسيد الكبريت، والأدخنة المنبعثة من الكمائن والذرات الدقيقة. وترتبط هذه العوامل بالربو من خلال تكون أحماض الكبريت والنيتروجين .

وترتبط جوائح الربو غير الوبائي بالأمطار الغزيرة، وانخفاض درجات الحرارة والضغط، وضربات الصواعق وارتفاع معدلات الرطوبة ويمكن أن تحدث كلها أثناء العواصف مما يجعلها ترتبط بحدوث وباء الربو.

عادة ما يكون المصابون بالربو المرتبط بالعواصف من البالغين في عمر الشباب والمصابين بالتحسس ولا يتناولون الكورتيزون المستنشق وغالباً ما تكون أولى إصاباتهم أثناء هذا الوباء. كما يتعرض الأشخاص ذوي الحساسية لحبوب اللقاح الذين يتواجدون أثناء العاصفة لاستنشاق الهواء المحمل بحبوب اللقاح الذي يتسبب بإصابتهم بنوبة الربو.

على الأطباء الإلمام بهذه الظاهرة و احتمالات ظهور جائحة الربو أثناء الأمطار الغزيرة. وعلى العاملين في وحدات الطوارئ والعناية المركزة توقع أعداد كبيرة من الحالات ومن ثم يحضرون أجهزة التنفس الصناعي والاحتياطات الأخرى للإنعاش القلبي الرئوي . وعلى الطاقم الصحي التعاطي مع هذه الظاهرة بأسلوب علمي في المستقبل و يتطلب هذا العمل كفريق.

مفاتيح الكلمات: الربو المرتبط بالعاصفة، الوباء


Acute episodes of bronchial asthma are associated with specific etiological factors such as air pollutants and meteorological conditions including thunderstorms. Evidence suggests that thunderstorm-associated asthma (TAA) may be a distinct subset of asthmatics, and, epidemics have been reported, but none from Saudi Arabia.

The trigger for this review was the TAA epidemic in November 2002, Eastern Saudi Arabia. The bulk of patients were seen in the King Fahd Hospital of the University, Al-Khobar. The steady influx of acute cases were managed effectively and involved all neighboring hospitals, without evoking any "Major Incident Plan".

Three groups of factors are implicated as causes of TAA: pollutants (aerobiologic or chemical) and meteorological conditions. Aerobiological pollutants include air-borne allergens: pollen and spores of molds. Their asthma-inducing effect is augmented during thunderstorms.


Correspondence to:

Dr. Abdullah M. Al-Rubaish, Associate Professor, Department of Internal Medicine, College of Medicine, King Faisal University, Consultant Internist/Pulmonary, King Fahd Hospital of the University, P.O. Box 40085, Al-Khobar 31952, Saudi Arabia


Chemical pollutants include greenhouse gases, heavy metals, ozone, nitrogen dioxide, sulfur dioxide, fumes from engines and particulate matter. Their relation to rain-associated asthma is mediated by sulfuric and nitric acid.

Outbreaks of non-epidemic asthma are associated with high rainfall, drop in maximum air temperature and pressure, lightning strikes and increased humidity. Thunderstorm can cause all of these and it seems to be related to the onset of asthma epidemic.

Patients in epidemics of TAA are usually young atopic adults not on prophylaxis steroid inhalers.  The epidemic is usually their first known attack.  These features are consistent with the hypothesis that TAA is related to both aero-allergens and weather effects. Subjects allergic to pollen who are in the path of thunderstorm can inhale air loaded with pollen allergen and so have acute asthmatic response. TAA runs a benign course

Doctors should be aware of this phenomenon and the potential outbreak of asthma during heavy rains. A & E departments and ICU should be alert for possible rush of asthmatic admissions and reinforce ventilators and requirements of cardio-pulmonary resuscitation. Scientific approach should be adopted to investigate such outbreaks in the future and must include meteorological, bio-aerosole pollutants and chemical pollutant assessment. Regional team work is mandatory.  

Key Words: Thunderstorm-associated asthma, epidemic.


The prevalence of bronchial asthma is increasing and its etiology remains obscure, but acute episodes have been associated with specific etiologic factors. These include air pollutants such as ozone, nitrogen dioxide, sulfur dioxide and other chemicals, as well as particulate matter of respirable diameter (e.g. fog, organic dust, and aero-biological products). It is difficult to standardize "measures of exposure". Accordingly, researchers employ ecological designs to seek associations between, on one hand, "exposure" measured in terms of the environmental factors and, on the other hand, "outcome" measured as individuals' asthma attacks or their utilization of health care facilities. In spite of the volume of research done, the assertion that air pollution causes asthma remains controversial.1.

      Some reports suggest a "point source" of environmental causative agents. An example is the Barcelona asthma epidemic which was linked to soya bean dust.2 Other reports of asthma epidemics have implicated meteorological conditions such as thunderstorms and sudden changes in atmospheric temperature or pressure.3-5 Factors associated with non-epidemic asthma differ from those associated with the epidemic form. This suggests that patients attending Accidents and Emergencies (A & E) departments with reversible airway obstruction related to rain ("Thunderstorm-associated asthma"), may be a distinct sub-set of asthmatics who are more sensitive to environmental stimuli.6 Indeed, epidemics of thunderstorm-associated asthma have been documented in the literature, but no Saudi experience has been reported.

      Throughout Saturday, 2 November 2002, an epidemic of acute episodes of asthma after a heavy downpour of rain was observed by the A & E Department, King Fahd Hospital of the University (KFHU), Al-Khobar, Eastern Province. It has been observed that the number of asthmatics requiring emergency room services increases during and following rains or thunderstorms. The KFHU epidemic, however, was striking for two reasons: the number of patients affected was large, and, the geographic area involved was wide. Thus, on that day, other hospitals in the Eastern Province reported a similar pattern of cases. 

      None of the treating hospitals in the region evoked their "Major Incident Plan" although the number of additional patients in some of these hospitals was big enough to trigger a mass casualty response. The "Major Incident Plan" is also termed Mass Casualty Plan or Disaster Plan. This may be explained by at least two possibilities. First, there may have been a delay in appreciating and accepting that extraordinary measures were necessary because the influx of patients had resulted from a "medical incident" rather than a major accident. Secondly, most patients were not severely affected. The majority were treated and discharged home; only a few required admissions, and less than 1% needed to be in the Intensive Care Unit (ICU).

      However, if a higher proportion of those admitted had needed to be in the ICU, there would have been serious logistical problems.  This is because in major incidents, the hospital's capacity to handle patients requiring resuscitation and artificial ventilation is a limiting factor.  Once a designated hospital becomes saturated, patients are diverted to supporting hospitals in the same region. Thus, should all hospitals in an area be affected simultaneously in asthma epidemics, even greater logistical and management problems would ensue.


Three groups of factors have been suggested as causes of TAA, but it is not yet known which ones play the major role. The groups are (1) Aero-biological pollutants, (2) Chemical pollutants and (3) Meteorological conditions.

1.   Aero-biological pollutants

A sudden rise in bio-aerosol concentrations has been observed during thunderstorms. Recent studies of the kinetics of the release of aero-allergens (air-born allergens) and their effects on patients have confirmed the presence of high concentrations of pollen grains and mold spores in the surrounding atmosphere.

      Pollen is a fine powdery substance produced by flowers. Insect and natural agents such as air, rain and storm transfer pollen from one plant to another for pollination.  Pollen is responsible for most asthmatic attacks in flowering seasons. Produced in large quantities, pollen is of respirable size2-10 and, therefore, enters the airways. It is readily carried long distances by winds and therefore affects individuals miles away from source. The maximal concentration in the atmosphere occurs before sunrise and after sunset.

      Molds are plant species which grow in damp areas with high humidity. They are microscopic, reproduced by the release of millions of spores into the air which then settle on organic matter and grow. Inhaled air-borne spores can cause asthmatic attacks.

      Raised concentrations of bio-aerosol during thunderstorm is attributed to sudden onset of high winds which trigger the sudden release of spores and pollen into the atmosphere. This is probably responsible for asthma epidemics. Winds associated with thunderstorms may have re-suspended residual pollen locally. It is conceivable that aero-allergens are carried, firstly, up in the rapid up-lift of air associated with connective storms,7 and secondly, horizontally with the storm. They are then re-deposited by a cold downdraft ahead of the rainstorm.  Lastly, rainfall itself causes rapid changes of humidity or temperature or both. This may lead to a rapid rise in respirable allergens. Exposure to allergen can increase non-specific bronchial reactivity; the magnitude and duration are proportional to the last asthmatic response.8,9 If recent exposure to allergens increased bronchial responsiveness, acute airway narrowing might then be triggered by a variety of precipitants.

2.   Chemical Pollutants 

Air pollution, a side effect of global industrialization and urbanization, has become a fact in today's world.  The earth is a closed system; nothing gets out. Today's greenhouse gases, heavy metals and other compounds, accumulate as they are produced in greater quantities than nature can absorb. It is like smoking in a closed room. Today's world harbors millions of people and machines.  Gas, diesel engines and industrial pollutants result in a haze of smog hanging over most major cities around the world.

      Ozone, nitrogen dioxide, sulfur dioxide and particulate matter are the main forms of air pollution of the out-doors. These oxidizing gases are formed as by-products of combustion and can cause airway inflammation in humans whether or not they have asthma.  Since the level of ozone and pollutants increases and temperatures also increase, the phenomenon of global warming threatens to make this a continuing problem.

      An average human consumes 12 kg of air per day to form carbon dioxide. It is about twelve times higher than the food we take. Hence, even small concentrations of pollutants in the air become more significant in comparison to similar levels present in food.  Nearly 15 kg of air is consumed to burn one liter of fuel in automobiles. Carbon monoxide, lead and hydrocarbons are emitted in high quantities in petrol combustion. These can cause the loss of visual accuracy and mental alertness.  Diesel combustion emits considerably higher amounts of nitrogen dioxide, particulate matter and sulfur dioxide.  Pollutants of diesel combustion are important trigger factors which aggravate asthma.  A consensus on research studies indicate that air pollutants cannot induce asthma in a person who is not predisposed to it (except ozone effect), but they can trigger an acute attack in asthmatic patients, and can cause other lung diseases such as chronic bronchitis in healthy, non-asthmatic persons.

The relation of Chemical Pollutants to Rain-associated Asthma 

Air pollution is a major cause of acidic deposition or acid rain as it is commonly known. It occurs when emissions of sulfur dioxide (SO2) and nitrogen dioxide mix in the atmosphere with water, oxygen and oxidants to form mild solutions of sulfuric and nitric acid. Sunlight increases the rate of these reactions. These compounds then fall to the earth in the wet forms of rain, snow, fog or in dry forms as gas and particles.  About half of the acidity in the atmosphere falls back to earth through these dry depositions which the wind blows into buildings, cars and homes.  Prevailing winds transport these compounds, hundreds of miles across countries and national borders, resulting in a significant negative impact on health.

3.   Meteorological Conditions

Climate variation has only marginal effect on normal persons.  However, for asthmatic patients who are prone to dust, humidity, high temperature and changes in atmospheric pressure, bivariate and multivariate analyses have shown significant association between lightning strikes and asthma presentations.  Celenze et al, using multivariate analysis of environmental factors, showed that between one and nine lightning strikes a day was associated with increased asthma presentations by a factor of 2.21 compared with when there was no lightning (P<0.05). 

      Bivariate and multivariate analyses of other meteorological variables suggest that there are significant associations of increased cases of non-epidemic asthma with the following four variables: high rainfall, drop in maximum air temperature, fall in air pressure and increased humidity. A sudden thunderstorm causes the greatest sudden fall in temperature and air pressure as well as the most pronounced increase in humidity, rainfall, and lightning strikes. Hence, it seems to be related to the onset of asthma epidemic.


During the epidemic of thunderstorm-associated asthma (TAA), characteristically, the patients were young atopic adults. A high prevalence of atopy was also a feature of similar outbreaks.10  In a significant number of the patients, the episode was the first known attack of asthma.  Most gave a history of asthma, but were probably not on prophylaxis with steroid inhalers.  A history of hay fever and allergy to rey grass were found to be strong predictors for asthma exacerbation during thunderstorms.11 These are consistent with the hypothesis that TAA is related to aero-allergens as well as the effect of weather. Subjects allergic to pollen who are in the path of thunderstorm are likely to inhale air which is heavily loaded with pollen allergen and consequently experience an acute airway asthmatic response.

      TAA seems to have had a benign course in most patients in the epidemic alluded to, as they did not require hospital admission. However, there should be no complacency in the treatment of many patients presenting to A &E departments with acute asthma.


1.       Doctors should be aware of this phenomenon, which may not however, merit the "asthma weather alerts." Adding fuel to the flames of the tabloid press is counter-productive to developing a wider understanding of asthma and its prevention.

2.       Hospital accident and emergency departments in the area should be aware of the potential outbreak of asthma during heavy rains, and take measures to set up departments with the necessary equipment.

3.       Physicians in Intensive Care Units should be on high alert for possible rush of admissions and demand for ventilators, and cardio-pulmonary resuscitation.

4.       A systematic, organized scientific approach and collaborative effort should be adopted in the future to investigate factors relating to such outbreaks involving meteorological, bio-aerosole pollutants and chemical pollutants.      


1.     Barnes P.  Air pollution and asthma.  Postgraduate Med 1994;70:319-24.

2.     Anto JM, Sunyer J.  A point source asthma outbreak, Lancet 1986; ii:900-3.

3.     Morrison I.  It happened one night.  Med J Aust 1960; 47:850-2.

4.     Logan WPD.  Mortality in the London fog incident, 1952, Lancet 1953; I:336-8.

5.     Anto JM, Sanyer J, Rodrigrez-Roisin R, Suarez-cervera M, Vazquez L.  Community outbreaks of asthma associated with inhalation of Soybean dust.  N Engl J Med 198;320:1097-102.

6.     Antonio Celenza, Forthergill J Kupek E , Shaw RJ.  Thunderstorm associated asthma: a detailed analysis of environmental factors.  BMJ 1996; 312:604-7.

7.     Norris-Hill J, Emberlin J.  The incidence of increased pollen concentrations during rainfall in the air of London.  Aerobiologia 1993; 9:27-32.

8.     Cartier A, Thomso NC, Frith PA, Roberts R, Hargreave FE.  Allergen-induced increase in bronchial responsiveness to histamine: relationship to the late asthmatic response and change in airway caliber. J Allergy Clin Immunol 1982; 70:170-7.

9.     Cockroft DW.  Mechanism of perennial allergic asthma.  Lancet 1983; ii:253-6.

10.   Packe GE, Ayres JG.  Aeroallergen skin sensitivity in patient with sever asthma during a thunderstorm.  Lancet 1986; i: 850-1.

11.   Girgis ST, Mrks GB, Downs SH.  Thunderstorm associated asthma in an inland town in South-eastern Australia who is at risk? Eur Respir J 2000; 16:3-8.