Case 2.

01 The Stabbing
1. Anatomy of the thorax

Thorax consists of: 1. Chest wall ribs, sternum and vertebral column (T1 T12) (provide most of the structural support) 2. 2 pleural cavities surrounding the lungs 3. The area between theses cavities the mediastinium, in which are found the heart, great vessels, trachea, oesophagus, vagus and phrenic nerves, thymus gland and the thoracic duct. 4. The mammary glands are also found on the externolateral chest wall. The thorax is separated from the abdomen by the diaphragm. It is continuous with the neck at the thoracic inlet between the sternum and T1. Structures pass between the thorax and the neck through this inlet.

(aka outlet as the subclavian artery passes OUT of the thoracic inlet) The ribs articulate with the vertebral column behind and the sternum, in front. These articulations permit the movement of breathing. Intercostal spaces between the ribs are occupied by muscle and a neurovascular bundle that supplies the muscles, the skin over them and the lining of the pleural cavity deep to then. The repeating pattern of the ribs, vertebrae and neuromuscular bundles is an example of segmentation. Vertebral levels and surface markings The suprasternal or jugular notch is at T2 The sternal angle of Louis is at T4 (if you palpate this angle and then move laterally you can palpate rib 2. From here you can count downwards through the intercostal spaces and ribs.) The xiphisternum or xiphoid process is at T9 Bones and Joints of the chest wall The chest wall is made up of 12 pairs of ribs., the sternum and intercostal muscles. The ribs are numbers 1-12 superiorly inferiorly and articulate with the vertebral column posteriorly and the sternum(mostly) anteriorly. The sternal end of the ribs is lower than the vertebral end. Ribs are united at the anterior end by costal cartilage with primary cartilaginous joints. Vertebrae A thoracic vertebral is identifiable because of its facets(flat areas) for articulation with ribs. Vertebrae T2-T9 have 2 demifacets on each side whereas the rest only have one.

Ribs each rib has a head a neck a tubercle and a shaft. There are typical and atypical ribs (1.11 and 12). You only need to know about the 1st of the atypical ribs. It has a scalene tubercle in the upper surface to which the scalenus anterior muscle attaches. There is a groove for the subclavian vein anterior to this tubercle and a groove for the subclavian artey posterior. Sternum has 3 parts, from superior to inferior. The manubrium, body and xiphoid process. There may be a hole in the centre of the body as it is formed by any number of individual sternebrae that should fuse but may fail to do so. Joints between vertebrae and ribs typical ribs have 3 synovial articulations with the vertebrae. The head has upper and lower articular facets set almost at a right angle to each other, the lower articulating with the vertebrae corresponding in number to the rib and the upper with the vertebrae above. Ribs 1, 10, 11 and 12 have only one facet and only articulate with the numerically corresponding vertebrae. The tubercle of most ribs (not 11 or 12) articulates with the transverse processes of the corresponding vertebrae. These joints allow the ribs to move white breathing.

Ligaments these are not of great importance. They include: Triradiate ligament from the head of the rib to the vertebrae above, the intervertebral disc and the vertebrae below. Costotransverse ligaments between the vertebral transverse process and the tubercle of the rib. Joints between the ribs , sternum and vertebral column the first costal cartilage is continuous with the manubrium (primary cartilaginous joint) and remains so throughout life until it ossifies completely. Costal cartilages 2-7 have synovial articulations with the sternum. The second costal cartilage articulates at the sterna angle with the manubrium AND the body of the sternum. Costal cartilages 8-10 have synovial articulations with

the costal cartilage immediately above. Costal cartilages 11-12 are free of any anterior articulation but provide attachments for muscles. Ribs 1-7 are vertebrosternal or true ribs Ribs 8-10 are vertebrochondral or false ribs Ribs 11-12 are floating ribs Muscles of the chest wall Intercostal muscles and spaces There are three layers of tissue between ribs, partly muscle and partly membrane external, internal and innermost intercostals, with the intercostals neurovascular bundle running between the internal and innermost. The area between the ribs occupied by these intercostals muscles is the intercostal space. External intercostal muscle. Muscle at the back and sides. Membrane anteriorly. Fibres pass from the upper rib downwards and forwards to the upper border of the rib below. Internal intercostal muscle. Muscle at the front and sides, membrane posteriorly. Fibres pass upwards and forwards, more or less at right angles to those of the external intercostals. Innermost intercostal muscle. As Internal intercostal. Inside the chest wall there are usually muscle fibres that fan out from the sternum to the internal aspect of ribs 3-6. This is transverse thoracis and is equivalent to transverse abdominis in the abdomen (it is not important) Neurovascular bundle costal groove These muscles are supplied by the segmental intercostal nerve corresponding in number to the intercostals space. The rib has a groove underneath most of its length on the internal aspect. The intercostals groove provides some shelter for the intercostal neurovascular bundle. Within the groove the bundle is arranged from top to bottom, VAN vein, artery, nerve. In each intercostals space there are also smaller branches of the intercostals nerve and atery (collateral branches) which run on the top of the rib below.

Muscles of the pectoral girdle Overlying the ribs and intercostals are muscles which attach the upper limb (humerus, clavicle and scapula) to the trunk: Pectoralis major and minor, latissimus dorsi, levator scapulae, rhomboids and trapezius.

Blood Supply of Chest Wall Posterior intercostal arteries

Are branches of the aorta and are called segmental arteries, apart from the first and second which come from the costocervical trunk, a branch of the subclavian artery(not from the aorta because it does not pass high enough in the thorax) Anterior Intercostal arteries

Arise from the right and left internal thoracic arteries, branches of the subclavian which run internally down the chest wall 1-2cm lateral to the sterna border. They are important in supplying the breast. Lateral thoracic artery - Important for the breast Other branches of the subclavian/axillary arteries thoracoacromial, superior thoracic.

Veins Anterior intercostals veins drain to the internal thoracic veins, then to the subclavian braciocephalic superior vena cava. Posterior intercostals veins drain to the azygos system and the superior vena cava. As the first one or two posterior intercostals arteries arise differently to the rest the first posterior intercostals veins drain differently to the rest, to the brachiocephalic veins. Intercostal nerves These are ventral rami of the thoracic segmental nerves. The run in the costal groove of each of each rib and supply the intercostals muscles, a strip of skin overlying the intercostals muscles and a similar strip of parietal pleura on the internal aspect of the chest wall. Anteriorly when the ribs turn upwards, the neurovascular bundle parts company with the ribs and continues in the direction already established. Lower intercostal nerves will also supply skin of most of the anterior abdominal wall. And the parietal peritoneum deep to it. Intercostal nerves contain both motor and sensory fibres. Cell bodies of motor fibres to skeletal muscle are in the ventral horn of the grey matter of the correspondingly numbered spinal cord segment. Cell bodies of sensory fibers in an intercostals nerve are in the dorsal root ganglion of the parent segmental nerve. This arrangement gives rise to the concept of segmental innerveration, and allows autonomic reflex in one area a physiological phenomenon particularly important clinically in the limbs 2. Anatomy of the Respiratory Organs Principle organs of the respiratory system are the nose, pharynx, larynx , trachea, bronchi, and lungs. Nose Warms, cleanses and humidifies air. The external nose is supported and shaped by bone and cartilage. Superiorly it is supported by nasal bones medially and maxillae laterally. The inferior half is supported by lateral and alar cartilages. Dense connective tissue shapes the flared portion called the ala nasi which forms the lateral wall of the nostrils. The nasal cavity extends from the anterior nares/nostrils to the posterior nares/choanae. The dilated chamber inside the ala nasi is called the vestibule. This has stiff nasal hairs called vibrissae. The nasal septum divides the nasal cavity into right and left chambers called the nasal fossae. These fossae have folds called conchae that increase the surface

area so the air is warmed and humidified. The nasal cavity is separated from the oral cavity by the palate. Pharynx A muscular funnel that is about 13cm long. Air turns 90 degrees to head downwards when it meets the nasopharynx. The oropharynx is the part of the pharynx that starts at the back of the tongue. The laryngopharynx connects the oro and nasopharynges. Larynx This is also known as the voicebox. It is a cartilaginous chamber about 4cm long. Its primary role is to keep food out of the airway but it has also evolved to produce sound. The superior opening is called the glottis; it is guarded by a flap called the epiglottis. The framework of the larynx consists if 9 cartiages. The epiglottic cartilage, which is superior is made of elastic cartilage but the rest are hyaline cartilage. The walls of the larynx are muscular. Trachea Aka windpipe, is a rigid tube about 12cm in length and 2.5cm in diameter. It is anterior to the oesophagus and is supported by 16-20 C-shaped rings of hyaline cartilage. These rings reinforce the cartilage and prevent it from collapsing during inhalation. The open part of the C faces posteriorly where it is spanned by smooth trachealis muscle. The gap in the C allows the oesophagus to expand as food passes through. The trachealis muscle can contract and relax to adjust tracheal airflow. The larynx and trachea are mostly lined by ciliated pseudostratified columnar epithelium which function as a mucociliary escalator where the mucus traps debris and the cilia beat and drive it up to the pharynx so it can be swallowed. Lungs Each lung is conical and has a concave base resting on the diaphragm and an apex that projects slightly superior of the clavicle. The broad costal surface presses against the ribcage and the smaller concave mediastinal surface faces medially. The lung receives the bronchus, blood vessels, lymphatic vessels and nerves through the hilum, which is on the mediastinal surface. These structures entering the hilum constitute the root of the lung. The left lung is smaller than the right and has an indentation called the cardiac notch to accommodate the heart. The left lung has a superior lobe and an inferior lobe with a deep fissure between them called the oblique fissure. The right lung has 3 lobs the superior, inferior and middle which are divided by the oblique and horizontal fissures. The lung has spongy parenchyma containing the bronchial tree, a highly branched system from the primary bronchus to about 65000 terminal bronchioles. The two primary bronchi arise from the trachea at the level of the angle of Louis. Each bronchi continues for 2-3cm and enters the hilum of its respective lung. The right bronchus is slightly wider and more vertical than the left. The bronchi are supported by C-shaped hyaline cartilage as well. All divisions of the bronchial tree have a substantial amount of elastic connective tissue, which helps to expel air from the lungs by recoiling. After entering the hilum the bronchus separates into lobar bronchus for each pulmonary lobe. Thus there are 2 secondary bronchi in the left lung and 3 in the right. Each secondary bronchus separates into tertiary or segmental bronchi (10 in the right lung and 8 in the left). The portion of lung supplied by each tertiary bronchus is called a bronchopulmonary segment. Secondary and

tertiary bronchi are supported by overlapping plates of cartilage. Branches of the pulmonary artery closely follow the bronchial tree on the way to the alveoli. The bronchial tree itself is nourished by the bronchial artery which arises from the aorta and contains systemic blood. Bronchioles are continuations of the airway that are 1mm or less in diameter and lack cartilage. A well developed layer of smooth muscle in their walls enables them to dilate and constrict. The portion of the lung ventilated by one bronchiole is called a pulmonary lobule. Each bronchiole divides into 50-80 terminal bronchioles, these measure less that 0.5mm in diameter and have no mucous glands or goblet cells. They do, however contain cilia, so mucous can be beaten away from the terminal bronchioles and alveoli. Each terminal bronchiole gives off 2 respiratory bronchioles that have scant smooth muscle and divide into thin walled passages called alveolar ducts that end in irregularly shaped spaces called alveolar sacs. Alveoli bud from the walls of respiratory bronchioles, alveolar ducts and alveolar sacs. The presence of alveoli indicates where gas exchange with the blood occurs. There are about 150 million alveoli in the lungs. An alveolus is a pouch about 0.2-0.5mm wide. It consists of: (Predominantly) squamous (type I) alveolar calls thin cells that allow rapid diffusion of gas between the alveolus and the bloodstream (5%) round cuboidal great (type II) alveolar cells secrete a detergent like lipoprotein called pulmonary surfactant which forms a thin film inside the alveoli and the bronchioles Alveolar macrophages (dust cells) patrol the lumens of the alveoli and the connective tissue between them.

Scanning e.m. showing some of the 300 million alveoli in the human lung.

Capillary

Alevolus

Type II pneumocyte

Each alveolus is surrounded by a basket of blood capillaries supplied by the pulmonary artery. The barrier between alveolar air and blood (respiratory membrane) consists only of squamous (type I) alveolar cells, the squamous endothelial cell of the capillary and their fused basement membranes. These have a total thickness of 0.5micrometres. Pulmonary circulation has very low blood pressure.

Pleurae The surface of the lung is covered by a moist serous membrane called the visceral pleura which extends into the fissures. At the hilum the visceral pleura folds back on itself and forms the parietal pleura, which adheres to the mediastinum, the superior surface of the diaphragm and the inner surface of the rib cage. The space between the visceral and parietal pleurae is called the pleural cavity. The two membranes are separated by a film of slippery pleural fluid. The pleurae and pleural fluid have 3 functions: 1. Reduction of friction pleural fluid acts as a lubricant that enables the lungs to expand and contract with minimal friction. 2. Creation of pressure gradient pressure in the pleural cavity is lower than atmospheric pressure and this assists in inflation of the lungs 3. Compartmentalisation the pleurae, mediastinum and pericardium compartmentalise the thoracic cavity and prevent infections of one organ spreading easily to another organ. Lung surfactant: dipalmitoylphosphatidylcholine (DPPC) + lipids and proteins

Reduces alveolar surface tension, during inspiration promotes inflation of all rather than some alveoli, increases lung compliance, prevents alveolar collapse at and of expiration Law of Laplace P=2T/r surfactant ensures this balance is maintained. Lung surfactant ensures that if two alveoli have equal radii but different tensions that the tension is reduced so they both expand to take in equal amounts of air. If there are two alveoli of equal tensions but different radii the lung surfactant reduces the tension more in the smaller alveolus. Lack of surfactant can result in alveolar collapse (atelectasis). This is more likely to occur at the end of expiration when the radius is minimal. Surface Markings of the lungs The pleura extends above the clavicle in the neck (vulnerable to stab wounds) Pleura also descends below the costal margin in the right costosternal margin and between the 12th rib and the vertebral column on the left and right. Lung tissue is the same as the pleura except it doesnt extend much below T1 These structures do, however, move during breathing and change with posture. Everything is lower when you are standing erect than when you are lying down. Diaphragm The diaphragm accounts for 75% of the change in intrathoracic volume during quiet inspiration. It is attached around the bottom of the thoracic cage. It arches over the liver and moves downwards when it contracts. The distance it moves ranges from 1.5cm to 7cm with deep inspiration. The diaphragm has 3 parts: Costal portion made up of muscle fibres that are attached to the ribs around the bottom of the thoracic cage. Crural portion made up of fibres that are attached to the ligaments along the vertebrae. Pass either side of the oesophagus and can compress it when they contract. Central tendon the crural and costal portions insert into this. This is also the inferior portion of the pericardium. The costal and crural portions are innervated by different parts of the phrenic nerve and can contract separately.

Xiphoid sternum

Domes

Abdominal organs

3.

Physics of respiration

The respiratory system is made up of as gas-exchanging organ (the lungs) and a pump that ventilates the lungs. The pump consists of the chest wall, respiratory muscles and the areas of the brain that control these and the nerves that connect the muscles to the brain. At rest a normal human being takes about 12-16 breaths per minute. About 500ml of air is taken in per breath. Partial pressures Gases expand to fill the volume available to them (unlike liquids). The volume occupied by a given number of gas particles is the same regardless of the composition of gas at a given temperature and pressure. Therefore the pressure of any one gas(the PARTIAL PRESSURE) in a mixture of gases is equal to the total pressure multiplied by the fraction of the total amount of gas it represents. Gases diffuse from areas of high pressure to areas of low pressure. The rate of diffusion depends on the concentration gradient and the nature of the barrier between the 2 areas.

Inspiration This is an active process. The contraction of inspiratory muscles increases intrathoracic volume. When the diaphragm is stimulated by phrenic nerves it flattens. The external intercostals also contract as do the scalenes so the ribs swing upward and out. As the ribcage expands and the diaphragm drops the parietal pleura clings to them. Because of surface tension in the pleural fluid, the visceral pleura clings to the parietal pleura and so the lungs are also pulled out and expand and the pressure in the airways becomes slightly negative. Therefore air flows into the lungs from an area of higher pressure to an area of lower pressure. Inhaled air is also warmed as it enters the lungs and this causes its volume to increase so this inhaled air also causes the lungs to inflate. Expiration At the end of inspiration the lung recoil begins to pull the lungs back into the expiratory position where recoil pressures of the chest wall balance. The air pressure in the lungs becomes slightly positive and the air flows out of the lungs as there is lower atmospheric pressure. Expiration is passive as no muscles which decrease intrathoracic volume contract. However, there is some contraction of inspiratory muscles in early expiration which act as a braking force to slow expiration. To exhale more completely than usual the internal intercostal muscles must be contracted, which depress the ribs. Abdominal muscles can also be contracted. This causes the intrapulmonary pressure to rise much higher than normal (20-30 mmHg) causing faster and deeper evacuation of the lungs. This is useful for singing and public speaking. Lung Volumes The amount of air that moves into the lungs with inspiration is called TIDAL VOLUME Air inspired with maximal inspiratory effort is called INSPIRATORY RESERVE VOLUME (expiratory reserve volume is with maximal expiratory effort air left in the lungs after maximal expiratory effort id called RESIDUAL VOLUME) VITAL CAPACITY is the largest amount of air that can be expired after maximal inspiratory effort.

4.

Physiology of gas exchange

Neural control of ventilation The heartbeat and breathing are the most evident rhythmic processes of the body. The heart has an internal pacemaker and continues to beat even if all nerves are severed, but breathing depends on constant stimulation from the brain. The reasons for this are that skeletal muscle requires nervous stimulation to contract and breathing requires coordination of multiple muscles that require a mechanism to make sure they contract at the right time. Neurons in the medulla oblongata and pons provide automatic control for automatic control of unconscious breathing. Neurons in the motor cortex of the cerebrum provide voluntary control. Medulla oblongata Contains inspiratory neurons and expiratory neurons(fire during forced expiration). Fibres from these neurons pass down the spinal cord and synapse with lower motor neurones in the cervical and thoracic regions. Then the fibres travel in the phrenic (diaphragm) and intercostal (intercostal muscles) nerves. The exact method for the rhythm of respiration is unknown. The medulla has 2 nuclei. The inspiratory centre or dorsal respiratory group (DRG) which contains inspiratory neurons. When these fire the muscles of inhalation contract. The more they fire for the deeper inhalation is, the longer they fire for the lower respiratory rate is as each breath is prolonged. The expiratory centre or dorsal respiratory group has inspiratory neurons in the middle and expiratory neurons

at the anterior and posterior ends. The expiratory neurons inhibit the inspiratory centre when deeper expiration is required. Pons Regulates ventilation by means of a pnemotaxic centre in the upper pons (and maybe an apneustic centre in the lower pons). The pnemotaxic centre sends a constant stream of inhibitory impulses to the inspiratory centre in the medulla oblongata. The impulse frequency controls how last inspiration lasts. High frequency = short breaths. Voluntary control With conscious attention it is possible to do things such as hold our breath, take a deep breath etc. This control originates from the motor cortex of the frontal lobe of the cerebrum that can bypass the brainstem respiratory centres by sending impulses down corticospinal tracts. There are limits to voluntary control as when CO2 levels get too high the automatic control overrides will. Air-water interface When air and water are in contact gases diffuse down their concentration gradient until the partial pressure of each gas is equal to its partial pressure in the water. If gas is more abundant in air than in water then in diffuses into the water. Therefore the greater the PO2 in the alveolar air than the more O2 the blood picks up. And since blood arriving at the alveolus has a higher PCO2 than air the blood releases its CO2 into the air. It is said to UNLOAD the CO2 and LOAD O2. Alveolar gas exchange Both the loading of oxygen and the unloading of carbon dioxide are dependant on erythrocytes (RBCs). The efficiency of these processes depends on how long the RBC spends in the capillary compared to how long it takes for O2 and CO2 to reach equilibrium concentrations in the capillary blood. It takes only 0.25 seconds for the gases to equilibrate and the RBCs spend at least 0.3 seconds in the alveolar capillary at highest blood flow. This process is so efficient for the following reasons: 1. High concentration gradients of both gases (O2s is higher) 2. Solubility of gases (O2 is more soluble that nitrogen and CO2 is more soluble than O2 so evens out the difference in concentration gradient. 3. Membrane thickness (very thin so little obstacle to diffusion) 4. Large membrane area (70m2) 5. Good perfusion of capillaries

5.

Histology of the lungs

Upper Respiratory Tract Ciliated, mucin-secreting cells line the upper airways The architecture of the nasal cavity and the paranasal sinuses provide a large surface area for warming and moistening inspired air and for trapping inhaled particles. Air enters the repiratory system through the nostrils. Skin extends a short distance into the vestibule of the nostril but then becomes non-keratinized squamous epithelium, although occasional patches of stratified squamous epithelium persist, most of the nasal and paranasal sinus cavities are lined by pseudostratified squamous epithelium. Many of the columnar cells bear numerous cilia. Scattered among these cells are mucus secreting or goblet cells with microvilli on their luminal surface. This pattern continues throughout most of the air conducting part of the respiratory tract and is known as RESPIRATORY-TYPE EPITHELIUM. The nasal and sinus mucosa is highly vascular and contains mucous and serous glands. Beneath the nasal epithelium the lamina propria contains many glands. 3 main glands can be distinguished. 1. Mucous glands which secrete mucous to supplement the goblet cells in the epithelium. 2. Serous glands containing basophilic granules which may produce small amounts of amylase 3. Serous glands contain eosinophilic granules which produce lysosome Inspired air is moistened by the secretions of the serous components of the glands and a sheet of mucus lies on the mucosal surface and traps inhaled particles. The mucus is then wafted by the cilia toward the pharynx where it is swallowed or expectorated. The lamina propria also contains immune cells such as plasma cells, macrophages and a few neutrophils and eosinophils. Eosinophils are numerous in those who suffer with allergic rhinitis. The highly vascular aspect of the lamina propria is also a major contributant to warming the air. Paranasal cavities are useful because they provide a large surface area for warming and moistening air and because they play a role in the nature of sounds in speech.

The nasopharynx is a posterior continuation of the nasal cavities and becomes the oropharynx at the level of the soft palate. It is lined by columnar ciliated epithelium containing the occasional goblet cell and has frequent patches of squamous epithelium. The patches of squamous epithelium arise by metaplasia and increase as you near the oropharynx and also with age. In the nasopharynx there is also abundant mucosa associated lymphoid tissue in the submucosa. This tissues samples inhaled antigenic materials and enables defence mechanisms against it. Larger nodule aggregates of this tissue make up the tonsils. Olfactory mucosa is located in the roof of the nasal cavity. The laryngeal region has a complex architecture which: 1. Prevents inspired air entering the oesophagus 2. Prevents ingested food entering the trachea 3. Permits the production of complex sounds It therefore contains the epiglottis, the true vocal cords and the ventricular vocal cords. Laryngeal architecture is maintained by a series of cartilaginous plates, these are joined by collagenous ligaments and mobilised by striated muscle.

The trachea is lined with respiratory mucosa and is braced with cartilage. One narrow strip of the tracheal wall is deficient in cartilage. Here the gap is bridged by dense fibrocollagenous ligament that is rich in elastic fibres and bundles of smooth muscle. This allows some constriction of the tracheal lumen. The ligament connecting the two cartilage ends prevents dilation. The internal lining is pseudostratified ciliated columnar epithelium containing scatted goblet cells. Subepithelial seromucous glands are particularly numerous in the posterior band devoid of cartilage.

The main bronchi are extrapulmonary and enter each lung at the hilum. They then divide into lobar bronchi and then segmental bronchi they further subdivide for a variable number of generations. Throughout their course the bronchi have a similar structure to the trachea but there are variations. The basic structure is: Pseudostratified columnar epithelium Subepithelial fibrocollagenous tissue containing variable quantities of seromucous glands Variable amounts of smooth muscle, with elastic fibres arranged in longitudinal bands Variable amounts of partial cartilaginous ring The bronchial tree is lined by pseudostratified columnar epithelium which is pseudostratified in larger bronchi and becomes less complex in smaller peripheral branches. The epithelium contains ciliated columnar cells, mucus-secreting goblet cells and neuroendocrine cells Ciliated cells are columnar in most of the bronchial tree but are shorter and almost cuboidal in most of the peripheral branches they have a basal nucleus, and lysosomes and numerous mitochondria in their supranuclear cytoplasm. The luminal surface bears about 200 cilia and microvilli. Basal cells lie on the basement membrane and are small cells that are not in contact with the lumen. They form a stem cell population from which other cells develop. Intermediate cells are stem cells that are mid transformation into ciliated or mucous secreting goblet cells. Goblet cells are scattered between goblet cells and are most numerous in the main and lobar bronchi, becoming less common in the smaller branches. Neuroendocrine cells are small round cells with dark staining nuclei and clear cytoplasm. They are located in the basement membrane. They are most numerous in the smaller bronchi. They possess cytoplasmic processes that contain neuroendocrine granules. They secrete hormones and active peptides. They may be scattered or congregate in clumps. Smooth muscle, lymphoid tissue and seromucous glands are present in the walls of the bronchi. There are also elastic fibres of fibrocollagenous stroma arranged in longitudinal bands. In the main bronchi the smooth muscle is mainly confined posteriorly due to the cartilaginous rings, it persists in the smallest branches long after the cartilage ceases to be present. The submucosal bronchial glands are seromucous glands that empty into the lumen via short ducts. The serous component is thought to secrete lysozomes and glycoproteins. The mucus is thin and traps inhaled matter and microorganisms. The ciliated columnaer epithelium waft this matter upwards Myoepithelial cells lie between the secretory and duct lining cells and their basement membrane and some neuroendocrine cells are also present.

The bronchial wall contain MALT (mucosa associated lymphoid tissue). Lymphocytes and IgA are closely associated with the bronchial glands and lymphoid aggregations are common, being most evident at bifurcations. Bronchi of all sizes contain some cartilage main extrapulmonary bronchi have regular incomplete rings of cartilage but the intrapulmonary bronchi have an irregular roughly circumferential arrangement of cartilage plates connected by dense fibrocollagenous bands. As the bronchi get smaller and more peripheral the cartilage plates decrease in size and number and are mainly concentrated at bifurcations. Bronchioles are distal airways that branch repeatedly. As they do so they reduce their luminal size. Smooth muscle becomes the main component of their walls. Bronchioles are lined with ciliated columnar epithelium without pseudostratification. The cells become lower and more cuboidal in the small peripheral branches. Occasional goblet cells persist, as do small numbers of neuroendocrine cells but there are no seromucous cells and a new cell called CLARA CELL is found. The Clara cell is neither ciliated nor mucus producing and is most numerous in the terminal bronchioles.

Distal respiratory tract Bronchioles are lined with cuboidal ciliated epithelium which merges with flattened epithelium lining the entrances to the alveolar ducts which are lined with alveoli. Alveoli have a polygonal air space of about 250 micrometers in diameter each when inflated, with a thin wall that contains pulmonary capillaries and forms the air-blood barrier. They also contain pores called the pores of Kohn which connect each alveolus to those adjacent to it. They provide direct communication from alveolus to alveolus which permits rapid and even distribution of air throughout the lobe of the lung during inspiration. However, a disadvantage is that pathogens can also use these pores to quickly spread through the lungs. Alveoli contain type I and type II pneumocytes, which lie on the alveolar basement membrane, and alveolar macrophages. Type I pneumocytes are very thin cells that allow gaseous diffusion. They represent about 40% of the alveolar cell population but form 90% of the surface lining of the alveolar sacs and alveoli. They are flat cells with flattened nuclei and are joined by tight junctions. They contain scanty mitochondria and the cytoplasm gives only a thin cover to the basement membrane which contributes to the thinness of the air-blood barrier.

Type II pneumocytes represent 60% of the alveolar call population numerically but only 5-10% of the surface area. These are rounded cells which are located at angles and bifurcations. Their nuclei are round and dark and their cytoplasm are rich in mitochondria and rER and sER. They also contain electron dense vesicles and spherical bodies of material which is rich in phospholipids, proteins and glycosaminoglycans which forms the basis of surfactant.

Alveolar macrophages phagocytose inhaled bacteria and particulate matter. Normally they lie on top of the alveolar lining cells and can be seen free in the alveolar space. They patrol airspaces and the interalveolar septa passing freely between the two. Apart from engulfing foreign particles and pathogens they remove extra surfactant and secrete enzymes. After phagocytosis they either pass to the terminal bronchioles and into the lymphatic system or they adhere to the mucus coated cilia and are carried out to be swallowed. They can also remain in the interstitium (septa). The alveolar wall also contains elastic tissue and this allows the lungs to stretch and accommodate air, recoil to expel air and also tethers the bronchioles to the lung parenchyma and therefore the pleura. Pulmonary vasculature Lungs have dual blood supply and venous drainage. Blood is provided by the pulmonary and bronchial arteries and veins. The bronchial system provides oxygenated blood to the larger components of the bronchial tree. The pulmonary vascular system is more important as this is the capillary component and therefore the site of gas exchange. They provide the lungs with deoxygenated blood from the right side of the heart. The proximal pulmonary artery branches are elastic arteries. They have a narrow intima which is single layer of endothelium lying on scanty collagen fibres and myofibroblasts, a media composed of layers of elastic fibres, smooth muscle cells and collagen and laminae that are formed of longitudinally running elastic fibres. The distal pulmonary arteries are muscular and the media of them is mainly circularly orientated smooth muscle. Continuous branching results in arterioles and the muscular layer becomes discontinuous and eventually disappears. The

oxygenated blood from the alveolar capillaries enters the venules which have a thin intima that lies on a narrow zone of collagen and elastic fibres. As they form larger and larger venules the numbers of myofibroblasts and smooth muscle cells increase in the media. The larger veins have distinct media with internal elastic lamina. Pleura The visceral pleura is composed of 5 ill-defined layers: Outer layer of flat mesothelial cells A narrow zone of loose, fibrocollagenous tissue with no basement membrane between it and the mesothelium An irregular elastic external layer An interstitial layer of loose fibrocollagenous stroma containing lymphatics, blood vessels and nerves and some smooth muscle fibres An internal elastic layer with short lengths of elastic fibre some of which merge with the interaveolar septa.

The parietal pleura is similar but more simple with only one layer of elastic fibres. It sits on a layer of adipose tissue, beneath which is a layer of dense collagenous tissue which is continuous with the periosteum of the ribs and the perimysium of the intercostals muscles.

6.

Reaction/effect of trauma sympathetic nervous system

Acute stress reaction (also called acute stress disorder or simply shock) is a psychological condition arising in response to a terrifying event. "Acute Stress Response", was first described by Walter Cannon in the 1920s as a theory that animals react to threats with a general discharge of the sympathetic nervous system. The response was later recognized as the first stage of a general adaptation syndrome that regulates stress responses among vertebrates and other organisms. The onset of a stress response is associated with specific physiological actions in the sympathetic nervous system, both directly and indirectly through the release of epinephrine and to a lesser extent norepinephrine from the medulla of the adrenal glands. The release is triggered by acetylcholine released from pre-ganglionic sympathetic nerves. These catecholamine hormones facilitate immediate physical reactions by triggering increases in heart rate and breathing, constricting blood vessels in many parts of the body - but not in muscles (vasodilation), brain, lungs and heart - and tightening muscles. An abundance of catecholamines at neuroreceptor sites facilitates reliance on spontaneous or intuitive behaviors often related to combat or escape. Normally, when a person is in a serene, unstimulated state, the "firing" of neurons in the locus ceruleus is minimal. A novel stimulus, once perceived, is relayed from the sensory cortex of the brain through the thalamus to the brain stem. That route of signaling increases the rate of noradrenergic activity in the locus ceruleus, and the person becomes alert and attentive to the environment. If a stimulus is perceived as a threat, a more intense and prolonged discharge of the locus ceruleus activates the sympathetic division of the autonomic nervous system (Thase & Howland, 1995). The activation of the sympathetic nervous system leads to the release of norepinephrine from nerve endings acting on the heart, blood vessels, respiratory centers, and other sites. The ensuing physiological changes constitute a major part of the acute stress response. The other major player in the acute stress response is the hypothalamic-pituitaryadrenal axis.

These catecholamine hormones facilitate immediate physical reactions associated with a preparation for violent muscular action. These include the following:

Acceleration of heart and lung action Inhibition of stomach and intestinal action General effect on the sphincters of the body Constriction of blood vessels in many parts of the body Liberation of nutrients for muscular action Dilation of blood vessels for muscles Inhibition of Lacrimal gland (responsible for tear production) and salivation Dilation of pupil Relaxation of bladder Inhibition of erection

7.

Emergency services ATLS

Advanced trauma life support is the standard method for the initial management of severely injured patients. The principle is simpletreat the greatest threat to life first. Loss of airway will kill before inability to breathe, and inability to breathe will kill before bleeding and loss of circulation. A definitive diagnosis is not necessary to treat the patient initially. The most important point to remember is that no harm should be done to the patient during treatment. The management of severely injured patients is divided into the primary and secondary survey. ABCDE of trauma Airway and cervical spine control Breathing and ventilation Circulation and haemorrhage control Disability and neurological status Exposure and environment Primary survey

The primary survey comprises a rapid evaluation of the patient, resuscitation, and institution of life preserving treatment. This process is called the ABCDE of trauma. Adjuncts to the primary survey include relevant imaging during resuscitation and re-evaluation. In practice, most of the steps of the ABCDE are carried out simultaneously by a trauma team. Anaesthetists will usually deal with the airway and intravenous access while the surgeon evaluates the chest, abdomen, and pelvis for potential life threatening injuries. Supine radiograph showing endotracheal tube 5 cm above carina (arrow)

Imaging is requested as part of the primary survey while the patient is assessed, life threatening injuries are dealt with, and resuscitation procedures instituted. Imaging should not be performed if it interferes with the rest of the primary survey or definitive care, and only investigations that may have a direct effect on the patient's initial problems should be done. Examples of imaging done as part of the primary survey include radiographs of the supine anteroposterior chest, supine pelvis, and lateral cervical spine (although this can be delayed if necessary); and limited ultrasonography (also known as FAST, focused assessment with sonography for trauma) Airways and cervical spine control

The airway should be assessed for patency. Foreign bodies and vomit should be removed and facial, mandibular, tracheal, and laryngeal injuries should be excluded clinically. Radiograph of supine pelvis may be requested for the primary survey. This radiograph shows no abnormality.

If the patient is conscious and talking, there is usually no immediate need for airway intervention. If the patient is unconscious and breathing spontaneously, an oropharyngeal airway may suffice as a temporary measure. Any patient who has a head injury and a score on the Glasgow coma scale of 8 or less should be intubated. However, intubation may be required for optimal control of airways in patients with higher scores. Glasgow coma scale score Eye opening (graded 1-4) Spontaneous4 To speech3 To pain2 None1 Best motor response (graded 1-6) Obeys command6 Localises pain5 Normal flexion4 Abnormal flexion3 Extension (decerebrate)2 None1 Verbal response (graded 1-5) Orientated5 Confused conversation4 Inappropriate words3 Incomprehensible sounds2 None1 Maximum score 15, minimum score 3

 Mild injury 14-15 Moderate injury 9-13 Severe injury 3-8 Coma 8 If the patient has been intubated, a chest radiograph should be taken to check the position of the endotracheal tube. The tip of the tube should not lie below the level of the aortic arch in a supine chest radiograph and a minimum of 3.5 cm (and preferably 5 cm) above the carina. Care should be taken to avoid worsening a potential cervical spine injury while establishing and safeguarding an airway. If the airway has been secured and the neck immobilised the cervical spine radiograph can be delayed. The cervical spine should be immobilised with a cervical collar, sandbag, and tape. Should the collar need to be removed, an experienced member of the trauma team should carry out in-line manual immobilisation of the head and neck. Breathing and ventilation

A patent airway does not guarantee adequate ventilation. The lungs, chest wall, and diaphragm must be assessed for potential injuries that could compromise ventilation acutely. These injuries include tension pneumothorax, tension haemothorax, flail chest, and open pneumothorax. It can be difficult to exclude these injuries in a patient with multiple trauma. A chest radiograph must be taken as soon as possible. If the patient is subsequently intubated or ventilated, a second radiograph should be taken to confirm that the endotracheal tube is in a satisfactory position and that life threatening injuries have not been made worse. Ventilation can cause a simple pneumothorax to become a tension pneumothorax.

Opaque left haemothorax with evidence of contralateral shift of the mediastinum.

Circulation and haemorrhage control

The patient's haemodynamic state must be assessed quickly and accurately because bleeding is a major cause of preventable death. Clinical evaluation is essential, in particular, the level of consciousness, skin colour, and pulse. Any external source of bleeding should be identified and dealt with immediately using manual pressure. When the examination or history suggests internal injury, a pelvic radiograph should be taken and limited ultrasonography (FAST) done to exclude hidden blood loss.

Main causes of hidden blood loss Chest, abdomen, and retroperitoneal injuries Pelvic fractures Multiple long bone fractures FAST can be performed by a physician, surgeon, or radiologist and has been shown to be valuable in the assessment of blunt trauma patients in the emergency room, especially in unstable patients with multiple injuries. Ultrasonography should be performed in five areas. These areas are the 5 Psperihepatic, perisplenic, and pelvis in the abdomen, and pericardial (to exclude a pericardial tamponade) and pleural (to detect fluid or a pneumothorax or consolidated lung) in the chest. The presence of a pelvic fracture or free fluid on ultrasonography mandates a specialist opinion. Disability (neurological examination) The patient's neurological state is assessed with the Glasgow coma scale. It is easy and quick to use and is a determinant of patient outcome and possible further management. All patients with a head injury should have computed tomography of the head, especially if they have lost consciousness, have amnesia, or severe headaches. Up to 18% of patients with mild head injuries (Glasgow coma scale 14-15) have abnormalities on computed tomography, and 5% of these patients may require surgery. Extradural haematoma and a subtle subdural haematoma (left), subdural haematoma (middle left), diffuse axonal injury (middle right), and combination injuries (right). If the patient has a head, scan itmissing a serious head injury may have catastrophic consequences Computed tomography should be done as soon as possible because morbidity and mortality rises substantially if surgery is delayed. The intracranial findings of computed tomography may include no abnormality, extradural haematoma, subdural haematoma, contusions and intracerebral haematomas, subarachnoid blood, diffuse axonal injury, and combination injuries. Supine anteroposeterior radiograph of normal chest with ABCDEs interpretation

The National Institute of Clinical Excellence (NICE) introduced UK guidelines for management of head injury in 2003 that support the advanced trauma life support guidelines. They emphasise that computed tomography must be done within an hour of the patient arriving at the hospital.

Exposure and environment The patient should be fully exposed (by cutting off all clothes) to allow a full examination. It is, however, critical to keep the patient warm with blankets and a heated emergency room. Large volumes of fluids may be infused, and these intravenous fluids should be warmed. Adjuncts to primary survey and resuscitation As a minimum, patients should have electrocardiography, their blood pressure monitored, pulse oximetry, a nasogastric tube, and a urinary catheter. Blood gases should also be monitored. If a fracture at the base of the skull is suspected, the nasogastric tube can be inserted after computed tomography of the head or an orogastric tube placed. ABCs interpretation of pelvic radiographs Alignment Check the pubic symphysis is symmetrical and not widened Carefully check that the sacroiliac joints are intact Bones Check that all three pelvic rings are intact Use a bright light to check iliac crests and hips Look at the lumbar spine and hip joints separately Cartilage Check the distance of the pubic symphysis Again check the sacroiliac joints Check both hips Soft tissues Check the soft tissue planes are symmetrical Look for obturator internus Carefully delineate the perivesical fat plane Make sure the gluteus medius and psoas fat planes are intact Interpreting primary survey images All imaging must be supervised and done without fuss or undue delay and with meticulous technique. Attention to detail is essential. In particular, the film must be labelled (including the patient's name and a side marker). Interpretation of the supine chest radiograph (ABCDEs) Airways Check trachea is clear and central

 Is airway patent? Check position of endotracheal tube Are there any teeth or foreign bodies? Check all lines and tubes Breathing Exclude tension pneumothorax and haemothorax Check there is no radiological flail segment Exclude rib fractures Check lungs are clear Circulation Check heart size and mediastinal contours are normal Make sure that the aortic arch is clearly seen Check the hila and vascular markings are normal Diaphragm Check that diaphragms appear normal (size, shape, and position) Can both diaphragms be clearly seen? Check under each diaphragm Edges Check the pleura and costophrenic recesses Exclude a subtle pneumothorax or effusion Soft tissues and skeleton Look for surgical emphysema Check clavicles and shoulders and exclude rib fractures Look at the paraspinal lines and check the spine The supine chest radiograph should be taken as soon as possible after the patient has been exposed and centred correctly. Attention must be paid to stop patients being rotated and keeping them in the middle of the trolley.

Radiograph of supine pelvis showing ABCDEs interpretation 8. Examination of the lungs

Palpation Palpation is the method of "feeling" with the hands during a physical examination. Percussion Percussion is a method of tapping body parts with fingers, hands, or small instruments as part of a physical examination. The purpose is to evaluate the size, consistency, borders, and presence or absence of fluid in body organs. Percussion of a body part produces a sound like playing a drum - that indicates the type of tissue within the organ: Lungs sound hollow on percussion because they are filled with air. Bones and joints sound solid. The abdomen sounds like a hollow organ filled with air, fluid, or solids. Auscultation The doctor will use a stethoscope to listen to the lungs and breath sounds. From a clinical point of view the following should be noted: - When you place a stethoscope on a patients back you are listening mainly to the lower lobe. There is a small area of upper lobe, but no middle lobe at all. - When you place a stethoscope on a patients anterior chest wall, you are listening mainly to the upper and middle lobes - You will listen to the middle lobe by placing the stethoscope at the side and in the axilla. - You cannot listen to individual pulmonary segments or even individual lobes. - When a patient is lying in bed on his back, the most dependant bronchopulmonary segments are the apical and posterior segments of the lower lobe. These segments are most often affected by lung infections in ill bedridden patients. - In normal breathing, lung tissue does not occupy the lower extremities of the costodiaphragmatic recesses, but it may in deep inspiration. This means in this region surface markings on the lungs is different from the surface markings of the pleural cavities. Abnormal Breath Sounds Rales: hissing, whistling, scrapping or rattling sounds are associated with increased airway resistance. These sounds are created by turbulent airflow past pus or mucus or past airways narrowed by

inflammation. Moist rales are gurgling sounds and are heard over fluids in conditions such as bronchitis, tuberculosis and pneumonia. Dry rales are heard in asthma and pulmonary oedema. Stridor: loud high pitched sound that can be heard without a stethoscope. Indicates acute airway obstruction such as partial blockage of the glottis by a foreign object. Wheezing: whistling sound that can occur I inspiration and expiration. Indicates airway obstruction sue to mucus build up or bronchospasms. Coughing: familiar sign of several respiratory disorders. It is primarily a reflex action that clears the airway but can also indicate irritation of the lining of the respiratory passageways. A productive cough ejects sputum, which can be ejected and analysed. Friction rub: distinctive crackling sound produced by abrasion between abnormal serous membranes.

You also may have the following tests: Chest X-rays

The posteroanterior radiograph is taken with the anterior of the patients chest touching the cassette holder and with the x-rays traversing the thorax form the posterior to the anterior aspect. It must not be even slightly oblique. If it is not the sternal ends of both clavicles should be equidistant from the vertebral spines. The following should be examined in systematic order:

1. Superficial soft tissues the nipples/breasts may be superimposed on the lung fields. The pectoralis major may also cast a soft shadow. 2. Bones the thoracic vertebrae are imperfectly seen. The cotransverse joints of the ribs should be examined from above downward and compared with the other side. Costal cartilages are not normally seen, but if they are calcified they will be visible. Theclavicles should be clearly seen crossing the upper part of each lung field. The medial borders of the scaplulae may be seen overlapping the periphery of each lung field. 3. Diaphragm should cast dome shaped shadows on each side. The right is slightly higher than the left. Beneath the right dome is the shadow of the liver. And beneath the left dome a bubble may be seen in the fundus of the stomach. 4. Trachea it will be a superimposed radiotranslucent air filled shadow. 5. Lungs dense shadows at the lung roots caused by blood vessels, large bronchi and lymph nodes. The lung fields due to the air content readily permit the passage of x-rays. The lungs are therefore more translucent on full inspiration than expiration. Pulmonary blood vessels are seen as shadows radiating from the lung root. 6. Mediastinum shadow is produced by various structures in the mediastinum, superimposed one on the other. The outline of the heart and great vessels are visible. The transverse diameter of the heart should not exceed half the width of the thoracic cage. On deep inspiration the vertical length of the heart increases as the diaphragm extends and the transverse diameter is narrowed. ALSO: - Arterial blood gases - electrocardiogram Tension Pnemothorax: Unilateral absence of breath sounds suggests pneumothorax; resonance to percussion and dilated neck veins suggest tension pneumothorax. When heard through a stethoscope, the breath sounds are decreased. Structures in the center of the chest (mediastinum) may appear to have moved. There may be air trapped in the tissue of the chest wall (subcutaneous emphysema), causing a spongy feeling when the chest is felt with the hands (palpation). Hamman's Sign (or 'Crunch') is a crunching systolic sound heard over the sternal edge in mediastinal emphysema or left apical pneumothoraces. Crepitus (crackling in the soft tissues beneath the skin) indicating surgical emphysema. The engorged veins in the neck suggest the patient has hypovolaemia and is a potential sign of tension pneumothorax.

An increase in negative intrathoracic inspiratory pressure increases venous return (the tension pneumothorax sends feedback that a deep inspiration is occurring because the intrathoracic pressure is so high and causes more deoxygenated to return to the heart to be oxygenated at the lungs (I THINK). Also pressure on the side of the heart where the pneumothorax is will cause increased output on that side of the heart.

Collapsed lung: Listening to the chest with a stethoscope may reveal decreased breath sounds on one side of the chest. There may be a bluish coloration of the skin caused by lack of oxygen. The affected person may have a rapid heart rate.

Diagnosis of tension pneumothorax using a needle and a cannula 12G intraveneous cannula with supporting needle inside and 50ml syringe

Right mid-clavicular line Once the chest wall has been penetrated,the needle is withdrawn leaving the catheter in place. In the presence of a tension pneumothorax air would rush out of the catheter under pressure.

9. Pneumothorax

Aortic rupture (a tear in the aorta, which is the major artery coming from the heart) can be seen on a chest xray. In this case, it was caused by a traumatic perforation of the thoracic aorta. This is how the x-ray appears when the chest is full of blood (right-sided hemothorax) seen here as cloudiness on the left side of the picture - Blunt or penetrating trauma - Requires rapid decompression and fluid resuscitation - May require surgical intervention - Clinically: hypovolaemia absence of breath sounds dullness to percussion - CXR may be confused with collapse

Pneumothorax occurs when air leaks from inside of the lung to the space between the lung and the chest wall. The lung then collapses. The dark side of the chest (right side of the picture) is filled with air that is outside of the lung tissue.

If fluid, such as blood, or air, gets into the pleural space, the lung can collapse, preventing adequate air exchange. Chest tubes are used to treat conditions that can cause the lung to collapse, such as: air leaks from the lung into the chest (pneumothorax) bleeding into the chest (hemothorax) after surgery or trauma in the chest (pneumothorax or hemothorax) lung abscesses or pus in the chest (empyema).

If air enters the pleural space, the lung will collapse. This is called a pneumothorax. If the chest wall is penetrated, which may occur as a result of an injury, air can enter the pleural space from the outside. Air can also enter from the inside, from the lung itself, if the lung is torn or ruptured. One of the most common causes of spontaneous non-traumatic pneumothorax is a pulmonary bleb. This is a weakness and out-pouching of the lung tissue, which can rupture. This introduces air into the pleural space.

Pneumothorax may result from chest trauma, excess pressure on the lungs, or a lung disease such as COPD, asthma, cystic fibrosis, tuberculosis, or whooping cough. In some cases, the cause is unclear. Symptoms Chest pain (stabbing). Decreased venous return Decreased cardiac output Low blood pressure Desaturation, not always Hypercarbia (too much carbon dioxide in the blood) Dyspnoea (shortness of breath)

Spontaneous pneumothorax Aeitiology Can be inherited by the autosomal dominant route with variable penetrance. Penetrance 21% in the Females. 50 % in the males. Marfans syndrome Ehlers Danlos syndrome.

There are two types of spontaneous pneumothorax:

Primary spontaneous pneumothorax Secondary spontaneous pneumothorax

Spontaneous means there is no traumatic injury to the chest or lung. Primary spontaneous pneumothorax occurs in people without lung disease. It occurs most often in tall, thin, young people. Sometimes people have a family history of this problem. People who have had one spontaneous pneumothorax are at higher risk of the same thing (on the same side or the other side) occurring again. Secondary spontaneous pneumothorax occurs in people who have underlying lung disease. The most common lung disease that causes spontaneous pneumothorax is chronic obstructive pulmonary disease (COPD). Other lung diseases associated with spontaneous pneumothorax include:

Asthma Cystic fibrosis Interstitial lung disease Lung cancer Pneumonia Tuberculosis

Symptoms often begin suddenly, and may occur during rest or sleep. They can include:

Abnormal breathing movement o Restricting chest wall motion when breathing to protect against pain o Splinting -- bending over or holding the chest to protect against pain Cough Rapid respiratory rate Shortness of breath Sudden chest pain or chest tightness o Breathing or coughing makes pain worse o Chest pain may be dull, sharp, or stabbing

Tension pneumothorax

A tension pneumothorax is a complete collapse of the lung. It occurs when air enters, but does not leave, the space around the lung (pleural space). Any condition that leads to pneumothorax can cause a tension pneumothorax. In uncomplicated pneumothorax, air can enter and leave the pleural space easily. In tension pneumothorax, however, air enters the pleural space with each breath and gets trapped there. As the amount of trapped air increases, pressure builds up in the chest. The lung collapses on that side and can push the important structures in the center of the chest (such as the heart, major blood vessels, and airways) toward the other side of the chest. The shift can cause the other lung to become compressed, and can affect the flow of blood returning to the heart. This situation can lead to low blood pressure, shock, and death. Symptoms

Sudden chest pain Shortness of breath Chest tightness Easy fatigue Bluish color of the skin due to lack of oxygen Rapid heart rate

Low blood pressure Decreased mental alertness Decreased consciousness Rapid breathing Bulging (distended) veins in the neck

Possible Complications

Acute respiratory failure Air in the mediastinal space, which can interfere with heart and lung function (pneumomediastinum) Very low blood pressure (shock) Death

Traumatic pneumothorax

A traumatic pneumothorax is a collection of air inside the chest, between the lung and inner chest wall, which causes the lung to collapse. Traumatic pneumothorax occurs when a physical injury causes the lung to collapse. It can be caused by chest injury from a gunshot or knife wounds. It may also be caused by automobile accidents, or can happen after certain medical procedures. High-risk medical procedures include transbronchial biopsy, pleural biopsy, thoracentesis, central venous catheter placement, intercostal needle anesthesia, and esophagoscopy. Hemothorax, a collection of blood between the lung and chest wall, often happens with traumatic pneumothorax. Symptoms History of recent chest injury or high-risk procedure, plus:

Chest pain Shortness of breath Breathing, rapid Chest tightness Hypoxemia (low oxygen level in blood)

10. Dressings for pneumothorax

Dressing sealed on three sides only. Acts as flap valve, allowing air flow through chest wall outwards but not inwards. Following application of the dressing sealed on three sides, the patient is positioned with the injured side down: The optimal treatment is the application of an Asherman chest seal. The skin may need to be shaved or wiped dry of sweat or blood to enable adequate adhesion. 11. Treatment of pneumothorax In general, if a health care provider suspects tension pneumothorax, treatment should start before tests are done. In an emergency, a small needle (such as a standard intravenous needle) may be placed into the chest cavity through the ribs to relieve pressure. Needle decompression

Tension pneumothorax is a rare prehospital event, particularly in blunt trauma. It is difficult to assess the exact numbers accurately as thoracocentesis is often performed in the absence of a true tension pneumothorax, but recent studies show a prevalence of 6%. Tension pneumothorax is more likely to occur in positive pressure ventilation. If the patient with multiple trauma is deteriorating, with an unknown cause, specifically look for tension pneumothorax. If localising features are not found consider the presence of bilateral pneumothoraces. Common features in patients who are awake include universal symptoms of chest pain and respiratory distress, with tachycardia and ipsilateral decreased air entry found in 5075% of cases. In ventilated patients, the universal findings are rapid onset deterioration with a decrease in oxygen saturations and blood pressure. High ventilation pressures, reduced chest wall movement and air entry are found in about 33% of cases. Technique of needle decompression. Avoid thick muscle, breast tissue or areas with surgical emphysema. The first choice of site is the 2nd intercostal space in the midclavicular line. Studies have shown that there is a low accuracy in correct anatomical placement and therefore practitioners should be familiar with the landmarks. The standard 14G cannula is 4.5 cm long, and depending on the body mass index of the patient this may not be long enough to decompress all tension pneumothoraces. The cannula may also fail to decompress the tension pneumothorax due to obstruction by blood, tissue or kinking. Therefore, the cannula should be inserted into the chest attached to a syringe and flushed with 2 ml of air, if there is no obvious air release on insertion. Other causes of failure include a localised tension pneumothorax in the patient with pre-existing lung disease, or the presence of a large air leak in which the air will collect in the pleural space quicker than can be drained by the narrow bore of the cannula. If the anterior approach fails due to suspected depth of chest wall, then the lateral approach should be attempted in the 5th intercostal space, anterior axillary line if the chest wall appears thinner at this site. Consider using a longer needle or a commercial device designed for this purpose. If needle decompression fails at both sites, the practitioner is certain of the diagnosis and is appropriately trained and competent: thoracostomy may be performed. After this an intercostal chest drain should be inserted or an Asherman chest seal over the open chest wound. Needle decompression should not be used for simple pneumothorax or haemothorax. There is considerable risk of iatrogenic pneumothorax if misdiagnosis and decompression is performed. Needle decompression in the absence of a pneumothorax may even create an iatrogenic tension pneumothorax. There is increasing concern regarding the number of needle decompressions being performed without the appropriate clinical indications, leading to significant morbidity and unnecessary interventions for the patient.

Continuing observation and reassessment is essential by a person who can repeat decompression if necessary: this includes during transfer. If the cannula fails to work and the patient is beginning to retension, repeat needle decompression should be performed adjacent to the initial successful site.

Surgical emergency Rx: emergency decompression before CXR Either large bore cannula in 2nd ICS, MCL or insert chest tube CXR to confirm site of insertion

Pneumothorax can be life-threatening. The immediate treatment for pneumothorax is tube thoracostomy, or the insertion of a chest tube. Explanation 1. Chest tubes are inserted to drain blood, fluid, or air and allow full expansion of the lungs. The tube is placed in the pleural space. The area where the tube will be inserted is numbed (local anesthesia). The patient may also be sedated. The chest tube is inserted between the ribs into the chest and is connected to a bottle or canister that contains sterile water. Suction is attached to the system to encourage drainage. A stitch (suture) and adhesive tape is used to keep the tube in place. The chest tube usually remains in place until the X-rays show that all the blood, fluid, or air has drained from the chest and the lung has fully re-expanded. When the chest tube is no longer needed, it can be easily removed, usually without the need for medications to sedate or numb the patient. Medications may be used to prevent or treat infection (antibiotics). Explanation 2. A long, flexible, hollow, narrow tube is inserted through the ribs into the pleural splace, and the tube is attached to a suction device. This allows the air to be evacuated from the pleural space, and allows the lung to re-expand. Chest tubes are generally inserted using local anesthesia. The chest tube is left in place until the lung leak seals on its own; this usually occurs within two to five days. Recovery from the chest tube insertion and removal is usually complete, with only a small scar. The patient will stay in the hospital until the chest tube is removed. While the chest tube is in place, the nursing staff will carefully check for possible air leaks, breathing difficulties, and need for additional oxygen. Frequent deep breathing and coughing is necessary to help re-expand the lung, assist with drainage, and prevent normal fluids from collecting in the lungs. Pulmonary blebs can be resected, preventing future pneumothorax. This is frequently done using a thoracoscopic surgical procedure. The patient is put to sleep using general anesthesia. Long, narrow

instruments, including one with a camera on the end to allow for visualization of the interior of the thorax, are introduced through small incisions in the chest wall

Pulmonary bleb

Explanation 3. An incision is made in the chest wall below the diagnostic cannula and distant from the wound (e.g. for Stephen - in 5th right interspace and in the midaxillary line). Blunt dissection (use of a large pair of scissors) is used to achieve full penetration of the chest wall. Insertion of a finger through the incision is useful to check that the pleural cavity has been penetrated. Having created access (for the chest drain) to the pleural cavity, two sutures are inserted - one at each end of the incision.These are initially left untied - they will subsequently be used to close the incision after the drain has been withdrawn.

The chest drain (a plastic tube) is inserted through the incision and into the pleural cavity. Insertion of the drain is sometimes aided by the use of a rod (trochar) within the lumen of the drain. The use of a trochar is not without risk and it is now considered preferable to manage without it. In the picture the drain has been inserted and the trochar is being withdrawn.

The chest drain is connected to its under water seal and fluid collection vessel. This must be positioned below the level of the patient or fluid will siphon into the pleural cavity.

A further suture (positioned close to the incision) is used to anchor the drain:

Explanation 4. The standard treatment is a chest tube, a large plastic tube that is inserted through the chest wall between the ribs to remove the air. The chest tube is attached to a vacuum bottle that slowly removes air from the chest cavity. This allows the lung to re-expand. As the lung heals and stops leaking air, the vacuum is turned down and then the chest tube is removed. Some people might need to stay in the hospital to have the chest tube checked, and because it can take several days for the affected lung to fully re-expand. Surgery may be needed if the problem happens again, or if the lung does not re-expand after 5 days with a chest tube in place. A stapling device is inserted into the chest during thoracoscopic surgery, and the segment of lung with blebs is stapled across and then removed. Most patients respond quite well to this procedure, and usually require one to three days in the hospital after surgery to recover. A chest tube is frequently left in place for one to two days after surgery to evacuate any residual air in the pleural space. ONLY REQUIRED FOR SPONTANEOUS PNEUMOTHORAX Complications of chest drains Insertional Direct trauma.

Positional Blockage. Kinking. Extra thoracic placement.

Infective

Entry site. Empyema.

12. Anaesthetics and Analgesics Anaesthetics General anaesthesia is the loss of awareness of general sensory inputs to the CNS and includes varying degrees of analgesia, amnesia and loss of consciousness. It may be accompanied by muscle relaxation

and loss of homeostatic control of respiration and cardiovascular function. An adequate level of general anaesthesia is essential for major surgical procedures. Modern general anaesthetics allow rapid and smooth induction of surgical anaesthesia with a short recovery phase. Anaesthesia is usually rapidly induced in adults as an intravenous bolus dose and is subsequently maintained by an inhalation anaesthetic.

General anaesthetics act on cell membranes. The stages of anaesthesia can be explained by the accessibility of the different neurones to the anaesthetic agent. Side effects: depress myocardial contractility, depress response of the respiratory centre, decrease liver blood flow. Reduce renal blood flow and renal vascular resistance, relax uterus, cause muscle relaxation, can produce post operative nausea and vomiting.

Local anaesthetics block the transmission of pain by reducing the ion fluxes that are responsible for the depolarisation of excitable calls, particularly the rapid influx of Na+ as well as the slower efflux of K+ . Local anaesthetics inhibit both afferent and efferent pathways as well as neuromuscular junctions. Pain pathways are more effectively inhibited than those involved in touch and pressure. A variety of mechanisms inhibit nerve transmission. Non specific membrane effects, specific intraneuronal receptor activity (therefore must be lipid soluble). Side effects: irritation and inflammation at the site of administration, can affect excitable membranes e.g. the heart. Techniques of administration affect the extent of local anaesthesia. Surface administration (slowly penetrate the skin), infiltration anaesthesia (a local injection of an aqueous solution of the salt of the base (e.g. hydrochloride), nerve trunk block (injected around a nerve trunk to produce anaesthesia distal to the site of injection), epidural (injection into spinal column but outside dura mata to produce anaesthesia above and below site of injection), spinal (injection into the lumbar subarachnoid space causes anaesthetic to flow in the direction of the posture of the patient ) Sympathetic fibres are particularly sensitive to local anaesthetics and this can result in cardiovascular complications particularly hypotension. From CALNet: Local anaesthetics produce a reversible blockade of action potential conduction in sensory and some other nerves when applied locally in effective concentration. The nervous system consists of a network of myelinated and unmyelinated nerves which collect sensory information from all parts of the body and relay it to the CNS where the information is processed for cognitive, mechanical and emotional responses. Sensory information travels along sensory nerves in the form of ACTION POTENTIALS (A.P.s) the cell membrane of each axon in the resting state is electrically polarised, being positively charged on the outside of the membrane and negatively charged on the inside. When a stimulus is applied the charges reverse which causes this reverse of charges to be conveyed along the neurone and to the CNS. Methods of achieving Local anaesthesia

Physical cooling when nerves are cooled sufficiently they fail to produce action potentials The maintenance of the nerve membrane is dependant on the Na+/K+/ATPase pump which slows down and stops as the temperature is reduced. This is why ice packs can give some pain relief in damaged extremities and why hands go numb in winter. When liquid ethyl chloride is sprayed on skin, the rapid evaporation of it removes heat from the skin, cooling the sensory nerves and producing a local anaesthetic effect. Physical pressure this reduces the ability of nerve fibres to conduct action potentials. However, there is risk of applying to much pressure and crushing which is why this is not used in medicine. Physical axonia the membrane potential is dependant on the Na+/K+/ATPase pump which is dependant on oxygen but this also has medical risks and so is not used medicinally. Irreversible chemical this is the method of permanently blocking sensory impulses using a chemical e.g. silver nitrate. Some toxins from animals and plants also have this affect by sodium blocking. Local anaesthetic drugs such as, cocaine, benzocaine, lignocaine, prilocaine, procaine. Local anaesthetics block voltage-gated sodium channels, thereby preventing the conduction of action potentials. Failure of action potential propagation in sensory nerves results in a local anaesthetic affect. Voltage gated sodium channels consist of a large protein with multiple membrane spanning domains which surround a central ion channel. The protein consist of four moieties each possessing six transmembrane domains which are linked by intracellular and extracellular amino acid chains. Sodium channels are found in the neurone membrane. In myelinated axons the channels only occur at the nodes of ranvier. In these axons the A.P jumps from node to node. This makes conduction in myelinated axons quicker. Unmyelinated axons have the channels in the membrane throughout the length of the axons, so the A.P. has to pass along the whole axon membrane. Sodium channels exist in about 3 different conformations 1. closed the membrane potential is about -70mV. Positively charged groups on some amino acids are positioned so they repel positively charged ions. 2. open the membrane is depolarised to about -50mV and this change in electrical field causes a change in the conformation in the membrane protein. The positively charged ions are no longer repelled and Na+ can pass through. However the channel will spontaneously inactivated after a few milliseconds. 3. inactivated the conformational change of depolarisation also results in a slower conformational change called the hinged lid mechanism. This will close preventing further access of Na+ ions.

Most clinically used local anaesthetic work by PHASIC BLOCK. The protonated anaesthetic binds to the channel. TONIC BLOCK is where the anaesthetic molecules increase surface pressureand distort the Na+ channel. Only benzocaine acts this way.

Local anaesthetics are weak bases mostly exist in a protonated (ionised) form. They are either esters or amides.

Practical aspects of local anaesthetics Local anaesthetics are administered either to the surface if the body (eye, skin, throat, suppositories) or by injection (I.V, Nerve block, spinal, epidural). All local anaesthetics will only produce local anaesthesia when applied locally to a nerve. All anaesthetics can produce effects on: the CNS (causing depression or convulsions), blood vessels (dilation), and the heart (decreased cardiac excitability). High concentrations of anaesthetic can cause restlessness, dizziness, acoustic/visual disturbances, tinnitus, tongue twitching, convulsions, and respiratory arrest. Many local anaesthetics are administered along with vasoconstrictors e.g. epinephrine or felypressin The reason for this is reduced bleeding from operative site prolongs action of local anaesthetic by reducing blood flow delaying absorption and so reducing unwanted affects enabling a smaller does of anaesthetic to be used and so reducing unwanted effects.

Lidocaine (lignocaine) This is a medicine that is used in neuropathic pain. It cannot be administered orally as it is potentially toxic when broken down. It is usually given as a loading dose by intravenous bolus injection followed by infusion. It is extensively metabolised in the liver into compounds to compounds with low anti-arrhythmic activity and one has convulsive properties. It has a short half life. Side effects: Nausea and vomiting, CNS toxicity (muscle twitching, convulsions, dizziness, drowsiness), negative inotropic (alters the force of muscle contractions) effect producing hypotension, bradycardia (slow heart beart). Analgesics Drug induced depression of consciousness.

Non-steroidal anti-inflammatory drugs (NSAIDs) and opioids are the major classes of pain-relieving (analgesic) drugs. They act at different levels in the pain relieving pathway to influence the production and recognition of pain. Neuropathic pain responds poorly to both classes of analgesic.

NSAIDs act mainly by blocking the generation of original nociceptive impulses and are most effective against peripheral pain of the musculoskeletal origins. They inhibit the production of prostaglandins thereby reducing the sensitivity of the nerve endings to agents released by damaged tissue which initiate pain, such as bradykinin. Opioids act in the spinal cord, especially the dorsal horn pathways associated with the paleospinothalamic pathway, and also have important supraspinal actions. The contribution of peripheral actions are smaller. They produce their effects via specific receptors which are closely associated with the neuronal pathways that transmit pain from the periphery to the CNS. 13. Pain Dictionary definition: An unpleasant sensation ranging from ranging from mild discomfort to agonized distress, associated with real or potential tissue damage. Pain is a response to impulses from the peripheral nerves in damaged tissue, which pass to nerves in the spinal cord, where they are subjected to gate control. This gate modifies the subsequent passage of the impulses in accordance with descending controls from the brain. Because attention is a crucial component of pain, distraction can act as a basis for pain therapy. Anxiety and depression focus the attention and exaggerate pain. If nerve pathways are damaged, the brain can increase the amplification in the pathway, maintaining the sensation as a protective mechanism.

Pain is a complex phenomenon that involves the generation of specific neuronal activity and the response of the patient to that activity. Stimuli that produce tissue damage initiate activity in the nervous system called nociception. Pain is a subjective sensation that results from the perception of these impulses. The response of an individual to the painful stimulus will be influence by psychological factors. This will determine whether or not pain produces or contributes to suffering or distress. Somatic pain is typically aching, stabbing, throbbing or pressure-like. Visceral pain is gnawing or cramp-like if it arises from a hollow viscus or similar to somatic pain when arising from other structures. Sharp pain stimuli are transmitted by fast fibres in the neospinothalamic pathway to the CNS, chronic visceral pain is transmitted by slow fibres in the paleospinothalamic pathway.

Pain management Appropriate management depends on its origin and severity. Acute pain usually has an obvious cause and is accompanied by anxiety. For rapid pain relief for a migraine for example a short acting drug can be used. For something more long term e.g. a sprain a long acting drug can be used. More severe acute pain can be treated with paracetamol or codeine or a combination of both, for very severe acute pain a strong opiod such as morphine can be used. Chronic pain (pain lasting more than 6 months) can be the result of chronic nocioceptive stimulation or can have a neuropathic origin. Other solutions than drug treatment are often more appropriate. The WHO use a concept called the analgesic ladder for choosing appropriate drug treatment for the level of chronic pain in patients. Insert box 19.2 14. PTSD There are a number of psychological disorders following trauma: Acute stress reaction, acute stress disorder, post-traumatic stress disorder, adjustment disorders, anxiety disorders and depressive disorders. Acute stress disorder increases risk of PTSD (70% ASD develop PTSD) PTSD has a number of catagories A exposure to an event involving actual or threatened death or serious injury or threat to physical integrity. A response of intense fear, helplessness or horror. B trauma persistently re-experienced Symptoms: recurrent and intrusive distressing recollections of trauma (thoughts, images, perceptions); recurrent distressing dreams; flashbacks; intense psychological distress at exposure to recollections, physiological reactivity to trauma stimuli C persistent avoidance of trauma stimuli or numbing of general responsiveness. Symptoms: Avoidance of thoughts, feelings or conversations associated with the trauma (include alcohol use); avoidance of activities, places or people associated with the trauma; marked diminished interest or activities; feelings of detachment or estrangement from others; restricted range of affect; foreshortened future. D persistent increased arousal Symptoms: Difficulty falling or staying asleep; irritability or outbursts of anger; difficulty concentrating; hypervigilance; exaggerated startle response. PTSD can be diagnosed if there is a duration of symptoms for one month or more, if it causes clinically significant distress or impairment in functioning (occupational, social or in other important area),

It is acute if the symptoms last for 1-3 months, it is chronic if the symptoms last for 3 months or more. It can also have delayed onset e.g. onset of symptoms 6 months after the stressor. Prevalence 1-2% of the general population 50% of sufferers recover within 3 months and 30% within 12 months. A distinct minority develop persistent disorder. The severity, duration and proximity of individuals exposure affect the likelihood of developing a disorder as do pre-existing mental disorders, social support, childhood experiences and personality variables. Treatments: Psychological treatments superior to drug treatments. In most cases but the most effective psychological treatments and drug treatments were equally effective. NICE guidelines: single session debriefing after trauma should not be routine practice. If symptoms are mild within 4 weeks, wait a further month before treatment, with severe PTSD within 4 weeks give trauma focused cognitive behavioural therapy. Cognitive behavioural therapy Exposure: habituation of anxiety through exposure to trauma related stimuli Anxiety management: learning how to cope Cognitive therapy: modification of thinking styles 75% of chronic PTSD will respond to CBT; supportive counselling has little effect; early intervention 1 month post trauma is effective; very early intervention (within 1 week) is ineffective Strongest support is found for the treatments that combine cognitive and behavioral techniques. Hypnosis, psychodynamic, anxiety management, and group therapies also may produce short-term symptom reduction. Imaginal exposure to trauma memories and hypnosis are techniques most likely to affect the intrusive symptoms of PTSD, while cognitive and psychodynamic approaches may address better the numbing and avoidance symptoms. Treatment should be tailored to the severity and type of presenting PTSD symptoms, to the type of trauma experience, and to the many likely comorbid diagnoses and adjustment problems. Although traumas such as rape, combat, assault, and tragic bereavement may appear quite different on the surface, victims of these events share what has been characterized as a violation of pre-existing schemata of the self and the world. Trauma has been described as shattering three basic assumptions: the belief in personal invulnerability, the perception of the world as meaningful, and the positive view of self. Regardless of the type of trauma experience, all victims must deal with the mental distress caused by the violation of these basic beliefs, and regardless of the type of treatment, a primary goal is to develop a realistic appraisal of both the danger and the choices for response that were available during the traumatic event. This typically involves the need to overcome avoidance of external and internal cues (e.g., conversations, places, thoughts, feelings) that trigger memories of the trauma by providing a safe environment in which the person can re-experience the event without becoming retraumatized. Some form of sustained emotional processing of the trauma memory appears to be essential to the effective treatment of PTSD, regardless of technique.

CognitiveBehavioral Treatments Although no therapy has been studied thoroughly as yet, the psychosocial treatments for PTSD that have received the most systematic research attention thus far are the cognitive behavioral interventions. These interventions include a variety of exposure techniques and anxiety-management procedures that have been studied alone and in combination with one another. Exposure Exposure-based approaches, all of which involve helping patients confront their fears, are based on a two-stage learning theory that suggests that fear and avoidance are acquired when neutral stimuli (words, thoughts, images) are paired with a traumatic event so that these neutral stimuli become aversive in themselves, and thus become capable of rendering many other associated stimuli also anxiety producing. In the second stage, avoidance responses develop as a means of decreasing the anxiety resulting from the presence of the conditioned stimuli. Clinical procedures based on learning theory emphasize direct therapeutic exposure for the reduction of PTSD symptoms. These interventions are designed to reduce anxiety by means of repeated or extended, real or imaginary, exposure to objectively harmless but feared stimuli. Available research suggests that direct therapeutic exposure is most effective in reducing the intrusive symptoms of PTSD, but appears to be less effective in reducing the symptoms of PTSD that relate to emotional numbing and avoidance. Both graded (e.g. systematic desensitization) and nongraded (e.g., prolonged exposure) forms of exposure have been used as treatments for PTSD. Systematic Desensitization This behavioral approach involves pairing graded imaginal exposure with relaxation. After patients learn relaxation techniques, they are confronted with the avoided stimuli (e.g., trauma memories and places) that have been categorized previously according to increasing levels of adversiveness. Although only two studies systematically have tested this therapy for PTSD, both found desensitization to be superior to no treatment, especially in terms of reducing the intrusive symptoms of PTSD. One of these studies found that reductions in nightmares, flashbacks, muscle tension, and hospital re-admissions persisted through the two-year follow up. Intensive Exposure Therapy Flooding and implosion both employ intensive exposure techniques involving prolonged or massed exposure to a safe but fear-related cue (e.g. situation, feeling, and person) until the anxiety and fear associated with that cue is reduced or extinguished. Both involve the continuous presentation of live or imagined trauma-related stimuli. They differ in that implosive therapy is supposed to add a component of exposure to psychodynamic cues, although most studies of implosive therapy do not describe having included this aspect. Available research suggests that intensive imagined exposure is an effective treatment for PTSD and can increase the effects of standard psychotherapy. Three controlled studies comparing these therapies to no treatment or standard care have reported limited improvement three to eight months following treatment in such varied outcomes as depression, fear, state anxiety, sleep disturbances, overall adjustment, and the intrusive symptoms of PTSD. It is possible that observed improvements might have been greater had these studies used optimal exposure conditions; the sessions in these studies were only 4550 minutes in duration, as opposed to the 90-

minute session length sometimes required to achieve a more complete reduction in anxiety. In addition, for clinical reasons, two of the three studies incorporated relaxation techniques, which also may have served to retard or negate the effectiveness of flooding. Despite the demonstrated effectiveness of flooding, it should be noted that cases of severe complications have been reported in the use of flooding for PTSD, including exacerbation of depression, relapse of alcoholism, and precipitation of panic disorder. Such complications were demonstrated most dramatically (though not exclusively) in two studies of live exposure. The more rigorous of these studies involved exposing combat veterans with chronic PTSD to a residential treatment program consisting of four weeks of exposure to military cues, including living in tents, wearing uniforms, weapons, artillery, and hand-to-hand combat training. Lebanon War veterans completing this program deteriorated considerably over the course of the next nine months, in contrast to an untreated control group who showed no such decline. While less-intensive real-life exposure (four 1-hour sessions) has been found to compare favorably with imagined flooding. In a civilian sample, the efficacy of both live and imagined exposure appears to depend on providing the patient with both control over the level of exposure and strong therapeutic support. Sertraline has been shown to reduce re-experiencing, avoidance/numbing, and arousal symptoms of PTSD, and it has recently been approved by the FDA as a treatment for PTSD. Additionally, Fluoxetine has been found to reduce acute symptoms of PTSD in victims of recent trauma. CBT is a short-term talking treatment that has a highly practical approach to problem-solving. It aims to change patterns of thinking or behaviour that are behind peoples difficulties, and so change the way they feel. This booklet is for anyone interested in knowing more about CBT. It explains who and what it's for, and how to find a therapist. What is cognitive behaviour therapy? Cognitive behaviour therapy (CBT) describes a number of therapies that all have a similar approach to solving problems, which can range from sleeping difficulties or relationship problems, to drug and alcohol abuse or anxiety and depression. CBT works by changing people's attitudes and their behaviour. The therapies focus on the thoughts, images, beliefs and attitudes that we hold (our cognitive processes) and how this relates to the way we behave, as a way of dealing with emotional problems. An important advantage of CBT is that it tends to be short, taking three to six months for most emotional problems. Clients attend a session a week, each session lasting either 50 minutes or an hour. During this time, the client and therapist are working together to understand what the problems are and to develop a new strategy for tackling them. CBT introduces them to a set of principles that they can apply whenever they need to, and which will stand them in good stead throughout their lives. CBT is a combination of psychotherapy and behavioural therapy. Psychotherapy emphasises the importance of the personal meaning we place on things and how thinking patterns begin in childhood. Behavioural therapy pays close attention to the relationship between our problems, our behaviour and our thoughts.

What's the history of CBT? In the 1960s, a US psychiatrist and psychotherapist called Aaron T. Beck observed that, during his analytical sessions, his patients tended to have an 'internal dialogue' going on in their minds, almost as if they were talking to themselves. was feeling. Beck realised that the link between thoughts and feelings was very important. He invented the term 'automatic thoughts' to describe emotion-filled or 'hot' thoughts that might pop up in the mind. Beck found that people weren't always fully aware of such thoughts, but could learn to identify and report them. If a person was feeling upset in some way, the thoughts were usually negative and neither realistic nor helpful. Beck found that identifying these thoughts was the key to the client understanding and overcoming his or her difficulties. Beck called it cognitive therapy because of the importance it places on thinking. It's now known as CBT because the therapy employs behavioural techniques as well. The balance between the cognitive and the behavioural elements varies among the different therapies of this type, but all come under the umbrella term cognitive behaviour therapy. CBT has since undergone scientific But they would only report a fraction of this kind of thinking to him. What's so important about negative thoughts? CBT is based on a 'model' or theory that it's not events themselves that upset us, but the meanings we give them. Our thoughts can block us seeing things that don't fit with what we believe is true. In other words, we continue to hold on to the same old thoughts and fail to learn anything new. What form does treatment take? CBT differs from other therapies because sessions have a structure, rather than the person talking freely about whatever comes to mind. At the beginning of the therapy, the client meets the therapist to describe specific problems and to set goals they want to work towards. discussing how to deal with them. Typically, at the beginning of a session, the client and therapist will jointly decide on the main topics they want to work on this week. They will also allow time for discussing the conclusions from the previous session. And they will look at the progress made with the 'homework' the client set for him- or herself last time. At the end of the session, they will plan another assignment to do outside the sessions. Doing homework Working on homework assignments between sessions, in this way, is a vital part of the process. What this may involve will vary. For example, at the start of the therapy, the therapist might ask the client to keep a diary of any incidents that provoke feelings of anxiety or depression, so that they can examine thoughts surrounding the incident. Later on in the therapy, another assignment might consist of exercises to cope with problem situations of a particular kind. The importance of structure The reason for having this structure is that it helps to use the therapeutic time most efficiently. It also makes sure that important information isn't missed out (the results of the homework, for instance) and that both

therapist and client think about new assignments that naturally follow on from the session. The therapist takes an active part in structuring the sessions to begin with. As progress is made, and clients grasp the principles they find helpful, they take more and more responsibility for the content of sessions. So by the end, the client feels empowered to continue working independently. Group sessions CBT is usually a one-to-one therapy. But it's also well suited to working in groups, or families, particularly at the beginning of therapy. Many people find great benefit from sharing their difficulties with others who may have similar problems, even though this may seem daunting at first. The group can also be a source of especially valuable support and advice, because it comes from people with personal experience of a problem. Also, by seeing several people at once, service-providers can offer help to more people at the same time, so people get help sooner. How else does it differ from other therapies? CBT also differs from other therapies in the nature of the relationship that the therapist will try to establish. Some therapies encourage the client to be dependent on the therapist, as part of the treatment process. The client can then easily come to see the therapist as all-knowing and all-powerful. The relationship is different with CBT. CBT favours a more equal relationship that is, perhaps, more business-like, being problem-focused and practical. The therapist will frequently ask the client for feedback and for their views about what is going on in therapy. Beck coined the term 'collaborative empiricism', which emphasises the importance of client and therapist working together to test out how the ideas behind CBT might apply to the client's individual situation and problems. How effective is it? CBT can substantially reduce the symptoms of many emotional disorders clinical trials have shown this. For some people it can work just as well as drug therapies at treating depression and anxiety disorders. And the benefits may last longer. All too often, when drug treatments finish, people relapse, and so practitioners may advise patients to continue using medication for longer. When patients are followed up for up to two years after therapy has ended, many studies have shown an advantage for CBT. This research suggests that CBT helps bring about a real change that goes beyond just feeling better while the patient stays in therapy. This has fuelled interest in CBT. The National Institute for Health and Clinical Excellence (NICE) recommends CBT via the NHS for common mental disorders, such as depression and anxiety. (NICE is an independent organisation responsible for providing national guidance on promoting good health and preventing and treating ill health.) Comparisons with other types of short-term psychological therapy aren't clear-cut. Therapies such as interpersonal therapy and social skills training are also effective. The drive is now to make all these interventions as effective as possible, and also, perhaps, to establish who responds best to which type of therapy. How does CBT work?

CBT is quite complex. There are several possible theories about how it works, and clients often have their own views. Perhaps there is no one explanation. But CBT probably works in a number of ways at the same time. Some it shares with other therapies, some are specific to CBT. The following illustrate the ways in which CBT can work. Learning coping skills CBT tries to teach people skills for dealing with their problems. Someone with anxiety may learn that avoiding situations helps to fan their fears. Confronting fears in a gradual and manageable way helps give the person faith in their own ability to cope. Someone who is depressed may learn to record their thoughts and look at them more realistically. This helps them to break the downward spiral of their mood. Someone with long-standing problems in relating to other people may learn to check out their assumptions about other people's motivation, rather than always assuming the worst. Changing behaviours and beliefs A new strategy for coping can lead to more lasting changes to basic attitudes and ways of behaving. The anxious client may learn to avoid avoiding things! He or she may also find that anxiety is not as dangerous as they assumed. Someone whos depressed may come to see themselves as an ordinary member of the human race, rather than inferior and fatally flawed. Even more basically, they may come to have a different attitude to their thoughts that thoughts are just thoughts, and nothing more. A new form of relationship One-to-one CBT can bring the client into a kind of relationship they may not have had before. The 'collaborative' style means that they are actively involved in changing. The therapist seeks their views and reactions, which then shape the way the therapy progresses. The person may be able to reveal very personal matters, and to feel relieved, because no-one judges them. He or she arrives at decisions in an adult way, as issues are opened up and explained. Each individual is free to make his or her own way, without being directed. Some people will value this experience as the most important aspect of therapy. Solving life problems The methods of CBT may be useful because the client solves problems that may have been long-standing and stuck. Someone anxious may have been in a repetitive and boring job, lacking the confidence to change. A depressed person may have felt too inadequate to meet new people and improve their social life. Someone stuck in an unsatisfactory relationship may find new ways of resolving disputes. CBT may teach someone a new approach to dealing with problems that have their basis in an emotional disturbance. 15. Progression from A +E to acute medical or surgical ALERT AND HANDOVER All time critical patients with chest injuries, or potentially serious chest injuries, should be pre-alerted to arrange appropriate trauma team standby at the receiving hospital. This should be done as soon as reasonably possible

as appropriate expertise for chest injuries may take longer to mobilise than other standby alerts. Consider selection of receiving hospital to allow for appropriate expertise (eg, on site cardiothoracic facilities). The information for the alert should include: - Mechanism of injury - Suspected injuries - Current observations including respiratory rate, pulse and blood pressure - Treatment given - Expected time of arrival. 16. Apathy of Bystanders The bystander effect (also known as bystander apathy, Genovese syndrome, diffused responsibility or bystander intervention) is a psychological phenomenon in which someone is less likely to intervene in an emergency situation when other people are present and able to help than when he or she is alone. Solitary individuals will typically intervene if another person is in need of help: this is known as bystander intervention. However, researchers were surprised to find that help is less likely to be given if more people are present. In some situations, a large group of bystanders may fail to help a person who obviously needs help. An example which shocked many people is the Kitty Genovese case. Kitty Genovese was stabbed to death in 1964 by a serial rapist and murderer. The murder took place over a period of about a half hour, after which it was reported that dozens of alleged "witnesses" failed to help the victim. For this reason, the name Genovese syndrome or Genovese effect was used to describe the phenomenon at the time. A 1968 study by John Darley and Bibb Latane first demonstrated the bystander effect in the laboratory. They ran some simple studies such as the following: A participant is placed alone in a room and is told he can communicate with other participants through an intercom. In reality, he is just listening to an audio recording and is told his microphone will be off until it is his turn to speak. During the recording, one participant suddenly pretends he is having a seizure. The study found that how long the participant waits before alerting the experimenter varies directly with the perceived number of other participants. In some cases, the participant never told the experimenter. A common explanation of this phenomenon is that, with others present, observers all assume that someone else is going to intervene and so they each individually refrain from doing so and feel less responsible. This is an example of how diffusion of responsibility leads to social loafing. People may also assume that other bystanders may be more qualified to help, such as being a doctor or police officer, and their intervention would thus be unneeded. People may also fear losing face in front of the other bystanders, being superseded by a superior helper, or offering unwanted assistance. Another explanation is that bystanders monitor the reactions of other people in an emergency situation to see if others think that it is necessary to intervene. Since others are doing exactly the same, everyone concludes from the inaction of others that other people do not think that help is

needed. This is an example of pluralistic ignorance and social proof. An alternative to explanations of rational motivation is that emotional cues to action can be as powerful as irrational ones, and the presence of a group of inactive others is a pre-rational emotional cue to inaction that must be overcome. To counter the bystander effect when you are the victim, a studied recommendation is to pick a specific person in the crowd to appeal to for help rather than appealing to the larger group generally. If you are the only person reacting to an emergency, point directly to a specific bystander and give them a specific task such as, "You. Call the police." These steps place all responsibility on a specific person instead of allowing it to diffuse. Furthermore, pluralistic ignorance is countered by the implication that all bystanders are indeed interested in helping, and social proof kicks in when one or more of the crowd steps in to assist. A Model of the Intervention Process An intervener must make a series of decisions. First, he must notice the event and then interpret it as an emergency. Then he must decide if he has responsibility to act, and if so what form of assistance he should use. Should he help directly or call the police? Then he must decide how to act and implement his choice. Of course, in a real emergency a person isn't so rational as this. Also, his decisions affect himself as much as the victim. The bystander can only gain with pride and a hero's status -- but he risks being a failure, getting sued, or even attacked or wounded himself.

Social Determinants to Bystander Intervention When a person happens upon an ambigious "situation", the person may look to other's behavior to see if they observe it as an emergency. An individual, seeing the inaction of others, will judge the situation as less serious that he would if alone". Males are expected to react to stress by being calm and collected. If they react to the emergency by intial calm inaction, this may be interpreted by others as an assessment of non-emergency. A 'pluralistic ignorance may develop. Thus, people may react less to an emergency if they are in a group situation than if they are alone. Experiment 1. Where There's Smoke, There's (Sometimes) Fire They had subjects began to fill out questionnaires in a room to which they began to add smoke. In one condition the subject was alone. In another three naive subjects were in the room. In the final condition one naive subject and two confederates who purposely noticed and then ignored the smoke (even when the room became hazy from all the smoke). 75% of alone subjects calmly noticed the smoke and left the room to report it. But only 10% of the subjects with confederates reported it. Surprisingly, in the three naive bystander condition only 38% reported the smoke. Most subjects had similar initial reactions. Those that didn't report it all concluded that the smoke wasn't

dangerous or was part of the experiment. No one attributed their inactivity to the presence of others in the room. Other studies have shown that togetherness reduces fear even when the danger isn't reduced. It may have been that people in groups were less afraid and thus less likely to act. Or people were inhibited to show fear in a group situation. However, from post-interviews it was clear that people didn't act because they concluded the situation wasn't a threatening situation. Experiment 2: Lady in Distress In this experiment subjects either waited alone, with a friend, with a passive confderate, or with a stranger in a room. The room was separated from another room by a curtain (which they passed on their way to their waiting room). The experimenter who led them there returned to other room and left, turning on a tape recorded that simulated a fall and subquent moaning about a hurt leg (total time 130 seconds). They measured the % who took action and how long it took them to act. Results Overall, 61% pulled back the curtain to check on the experimenter. 14% entered via another door, and 24% simply called out. Nobody went to report the accident. 70% of alone subjects reacted, but only 7% of those with passive confederates reacted. The subjects with confederates became confused and frequently looked over at the confederate. Only 40% of stranger pairs offered to help. 70% of friend pairs helped (same as alone group), which shows some inhibition because given the 70% alone rate we would expect a 91% rate with no inhibition. The interveners claimed they acted because the fall seemed serious and it was "the right thing to do". The noninterveners said they were unsure what happened but decided it wasn't serious, and some felt they didn't want to embarass the researcher. Again, people felt they weren't highly influence by others in the room. The results confirm results in the Smoke study. It seems that the risk of inappropriate behavior is less with friends, and friends are less likely to develop "pluralistic ignorance". All of the above experiments concerned whether a bystander noticed and concluded there was an emergency. He must also decide what responsibility he has and what form of assistance it would take. If there are multiple people at an emergency, the overall responsibility for one individual is reduced. Or they may assume that others have already responded to the emergency, so no one acts first.

17. Epidemiology of pneumothorax The incidence of TPT varies with the population studied and is not well establishedoften reflecting disease suspicion rather than true incidence. TPT was confirmed (hiss of air on decompression) in 5.4% of major trauma patients, (64% of whom were ventilated) treated by pre-hospital care doctors in London. Other studies have reported needle decompression rates (as a surrogate for potential TPT) in the pre-hospital environment varying from 0.7% to 30%. Earlier postmortem studies on patients dying in ICUs show rates of undiagnosed TPT ranging from 1.1% to 3.8%. Missed diagnosis was more probable if ventilation or cardiopulmonary resuscitation had occurred. In ventilated patients TPT is more likely if simple pneumothorax diagnosis is delayed. TPT would also seem to be more serious in ventilated patients reaching 91% mortality rates in one series. 18. Potential transmission of infection to healthcare workers See infection control document 19. WebCT

1. Parametric and nonparametric tests All statistical tests are either parametric (that is, they are based on the assumption that the data follows a distribution, usually a normal distribution) or nonparametric (the test doesn't rely on this assumption). In general, parametric tests are more powerful than non-parametric ones and so should be used if possible.

Non-parametric tests look at the rank order of the values (which one is the smallest, which one comes next, and so on) and ignore the absolute differences between them. For example, these could be derived variables (see the audio lecture MedStats 1 in Semester 1 Case 1) where the outcome variable is ranked. All commonly used non-parametric tests rank the outcome variable from low to high and then analyse the ranks.

Examples of parametric tests: Student's t-test Examples of non-parametric tests: Mann-Whitney U test Chi-squared (2) test

Wilcoxon matched pairs test 2. Paired and unpaired tests Students often find it difficult to decide whether to use a paired or unpaired statistical test to analyse their data. There is no great mystery about this. If you measure something twice on each subject - for example, blood pressure measured when the subject is lying and when standing - you will probably be interested not just in the average difference of lying versus standing blood pressure in the entire sample, but in how much each individual's blood pressure changes with position. In this situation, you have what is called 'paired' data, because each measurement beforehand is paired with a measurement afterwards.

In the example described above, it is using the same person on both occasions which makes the pairings, but there are other possibilities (for example, any two measurements of bed occupancy made of the same hospital ward). In these situations, it is likely that the two sets of values will be significantly correlated (for example, my blood pressure next week is likely to be closer to my own blood pressure last week than to the blood pressure of a randomly selected adult last week). In other words, we would expect two randomly selected paired values to be closer to each other than two randomly selected unpaired values. Unless we allow for this, by carrying out the appropriate paired sample tests, we can end up with a biased estimate of the significance of our results. 3. One- and two-tailed tests

The term "tail" refers to the extremes of the distribution - the areas at the outer edges of the bell in Fig 1. Case: dietary sodium and blood pressure Let's say that the graph in Fig 1. represents the diastolic blood pressures of a group of people of which a random sample are about to be put on a low sodium diet. If a low sodium diet has a significant lowering effect on blood pressure, subsequent blood pressure measurements on these subjects would be more likely to lie within the left tail of the graph. Hence we would analyse the data with statistical tests designed to show whether unusually low readings in this patient sample were likely to have arisen by chance. But on what grounds may we assume that a low sodium diet could only conceivably put blood pressure down, but could never do the reverse, put it up? Even if there are valid physiological reasons in this particular example, it is certainly not good science always to assume that you know the direction of the effect which your intervention will have. A new drug intended to relieve nausea might actually exacerbate it, or an educational leaflet intended to reduce anxiety might increase it. Hence, your statistical analysis should, in general, test the hypothesis that either high or low values in your dataset have arisen by chance. In the language of the statisticians, this means you need a two tailed test, unless you have very convincing evidence that the difference can only be in one direction. 4. Outliers Unexpected results may reflect: idiosyncrasies in the subject (for example unusual metabolism), errors in measurement (faulty equipment), errors in interpretation (misreading a meter reading), or errors in calculation (misplaced decimal points). Only the first of these is a "real" result which deserves to be included in the analysis.

Outliers can be shown in box-and-whisker plots (as dots above the whisker in Fig 2), but statistically correcting for outliers (for example, to modify their effect on the overall result) requires sophisticated analysis which would be done by a statistician. Box-and-whisker plots were described in the audio lecture MedStats 2, Displaying the Data, in semester 1.