IMMOBILIZATION Effects.pptx

Immobilized

1. Physiological responses to immobilization

2. Immobilization refers to reduction or elimination of motion of the body or a part by mechanical means or by strict bed rest. Deconditioning is a complex process of physiological change following a period of inactivity, bedrest or sedentary lifestyle. It results in functional losses in such areas as mental status, degree of continence and ability to accomplish activities of daily living. Introduction

3. Bed rest and immobilization is often used to treat a wide variety of medical conditions. Although it often benefit the affected part of the body, they sometimes harm the rest of the body. Many types of immobilizations can lead to complications: -enforced bed rest (illness or convalescence); paralysis; -immobilizations of body parts with braces, casts, or corsets; -joint stiffness and pain with protective limitations of motion; -mental disorders (catatonia, hysterical paralysis) -loss of sensation: discomfort does not dictate change of position.

4. Chronically ill, disabled, and geriatric people are particularly at risk. These people already have little or no reserve physiologic function, and any additional difficulties created by immobilization result in functional losses.

5. Effects of immobilization on different systems

6. FLUID When the body is upright, the fluids within it are continually exposed to the effects of gravity. This encourages lymph and, particularly, blood to move down into the lower limbs . When a person is confined to bed, there is a gradual shift of fluids away from the legs towards the abdomen, thorax and head. Cardiovascular system

7. Bedrest of longer than 24 hours results in a shift of around 1L of fluid from the legs to the chest. This temporarily increases venous return to the heart and elevates intracardial pressure.

8. STROKE VOLUME AND HEART RATE According to Starling’s law of the heart (the Frank-Starling principle), the greater the volume of blood entering the heart during diastole (when the ventricles are relaxed), the greater the volume of blood ejected during systolic contraction (stroke volume). Since prolonged bedrest leads to a reduction in blood volume and limits the effectiveness of venous return, there is a gradual decrease in the diastolic volume and so stroke volume falls . The body’s mechanism to counteract this decrease in stroke volume and keep sufficient cardiac output is to gradually increase the heart rate.

9. WATER BALANCE Increases in blood volume and venous return stretch the right atrium in the heart and stimulate the release of atrial natriuretic peptide (ANP). This is a powerful diuretic and increases urine output while decreasing blood volume. A drop in blood volume and pressure are detected as reduced stretch by the baroreceptors in the aortic arch and carotid sinus. This initiates the release of anti-diuretic hormone (ADH) from the posterior pituitary gland. ADH stimulates the kidney to reabsorb water , which reduces urine output and increases blood volume.

10. In long periods of bedrest , the delicate balance between these two hormones is disrupted . When a person is supine, the shift of blood from the legs into the thorax increases atrial stretch, stimulating the release of ANP. This initiates diuresis leading to significant water loss. This same shift of blood stretches the aortic arch and carotid sinus baroreceptors , which reduces ADH release from the posterior pituitary . As the levels of plasma ADH fall, less water is reabsorbed in the kidney, further increasing the diuretic effect of ANP.

11. The result is an increase in urine output and a progressive reduction in blood volume that can often lead to dehydration.

12. MUSCLE PUMP Prolonged bedrest rapidly leads to skeletal muscle atrophy throughout the body. Loss of muscle mass from the legs impairs the skeletal muscle pump, significantly reducing venous return. Insulin promotes the uptake of glucose by the muscles, providing energy for muscle contraction. With prolonged bedrest , muscle fibres become less sensitive to insulin and, as a result, there is less glucose to power muscular contraction. Loss of muscle tissue in the legs reduces the muscle mass available to squeeze the walls of the veins, thereby impairing the skeletal muscle pump function and significantly reducing venous return.

13. ORTHOSTATIC HYPOTENSION Orthostatic hypotension occurs when the cardiovascular system does not adapt normally to an upright posture. It occurs after 3 weeks of bed rest (earlier for the elderly) because of excessive pooling of blood in the lower extremities and a decrease in circulating blood volume . This, along with a rapid heart rate, results in diminished diastolic ventricular filling and a decline in cerebral perfusion. The circulatory system is unable to restore a stable pulse and blood pressure level.

14. CARDIAC DECONDITIONING Like skeletal muscle, the cardiac muscle fibres within the myocardium (muscular layer of the heart) need the stress of physical work to stay healthy. The principle of ‘use it or lose it’ is key . As stroke volume decreases, the myocardium is required to do less work and begins to atrophy. Myocardial thinning, particularly in the ventricular regions, is common.

15. CARDIOVASCULAR RISK C-reactive protein (CRP) and cystatin C are biomarkers associated with general inflammation in the body, including the inflammatory events involved in atherosclerotic occlusion (where fatty plaque is deposited on the arterial walls). Bedrest has been shown to increase the levels of both CRP and cystatin C, suggesting that longer periods of bedrest may augment the risk of atherosclerosis. Elevated cystatin C is also associated with major cardiovascular diseases such as coronary artery disease, myocardial infarction, hypertension and heart failure, as well as with non-cardiovascular conditions such as diabetes and chronic renal disease.

16. MUSCLES With only a few days of bed rest, skeletal muscle atrophies due to disuse and lead to weakness, discoordination and balance difficulty . The first muscles to become weak and atrophic are those in the lower limbs that normally resist gravitational forces in the upright position. Skeletal muscles lose tone when the feet no longer bear weight. Musculoskeletal system

17. The stiffening and shrivelling of muscles leads to a dramatic reduction in muscle mass, and a patient on prolonged bed rest exhibits a weight loss attributed both to this, and the loss of fat content . When muscles are immobilised , they shorten. The number of sarcomeres decreases with muscles kept in a shortened position. The extent of atrophy is significantly increased if the muscle is kept in the contracted position.

18. CONNECTIVE TISSUE Along with muscle, connective tissue undergoes changes when subject to immobility , since connective tissue such as tendons, ligaments and articular cartilage require motion to maintain health. Most of these changes are due to a change in the structure of collagen fibres . Tendons are stiff connecting fibres connecting muscle onto bone. Bed rest decreases the stiffness of tendons and increases their viscosity. This affects the transmission from muscle fibres to bone and reduces the ability to produce dynamic force – rendering a weaker and more exhausted patient.

19. CONTRACTURE Any decrease in normal range of motion is termed a ‘contracture ’. Muscle atrophy plays a role in the development of contractures, abnormally shortening and weakening the muscle. Contractures can develop over joints, often when there is an imbalance in the muscle strength of antagonistic muscle groups. If this is allowed to progress, the contracture may develop to involve the muscles, tendons, ligaments and joint capsule, rendering a stiff joint , limited in its full use and range of motion.

20. Collagen is arranged in fibres . In areas of frequent movement, the collagen fibres are arranged in a loosely coiled arrangement which permits normal stretching and activity. Immobilisation causes these loosely coiled fibres to change into a mass of shortened, straightened and more densely packed fibres . Immobilisation can cause a fibro-fatty infiltration of joints that can develop into strong adhesions and might destroy cartilage. In peri-articular connective tissue , increased cross-linking between existing collagen and new abnormal type 1 collagen deposited in the matrix, contributes to contracture formation.

21. BONE Bone is a dynamic tissue and in normal health and levels of activity, a constant equilibrium is maintained in bone formation and resabsorption . O steoblasts rely on the stress of mobility and weight bearing to perform their function. During immobility and bed rest, the process of building new bone therefore stops, but the osteoclasts still continue to perform their function and break down bone. This results in a loss of bone density and a deterioration in the make up of bone, leaving the bone structure soft and weak.

22. Alarmingly, during immobilisation the mineral content of bone tissue changes such that the rate of calcium loss from bone begins to exceed the rest of deposition. Because both the mineral content and matrix of the bone deteriorate following prolonged bed rest, people develop soft spongy bones which can easily compress, become deformed or fracture.

23. In just a few days, the plasma calcium levels rise and there are measureable increases in the urinary losses of calcium. If the period of immobility continues, this can lead to the formation of calcium containing kidney stones ( urolithiasis ). Despite the lack of calcium in the bone, a diet high in calcium will not enhance bone uptake of calcium, instead, it will add to the excess calcium already excreted in the urine and in certain circumstances calcium will be deposited in soft tissues which normally do not undergo calcification, a condition called heterotopic calcification or myositis ossificans . This may occur in muscles, vessel walls or cardicac valves, where it may interfere with joint or muscle function, or even impact on cardiovascular function.

24. LUNG VOLUME CHANGES Tidal volume: This is the volume of air exchanged during normal breathing and is typically around 500ml. In a supine person, the weight of the body restricts the free movement of the rib cage, reducing tidal volume . During prolonged bedrest , patients may develop fixed contractures of the costovertebral joints, further reducing tidal exchange and potentially leading to permanent restrictive pulmonary disease Respiratory system

25. Residual volume: This is the air remaining in the lungs after a full forced breath out and is typically around 1.5L. The residual volume of the lungs drops in bedridden patients, potentially increasing the risk of portions of the lung collapsing. This reduction in residual volume appears to be due to : Movement of blood away from the lower limbs into the abdomen and thorax, increasing pulmonary blood volume; A shifting of the internal abdominal organs towards the thorax , which press on the diaphragm and compress the lungs.

26. FVC and FEV1: Forced vital capacity (FVC) is the amount of air that can be forced out of the lungs after a maximum intake of breath, and is typically around 4.5L. The supine position reduces both FVC and another measure called forced expiratory volume in one second (FEV1). It is thought these effects are due to a combination of : Airway obstruction, potentially due to pooled mucus ; Increased resistance in the airways and a loss of elastic recoil as a result of structural changes within the lungs

27. STRUCTURAL CHANGES When a patient is confined to bed there is a tendency for mucus to pool , under the influence of gravity, in the lower part of the airway.These accumulated secretions can swamp the lower portion of the ciliary escalator, reducing its function . These effects are often compounded in bedridden patients by dehydration , leading to the pooled mucus becoming thick and difficult to expectorate .

28. The diameter of the airways, particularly the bronchioles, decreases after a period of immobility . This reduction in airway size, together with pooled mucus and the extra weight the recumbent body places on the rib cage, combine to make breathing more laboured , and patients tend to take fewer deep breaths . The results can include the collapse of airways and small areas of lung tissue ( atelectasis ), which reduces the area available for gaseous exchange.

29. Prolonged bedrest dramatically increases the risk of respiratory tract infections. People cannot cough as easily or as well, which allows pooled mucus to stagnate and reduces the clearance of potentially pathogenic material and irritants.

30. INCREASED CORTISOL SECRETION One of the major complications of prolonged bedrest is a progressive loss of muscle mass, known as sarcopenia.This is exacerbated by changes in the levels of adrenal glucocorticoid hormones . Physical injury or starvation prompts the release of the stress hormone cortisol , a natural anti-inflammatory that also promotes gluconeogenesis (generation of glucose derivatives from proteins and fat). In people confined to bed after an injury and/or surgery, cortisol secretion increases ( hypercortisolemia ). This leads to skeletal muscle breakdown and the release of amino acids into the blood. Prolonged bedrest also sensitises skeletal muscles to the catabolic effects of cortisol , thereby accelerating muscle atrophy. Endocrine system

31. METABOLIC CHANGES Inactivity and immobility lead to a progressive drop in the metabolic rate reflecting the decline in lean muscle mass as a result of disuse. RENIN ANGIOTENSIN CASCADE In people who are confined to bed, plasma volume falls significantly, largely as a result of increased urine output. This loss in blood volume, together with sodium loss during diuresis , initiates the renin-angiotensin-aldosterone cascade , which has the effect of increasing plasma renin activity and plasma aldosterone levels. This stimulates the kidneys to reabsorb more sodium, helping to maintain blood volume and arterial pressure .

32. BLOOD VISCOSITY The diuresis associated with bedrest causes a gradual reduction in plasma volume . In the early stages of bedrest , the total red cell mass remains relatively constant, but, as plasma volume is lost, there is an increase in the haematocrit (packed red cell volume), leading to a significant increase in blood viscosity. Haematological system

33. RBCs AND HAEMOGLOBIN Because of skeletal muscle atrophy associated with bedrest , there is a gradual reduction in oxygen demand. This can cause drop in erythropoiesis (generation of erythrocytes) in the bone marrow, resulting in a drop in erythrocyte numbers, total red cell mass and total haemoglobin level.

34. OXYGEN TRANSPORT In bedridden patients, reductions in lung function, plasma volume and erythrocyte number also lead to a drop in arterial oxygen saturation . At the same time, blood carbon dioxide concentrations increase .

35. VIRCHOW’S TRIAD Virchow’s triad refers to a combination of three factors – venous stasis , hypercoagulability and blood vessel damage – which, when present together, dramatically increase the chances of deep vein thrombosis developing . 1. Venous stasis: As the skeletal muscle pump becomes less efficient , blood flow within the veins of the lower limbs can become sluggish . In some veins, blood flow may cease completely, leading to the pooling of blood and venous stasis.

36. 2. Hypercoagulability: Because blood is pooling in the veins of the lower limbs, clotting factors are not cleared as quickly by the liver. This , together with reduced plasma volume and the increased haematocrit seen in bedridden patients, increases the viscosity of the blood and further increases the likelihood of clot formation (thrombosis). 3. Blood vessel damage: The continual weight of the supine body compresses blood vessels and can cause damage to the vulnerable endothelium. This mechanical damage, often made worse by the pooling of blood and venous stasis, leads to the death of endothelial cells, exposing the collagen-rich tissue beneath. Platelets rapidly stick to the exposed collagen fibres and become activated, prompting the formation of blood clots.

37. POTENTIAL FOR EMBOLI   After the development of DVT, there is a danger of a vessel becoming blocked by a clot, a process known as embolisation . Clots most commonly develop close to venous valves within the calf areas . When the patient moves, the contraction of muscles increases venous blood flow and clots may detach to form emboli . These can travel to distant areas where they become trapped in small vessels, cutting off blood flow.

38. BLUNTING OF BARORECEPTOR RESPONSE There is blunting of baroreceptor responses , which increases the risk of orthostatic hypotension. Prolonged bedrest is associated with sensorimotor dysfunction that commonly manifests as postural instability and a dysregulated sense of balance. This, together with reduced muscle mass and strength, increases the risk of falls. Nervous system

39. SENSORY DEPRIVATION AND LEARNT HELPLESSNESS Patients who are confined to bed in hospital often experience a reduction in environmental and psychosocial stimuli, because of limited opportunities for interactions outside of their immediate environment . This restriction, called sensory deprivation, can have a knock-on effect on behaviour . It is often associated with: Restlessness ; Increased aggression; Insomnia ; Reduced pain threshold

40. GASTRIC REFLUX Swallowing is more difficult in the recumbent position , and food takes longer to pass through the stomach . Gastric secretions may collect around, and press against, the lower oesophageal sphincter , causing irritation. Patients confined to bed may, therefore, experience symptoms of gastro- oesophageal reflux disease , such as regurgitation and heartburn ; they also appear to be at greater risk of gastric ulceration. Gastrointestinal system

41. CONSTIPATION In patients confined to bed, smaller food intake and slower peristaltic rate lead to reduced motility in the gut, which is associated with atrophy of the mucosal lining and shrinkage of glandular structures. Increased transit times slow down the movement of faeces through the colon and rectum , increasing water reabsorption , and stools progressively harden.

42. DECRERASED FOOD INTAKE Changes in the gut and the reduced appetite that is often reported in patients who are confined to bed can lead to decreased food intake, potentially causing: Reduced calorific intake; Vitamin and mineral deficiencies. As tissue healing and recovery from infection require an adequate intake of calories and macro- and micro-nutrients, the detrimental effects of bedrest on the gastrointestinal system can delay recovery.

43. I f a patient is enduring a period of confined immobility or has decreased sensation, altering their body weight may not be possible. This will result in prolonged pressure on skin capillaries, and ultimately the death of skin tissue ( ischaemia ). During bed rest, a large surface area of skin bears weight and is in constant contact with the bed surface. Areas where skin is stretched tautly over bony prominences are at highest risk for breakdown. Here the possibility of ischaemia is at its greatest, since skin capillaries are being compressed between a hard surface such as a bed or chair, and the bone . The impairment of lymph and blood flow results in an ischaemic lesion of the skin, commonly known as a decubitius ulcer or pressure sore. Skin

44. Fat and other subcutaneous tissues have a poorer blood supply than the skin and are affected first . Prolonged pressure (greater than capillary pressure of 32mm Hg) can result in ischaemia and necrosis of underlying tissues. The longer the duration and the greater the magnitude of pressure, the greater the chances of developing a pressure ulcer.

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