UNIT 2 PHYSIOLOGICAL REACTION TO INJURY

PRESENTER: CHAPIMA F. BSc N, DipRN, ROTN, Cert. OP, Adv.Cert PA (UNZA), Cert. ED (TVTC)

INFLAMMATION
Definition: Inflammation is the body's natural response that occur immediately following tissue damage. Its main functions are to defend the body against harmful substances, dispose of dead or dying tissue and to promote the renewal of normal tissue.

 Inflammation is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. In the absence of inflammation, wounds and infections would never heal and progressive destruction of the tissue would compromise the survival of the organism. However, chronic inflammation can also lead to a host of diseases, such as rheumatoid arthritis. It is for that reason that inflammation is normally closely regulated by the body.

Causes Burns Chemical irritants Frostbite Toxins Infection by pathogens Physical injury, blunt or penetrating Immune reactions due to hypersensitivity Ionizing radiation Foreign bodies, including splinters

Process of Acute Inflammation

1. Tissue Injury Tissue damage may occur from trauma such as a tackle in football, collision or from an awkward fall. 2. Release of Chemicals When tissue cells become injured they release a number of chemicals that initiate the inflammatory response. Examples of these are kinins, prostroglandins and histamine.

 These chemicals work collectively to cause increased vasodilatation (widening of blood capillaries) and permeability of the capillaries. This leads to increased blood flow to the injured site. These substances also act as chemical messengers that attract some of the body's natural defense cells- a mechanism known as chemotaxis. Although highly beneficial to the body's defense strategies some chemicals also increase the sensitivity of the pain fibers in the area and so the area becomes painful.

3. Leukocyte Migration Chemotaxis leads to the migration of certain white blood cells (leukocytes) to the damaged area. Two types of leukocyte are predominantly in the inflammatory response- macrophages and neutrophils. Neutrophils are first to reach the injured site and function by neutralizing harmful bacteria.

 Macrophages aid the healing process by engulfing bacteria and dead cells and ingesting them so that the area is clear for new cells to grow. They arrive at the injured site within 72 hours of the injury and may remain in the area for weeks after the injury.

Clinical Signs
Acute inflammation is a short-term process, usually appearing within a few minutes or hours and ceasing upon the removal of the injurious stimulus. It is characterized by five cardinal signs: Pain (Dolor) due to chemicals released by damaged cells. Swelling or Edema (Tumor) due to an influx of fluid into the damaged region.

 Redness (Rubor) due to vasodilatation- the widening of blood vessels.

Infected ingrown toenail showing the characteristic redness and swelling associated with acute inflammation

 Heat (Calor) due to an increase in blood flow to the area. Loss of function (Functio laesa) due to increased swelling and pain. These five signs appear when acute inflammation occurs on the body's surface, whereas acute inflammation of internal organs may not result in the full set.

 Pain only happens where the appropriate sensory nerve endings exist in the inflamed area e.g., acute inflammation of the lung (pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings.

Classification of Inflammation
Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes from the blood into the injured tissues.

 Prolonged inflammation, known as Chronic Inflammation, leads to a progressive shift in the type of cells which are present at the site of inflammation and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.

Outcomes of Inflammation
The outcome in a particular circumstance will be determined by the tissue in which the injury has occurred and the injurious agent that is causing it. Here are the possible outcomes to inflammation. Resolution The complete restoration of the inflamed tissue back to a normal status.

 Inflammatory measures such as vasodilatation, chemical production, and leukocyte infiltration cease, and damaged parenchymal cells regenerate. In situations where limited or short lived inflammation has occurred this is usually the outcome. Fibrosis Large amounts of tissue destruction, or damage in tissues unable to regenerate, can not be regenerated completely by the body.

 Fibrous scarring occurs in these areas of damage, forming a scar composed primarily of collagen. The scar will not contain any specialized structures, such as parenchymal cells, hence functional impairment may occur.

Scars present on the skin, evidence of fibrosis and healing of a wound

Abscess Formation A cavity is formed containing pus, an opaque liquid containing dead white blood cells and bacteria with general debris from destroyed cells. Chronic inflammation In acute inflammation, if the injurious agent persists then chronic inflammation will ensue. This process marked by inflammation lasting many days, months or even years, may lead to the formation of a chronic wound.

 Chronic inflammation is characterized by the dominating presence of macrophages in the injured tissue. These cells are powerful defensive agents of the body, but the toxins they release are injurious to the organism's own tissues as well as invading agents. Consequently, chronic inflammation is almost always accompanied by tissue destruction.

TRAUMA

Definition Trauma is defined as any body injury produced by sudden physical injury, as from accident, injury, or impact. Causes of Trauma Road Traffic Accidents Falls Firearms

Classifications of Trauma Blunt trauma, a type of physical trauma caused by impact or other force applied from or with a blunt object e.g. fist or ball. Penetrating trauma, a type of physical trauma in which the skin or tissues are pierced by an object. Crushing injuries, caused by a great or extreme amount of force applied over a long period of time.

Treatment Trauma patients may require specialized care, including surgery and blood transfusion, within the so-called golden hour of emergency medicine, the first sixty minutes after trauma occurs. This is not a strict deadline, but recognizes that many deaths which could have been prevented by appropriate care occur a relatively short time after injury.

 In many places organized trauma referral systems have been set up to provide rapid care for injured people. Research has shown that deaths from physical trauma decline where there are organized trauma systems.

SOFT-TISSUE INJURIES
Soft-tissue injuries include sprains, strains, dislocations and subluxation. These common injuries are usually caused by trauma. SPRAINS A sprain is an injury to ligamentous structures surrounding a joint, usually caused by a wrenching or twisting motion.

Classification of Sprains A sprain is classified according to the amount of ligament fibres torn. First degree involves tears of a few fibres resulting in mild tenderness and slight swelling. Second degree sprain is partial disruption of the involved tissue with more swelling and tenderness. Third degree sprain is a complex tearing of the ligaments a gap in the muscle may be apparent or felt through the skin of the muscle.

 Because these areas have nerve endings, the injury is extremely painful. The most common areas of sprain occur in the ankle and wrist.

STRAINS
A strain is stretching of muscles and its fascial sheath. Aetiology Acute soft tissue injuries are caused by falls, direct blows, crust injury, motor vehicle collisions and sport injuries.

Clinical Manifestation The clinical manifestation of sprains and strains are similar and include; History of traumatic injury of possibly of a twisting nature, or recent exercise activity. Pain, Oedema, Decrease in function of the affected limb. Bruising. Muscle spasms.

Management Investigations X-rays of the affected part are usually taken to rule out a fracture or widening of the joint structure. History from the patient. Treatment Apply crape bandage Analgesia is necessary to relieve pain (Mild analgesic, aspirin, ibuprofen.

 Administer tetanus prophylaxis if skin integrity is broken. Surgical repair may be necessary if the injury is significant enough to produce severe disruption of ligamentous or muscle structures, fracture or dislocation. Nursing Care Ensure airways, breathing and circulation. Assess neurovascular status of involved limb. Rest and limitation of movement.

 Application of ice to the injured area. Cold in several forms can be used to produce hypothermia to the involved part. Physiological changes that occur in soft tissue as a result of the use of cold include vasoconstriction, reduction in transmission of nerve impulses. These changes result in analgesia and anaesthesia, reduction of muscle spasm without changes in muscular strength or endurance, reduction of local oedema and inflammation and reduction of local metabolic requirements.

 Few unwanted side effects accompany the use of cold to treat a soft tissue injury. Cold is most useful when applied immediately after the injury had occurred. Ice application should not exceed 20 to 30 minutes per application, allowing a warm-down time for 10 to 15 minutes between applications. Compression of the involved extremity. Compression also helps in limiting swelling, which, if left uncontrolled could lengthen healing time.

 The elastic compression bandage can be wrapped around the injured part, but it should not be too tight or too loose. Elevation of the extremity and to prevent oedema. After the acute phase (usually lasting 24 to 48 hours), warm, moist heat can be applied to the affected part to reduce swelling and provide comfort. NSAIDS may be recommended to decrease oedema and pain.

 The patient is encouraged to use the limb provided that the joint is protected by means of casting, taping or splinting. Movement of the joints maintains nutrition to the cartilage, and muscle contraction speeds circulation and resolution of the haematoma.

Prevention To reduce sprains and strains, individuals are encouraged to stretching and warm-up exercises before vigorous activity. Pre-conditioning exercises protect an inherently weak joint, because slow stretching is tolerated better by biological tissues than quick stretching. The increased metabolism contributes to better oxygenation of muscle fibres during work. Put on low healed shoes.

TRAUMA TO INTERNAL INJURIES

Internal injuries, especially those involving the liver, spleen, stomach, colon, pancreas and blood vessels can be caused by motor vehicle accidents, blunt trauma or penetrating injuries. Further discussions will be done later.

HAEMORRHAGE

Definition
Hemorrhage is the loss of blood from a blood vessel. The blood lost is described as extravasated (outside the vessels). It may lie on the surface of the body, on the patient's clothing or on the floor.

Causes of Haemorrhage The blood loss may be large and sudden (acute), or small repeated bleeds may occur over a period of time (chronic). The various causes of haemorrhage are listed below: Trauma to the vessel wall e.g. penetrating wounds Spontaneous haemorrhage e.g. ruptures of an aneurysm, acute leukemia, scurvy.

 Inflammatory lesions of the vessel wall e.g. bleeding from chronic peptic ulcer, typhoid ulcers, blood vessels traversing a tuberculous cavity in the lung. Neoplastic invasion e.g. haemorrhage following vascular invasion in carcinoma of the cervix. Elevated pressure within the vessels e.g. cerebral and retinal haemorrhage in systemic hypertension, severe haemorrhage from varicose veins due to high pressure in the veins of legs or esophagus.

Effects of Haemorrhage The effects of blood loss depend upon 3 main factors: The amount of blood loss. The speed of blood loss. The site of haemorrhage. The loss up to 20% of blood volume suddenly or slowly generally has little clinical effects because of compensatory mechanisms.

 A sudden loss of 33% of blood volume may cause death, while loss of up to 50% of blood volume over a period of 24 hours may not be necessarily fatal. However, chronic blood loss generally produces iron deficiency anemia, whereas acute haemorrhage may lead to serious immediate consequences such as hypovolemic shock.

Classifications of Hemorrhages According to the source of haemorrhage Blood may be lost from all three types of vessel, the arteries, the veins or the capillaries. The type of haemorrhage is named accordingly. Arterial haemorrhage. The blood is bright red and spurts with the heart beat. The escape is from both ends of the vessel not only from that nearer to the heart. Blood loss is more rapid than from a vein of corresponding size.

Capillary haemorrhage. The blood oozes over the surface and is darkish red in colour. Oozing over several hours can result in considerable blood loss. Venous haemorrhage. The blood is dark in colour, there is no spurting and the rate of loss is much less severe than arterial haemorrhage. Since the large veins are big cave-like structures, injury to them is a serious matter. A further danger is that air may be sucked into the damaged veins, giving rise to fatal air embolism in which the blood and air may form 'foam'.

According to the Time It Occurs Bleeding which occurs as soon as the vessel is divided is known as primary haemorrhage. If the patient is collapsed the vessel may not bleed immediately, but as recovery takes place the blood pressure rises and bleeding occursthis is known as reactionary or intermediate haemorrhage. Primary haemorrhage is immediate, e.g. a cut finger or on an operative incision.

 Reactionary haemorrhage occurs in the first 24 hours after operation. The more severe the operation the more likely it is to occur, especially after the patient has recovered from circulatory collapse. Operation on the kidney, the thyroid and the breast as well as total hysterectomy are particularly liable to be followed by reactionary haemorrhage. Coughing or vomiting may increase the pressure in the veins and contribute to reactional hemorrhage.

 Secondary haemorrhage is due to sloughing of the wall of a blood vessel. The commonest cause is bacterial infection, but in the absence of infection it may be caused by the action of an enzyme, for example acid pepsin on a peptic ulcer. The pressure of a drainage tube, a bone fragment or the presence of carcinoma may also be factors. The vessel is eroded. The thinnest walled vessels, the capillaries, burst first and a few specks of blood are found on the dressing.

 This should be immediately reported. It is a warning that the larger vessels are also being eroded, and in another few days, commonly the 10th after operation, a main artery may burst, giving rise to a torrential, fatal haemorrhage. Most symptoms of blood loss complained of by patients in clinics are in fact small secondary hemorrhages.

Signs and Symptoms Restless and anxiety Cold and crummy skin Increased pulse rate Low blood pressure Pallor The patient is thirsty Air hunger Reduced urine out put Low CVP (central venous pressure) Reduce vision, tinnitus and coma in this order prior to death.

Treatment Treatment is covered under the following headings; Arrest of haemorrhage. Restoration of blood volume. Arrest of haemorrhage (external) Padding and bandaging at the bleeding site. Application of digital pressure. Elevation of the affected limb.

 Application of tourniquet (applies only to the limbs). Surgical ligation of the bleeding blood vessel. Coagulation with diathermy may be required. Styptics (drugs that causes contraction of body tissues and canals) such as snake venom or adrenaline may be used locally.

Arrest of Haemorrhage in Concealed Haemorrhage The organ is emptied of blood clot if possible. After evacuation of blood, the organ contracts as a result blood vessels also contract and haemorrhage is arrested. If it fails, the vessels are encouraged to contract by washing the organ with normal saline or sodium bicarbonate to which a few drops of adrenaline has been added (making adrenaline solution 1: 1000).

 Administration of vitamin K to the bleeding patient may increase coagulability of blood. Packing the organ with gauze soaked in adrenaline constricts the blood vessels hence arresting haemorrhage. Surgical ligature of the bleeding blood vessel. Antibiotics in secondary haemorrhage may be used. Blood transfusion: which will be discussed later.

Complications Shock Kidney failure Heart failure Blindness

BLOOD TRANSFUSION

Definition
Blood transfusion is the introduction of whole blood or components of the blood such as plasma, serum, erythrocytes, or platelets into the venous circulation.

The reasons for blood transfusions are as follows: To restore blood volume after severe hemorrhage. To restore the red blood cell level after severe and chronic anemia and to maintain blood hemoglobin levels. To provide plasma factors such as ant hemophilic factor (AHF) that are necessary to control bleeding.

Types of Blood Transfusion Direct transfusion Exchange transfusion Auto transfusion General Nursing Care of the Patient on Blood Transfusion Explain procedure to the client and the need for blood transfusion. The clients temperature, pulse rate, respirations and blood pressure are taken and recorded.

 If the temperature is raised, liaise with the doctor; these will be the baseline observations. Commence the transfusion if all these are in order. Check for signs of cloudiness, milkiness, clots etc in the blood. Instruct the client to report any abnormalities The observations while on BT are done and recorded every 5 minutes for the first 15 minutes, and then half hourly until the transfusion is completed.

 Also chart the time of commencement and completion. Continue vital signs half hourly for one hour after completion. Risks of Blood Transfusion Although technologic advances have made blood transfusions a relatively safe procedure, some risks are involved; therefore transfusions are given only when absolutely necessary. Mislabeling Errors: Faulty identification of containers can lead to a person receiving wrong type of blood.

 Fatal hemolytic reactions can occur if, for example, a patient with type A blood receives types B or AB blood. Transmission of Diseases. Syphilis, malaria, HIV and hepatitis can be transmitted by donors that are asymptomatic carriers. Although precautionary questions are asked when blood is donated, there is no proof method of detecting all carriers. The incidence of syphilis contracted through blood transfusions is rare now since the advent of serologic testing on all units of blood.

 Sensitivities. In most blood transfusions the donor's red cells have some antigenic factor that the recipient does not have. For the most part these factors are antigens, but occasionally some can evoke intense antibody formation. This creates a risk for the recipient when subsequent transfusions are given. Citrate Toxicity. Citrate toxicity can occur when massive transfusions are required such as six units of blood in less than 24 hours.

 Each unit of whole blood contains approximately 50 ml of acid-citrate dextrose (ACD) solution. Its purpose is to serve as an anticoagulant and to provide the red cells with sugar for metabolism. Iron Overload. Each unit (500 ml) of blood contains 250 mg of iron. For patients who have chronic anemia and who must have frequent transfusions, hemosiderosis develops.

 Hemosiderosis is the deposition of iron in the skin, liver, spleen, and other organs, and it can interfere with normal physiologic function.

SHOCK (CIRCULATORY SHOCK)

Definition
Shock also known as circulatory shock, is a serious, life-threatening medical condition characterized by a decrease in tissue perfusion to a point at which it is inadequate to meet cellular metabolic needs.

Pathophysiology of shock As the blood carries oxygen and nutrients around the body, reduced blood flow hinders the delivery of these components to the tissues, and can stop the tissues from functioning properly. The process of blood entering the tissues is called perfusion, so when perfusion is not occurring properly this is called a hypoperfusional (hypo = below) state.

 There are four stages of shock. As it is a complex and continuous condition there is no sudden transition from one stage to the next. Initial Stage: During this stage, the hypoperfusional state causes hypoxia, leading to the mitochondria being unable to produce adenosine triphosphate (ATP). Due to this lack of oxygen, the cell membranes become damaged, they become leaky to extracellular fluid, and the cells perform anaerobic respiration.

 This causes a build-up of lactic and pyruvic acid which results in systemic metabolic acidosis. The process of removing these compounds from the cells by the liver requires oxygen, which is absent. Compensatory (Compensating): This stage is characterized by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition.

 As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release of adrenaline and noradrenaline.

 Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate, whereas adrenaline predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. Renin-angiotensin axis is activated and arginine vasopressin (Anti-diuretic hormone; ADH) is released to conserve fluid via the kidneys. Also, these hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain.

 The lack of blood to the renal system causes the characteristic low urine production. Progressive (Decompensating): Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries.

 Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing slugging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.

 If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock. Refractory (Irreversible): At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death have occurred. Death will occur imminently.

Types of shock In 1972 Hinshaw and Cox suggested the following classification which is still used today. It uses four types of shock: hypovolemic, cardiogenic, distributive and obstructive shock. Hypovolemic shock This is the most common type of shock and is based on insufficient circulating volume. Its primary cause is loss of fluid from the circulation from either an internal or external source (most often haemorrhage).

 An internal source may be internal bleeding. External causes may include traumatic bleeding, or severe burns. Cardiogenic shock This type of shock is caused by the failure of the heart to pump effectively. This can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes of cardiogenic shock include cardiac arrhythmias, cardiomyopathy, congestive heart failure (CHF) or cardiac valve problems.

Distributive shock As in hypovolemic shock there is an insufficient intravascular volume of blood. This form of "relative" hypovolemia is the result of dilation of blood vessels which diminishes systemic vascular resistance. Examples of this form of shock are:
Septic shock Caused by an overwhelming systemic infection resulting in vasodilatation leading to hypotension.

 Septic shock can be caused by Gram negative bacteria such as (among others) Escherichia coli, Proteus species, Klebsiella pneumoniae which release an endotoxin which produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body, and other Gram-positive cocci, such as pneumococci and streptococci, and Gram-positive bacterial toxins. Anaphylactic shock Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes widespread vasodilatation, leading to hypotension and increased capillary permeability.

 Neurogenic shock Neurogenic shock is the rarest form of shock. It is caused by trauma to the spinal cord resulting in the sudden loss of autonomic and motor reflexes below the injury level. Without stimulation by sympathetic nervous system the vessel walls relax uncontrolled, resulting in a sudden decrease in peripheral vascular resistance, leading to vasodilatation and hypotension.

 Obstructive shock In this situation the flow of blood is obstructed which impedes circulation and can result in circulatory arrest. Several conditions result in this form of shock. These include;
Cardiac tamponate in which fluid in the pericardium prevents inflow of blood into the heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation with cardiac tamponate.

 Tension pneumothorax. Through increased intrathoracic pressure, blood flow to the heart is prevented (venous return). Aortic stenosis hinders circulation by obstructing the ventricular outflow tract.

Recently a fifth form of shock has been introduced. This is endocrine shock. Endocrine shock is based on endocrine disturbances. Causes are; Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.

 Thyrotoxicosis may induce a reversible cardiomyopathy as a result produces constrict pericarditis like effect on the heart.

Signs and Symptoms

Anxiety, restlessness, altered mental state due to decreased cerebral perfusion and subsequent hypoxia. Hypotension due to decrease in circulatory volume A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction

 Rapid and shallow respirations due to sympathetic nervous system stimulation and acidosis
Hypothermia due to decreased perfusion and evaporation of sweat Thirst and dry mouth, due to fluid depletion Fatigue due to inadequate oxygenation Distracted look in the eyes or staring into space, often with pupils dilated

Treatment of Shock It is difficult to know when shock actually exists and when therapy should begin. Treatment should generally be instituted for shock whenever at least two of the following three conditions occur.
Systolic BP 80 mm Hg or less. Pulse pressure of 20 mm Hg or less. Pulse rate of 120 or more.

Pulse pressure is calculated by subtracting diastolic BP from systolic BP. Normally pulse pressure is between 30 and 50 mm Hg.

Emergency Management Establish and maintain airway; anticipate need for intubation if respiratory distress is evident. Administer high flow humidified oxygen (100 per cent) by mask. Monitor vital signs, level of consciousness and cardiac rhythm every 30 minutes. Establish IV access with two large guage catheters and administer IV fluids (normal saline). Assess for external bleeding sites and apply pressure dressings.

 Assess for life-threatening injuries (haemothorax, cardiac tamponade, liver laceration and Pelvic fractures) and report to the doctor or clinician. Insert an indwelling catheter and nasogastric tube if indicated. Treat the cause. Position (after the chest-X-Ray have ruled and neck and spine injury) the patient in supine position with the legs elevated to an angle of 45 degrees to promote blood flow to the brain.

Prognosis The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock is readily treatable and respond well to medical therapy. Septic shock however, is a grave condition and with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse.

END OF LECTURE