Burn 3rd Lecture Pathophysiological changes of burns: 3rd Lecture Pathophysiological changes of burns:

BurnBurn

3rd LecturePathophysiological changes of burns:

3rd LecturePathophysiological changes of burns:

Pathophysiological changes of burnsThe basic pathophysiological consequence of the burn

injury is the loss of the capillary integrity, localized increase in the micro vascular permeability, generalized impairment in the cell membrane resulting in cell swelling and increase osmotic pressure of the burned tissues leading to further fluid accumulation and oedema formation, which is a result of the outpouring of the intravascular fluid into the interstitial spaces.

This process occurs at all areas of partial skin thickness burns and at the areas which are adjacent to and subjacent to the full skin thickness burns.

As the patient frequently splints the injured part because of pain and as a result of the direct damage to the lymphatic system, fluids of oedema accumulates and persists in tissue spaces around tendons, ligaments and joints, leading to the formation of new collagen fibres in this protein - rich oedema fluids and eventually leading to adhesions and loss of the normal elasticity of the supporting structures. In addition the prolonged immobilization fix the structures and produce joints morbidity.

Metabolic changes of burns: The ebb and flow phases:The immediate post-burn period is known as the

ebb phase, as nutrient flow and oxygen delivery to cells is decreased, leading to a decrease in the basal metabolic rate (B.M.R.), then there is a gradual increase in the metabolic rate reaching the normal B.M.R. (40±10% C/m2/hr) and exceeding this normal level up to twice or twice and half the normal value and this is the flow phase. This flow phase is due to the massive catecholamine release from the adrenal medulla and from the nerve endings of the sympathetic division of the autonomic nervous system, leading to systematic vasoconstriction, increased vascular resistance and poor peripheral circulation affecting skin, muscle and nerve, resulting in nerve function alterations.

Vascular complications:Vascular complications of hand and foot

occur from the predominating sympathetic tone and from the circumferential third degree burn, with a decreased arterial flow due to arterial compression, the compound effects of the predominating sympathetic tone and the circumferential third degree burn can lead to ischaemia namely pain, pallor, pulselessness and paralysis. So in this case Escharotomy is indicated to relieve compression.

Musculoskeletal complications:The frequency of musculoskeletal

complications is lower than those involving the neuromuscular system, but the effects can be equally devastating. Musculoskeletal complications include the direct and indirect effects of burns to bone, joint, and tendon as the Heterotopic ossification (HO), which can be defined as "the formation of new bone in tissues that normally do not ossify".

Heterotopic ossification may occur in soft tissue surrounding a joint, within a joint capsule and ligaments, or may form a bony bridge across a joint.

Heterotopic ossification formation is attributed to a disturbance in calcium metabolism as the prolonged immobility and trauma have been shown to increase calcium mobilization from bone and increase caluresis, leading to focal ectopic calcium deposits.

Asymptomatic effusion into a joint underlying a major burn is quite common skeletal complication leading to swelling and limitation of motion, also the common sites of bone involvement is the subcutaneous surface of the tibia and the extensor surface of the phalanges. Also osteoporosis, bone spurs, septic arthritis and tendonitis are another skeletal complications to burns.

Mechanisms of pain in burned patients:Pain in victims of burn has frequent and wide

fluctuations in intensity, and its control presents a formidable challenge to those responsible for patient care.

It has been postulated that, the pain mechanisms in the burned patients are the result of stimulation of the three pain receptors, thermosensitive, chemosensitive and the mechanosensitive pain receptors. The direct effect of the thermal injury on the thermosensitive pain receptors will lead to pain, then the chemical mediators (Prostaglandins histamine and bradykinin) via inflammation will stimulate the chemosensitive pain receptors and produce pain, and finally with the metabolic stress and the predominant sympathetic tone plus oedema and swelling will lead to compression and ischaemic pain, exaggerated by muscle spasm via stimulation of the chemosensitive pain receptors.

Mechanisms of pain in burned patients

Neuromuscular complications:A burn injury can have devastating effects on

the neuromuscular system as the patient complaints regarding weakness of lack of sensation often are rationalized as generalized sequelae of the injury and healing process. However, these symptoms may be due to peripheral neuropathies resulting from either impaired peripheral nerve axons, or myelin sheath, or both.

Neuropathies from burn injury:Nerves that are superficial and at significant risk

for damage are the ulnar nerve at the elbow and the superficial branch of the radial nerve on the dorsum of the hand in the upper limb. As well as the common personal nerve at the fibular head in the lower limb.

Neural tissue has a very low resistance to electric current and is particularly susceptible to injury in electrical burns as the peripheral nerve damage is caused by the direct influence of the current on the nerve and surrounding tissues and by swelling of the involved muscle compartment.

If chemical burns lead to full-thickness wounds, underlying nerves could be involved. Damage to a nerve would then be due to direct local action of the individual chemical.

Neuropathies from burn management:Positioning and splinting of patient's limbs must

be done properly to prevent deformities, but the improper positioning and splinting can lead to nerve injury. So three particular areas must be managed carefully to prevent nerve injury. The shoulder for the brachial plexus injuries, the elbow for the ulnar nerve lesions, and the knee for the peroneal nerve lesions. The peroneal nerve & its branches supply the dorsifiexors of the foot and toes and carry sensory fibres from the dorsum of the foot and lateral aspect of the lower half of the leg. Clinically, compression of this nerve is characterized by an acute onset of foot drop and occasionally is associated with sensory impairment in the region of the superficial or deep peroneal nerve.

The peroneal nerve is frequently injured as the nerve is vulnerable to compression by being exposed over the fibular head for about 4 to 5 cm, covered only by skin, fat, and superficial fascia. Compression of the nerve can occur during prolonged side-lying, from side rails on the bed, and from poorly fitting splints. The peroneal nerve also is susceptible to stretch injury because of limited longitudinal mobility. Prolonged "Frog leg" position due to medial thigh burns or oedema of the perineum can increase the stretch of the nerve. Preventive measures include altering side-lying positions constant vigilance to avoid the frog leg position and positioning the knees in extension and the ankles in dorsiflexion.

Operating room procedures:The operating room is a particularly

dangerous environment for causing iatrogenic injury debridement of devitalized soft tissue can injure nerves with the advent of early excision and skin grafting, neurological deficits may become more prevalent. Compression neuropathies can occur during surgery from prolonged application of an elastic tourniquet to create a bloodless field. Direct compression of underlying nerves and ischaemic injury to tissue distal to tourniquet are two possible mechanisms of injury.

Dressings:Tight, bulky dressings may cause direct pressure to

various nerves, although the peroneal is affected most frequently measures for prevention include: applying dressings with less compression; providing a window for the area and educating personnel performing dressing changes.

Injections:Injury to muscle and small nerve fibers may occur as a

result of failing to alternate sites for intramuscular injections. Damage caused by an inflammatory reaction due to the physical trauma from the needle, pressure from the volume injected, and toxicity of the drug.

Skeletal traction:Skeletal pins occasionally are used to achieve

elevation and immobilization of an extremity after skin grafting. Improperly applied traction may create undue stress on peripheral nerves. Also changes in position may alter the traction forces leading to excessive stretch on peripheral nerves.

Neuropathies from burn complication: Oedema:In burns grater than 25 percent of the body,

capillaries of both unburned and injected tissue become abnormally permeable. Plasma escapes into the interstitial space with subsequent oedema formation. Fluid resuscitation required to combat initial burn shock increases oedema. Normal skin expands to accommodate swelling, but skin with denatured collagen and destroyed elastic fibres is inelastic and lack this ability and if the burn is circumferential on the extremity, a tourniquet effect is exerted and progressive ischaemia may develop, involving peripheral nerves and soft tissue underlying and distal to the burn, after compressing the neurovascular bundles.

The cardiogenic shockIs caused by pump failure due to disease of the heart

muscle as in cases of myocardial infarction (heart attack) or due to an infection of the heart muscle leading to myocarditis. The injured or the diseased heart muscle is incapable of a forceful contraction and there is diminished output with each ejection. The cardiogenic shock is the inability of the heart to destined and fill before ejection. The heart is enclosed within a tissue sac known as the pericardium. In the normal states this sac is empty and allows the heart to distend and contract. In some disease states the sac may be filled with fluid or blood and constrict the heart, preventing its normal filling, this is known as temponade and us encountered most frequently when there has been direct penetrating trauma such as a gunshot or stab wound of the heart with filling of the pericardium with blood.

Neurogenic shockA primary shock caused by loss or

decrease of the vascular tone = or due to decrease of the blood pressure via the increase of the vagal tone. Increase vagal tone means increase the parasympathetic action of the cardio-pneumo gastric nerve which is called the verges nerve (verges means wandering). It is the 10th cranial nerve which send an important branches to the heart, lung and stomach. It also has a great distribution in the neck, thorax and abdomen, also it has a palate, pharynx and larynx. In abdomen it gives branches to stomach, gall bladder, large and small intestine.

The neurogenic shock: is due to sudden increase in vagal tone which inhibits the heart and decreases the vascular tone (peripheral vasodilatation) leading to a sudden drop in the blood pressure occurs independent of hypovolemia [means decrease B.P with normal blood volume]. decrease B.P leading to diminished venous return to the heart leading to decrease the cardiac output. Both the peripheral vasodilatation (decrease vascular tone) and the diminished output results in shock.

The increase in the vagal tone results from the action of psychogenic impulses or the sensory stimulation of somatic and autonomic origin upon the medullary centers.

The secondary shock or the hypovolemic shock

It is the shock which is caused by the loss of the circulating blood volume, may occur with the loss of the whole blood or the loss of plasma as in cases of serious burn injuries, Hemorrhage may be the result of trauma with laceration of a blood vessel or injury to an organ. If the injured vessel is in an extremity, the However, if the injures organ is in the abdomen or chest, the source of bleeding is hidden (not obvious) and the severity of the injured may be unrecognized till the victim develops shock

Fractures result in hemorrhage of the vessels in adjacent muscles that are torn coincident with the fracture. Careless moving of the fractured extremity may lead to the injured of other vessels or dislodge clots, causing further hemorrhage. Hemorrhage may result from disease rather than trauma. Ulcer of the stomach and duodenum may be complicated by rapid and massive hemorrhage with the patent appearing in shock. Loss of fluids and electrolytes with resultant decrease in circulating volume may be occur as a result of vomiting or diarrhea. The absorption of fluids and electrolytes by the mucosal lining of the gastrointestinal tract is diseased, this source of fluids is lost.

If vomiting and diarrhea occur, there is a loss of the gastrointestinal tract as the source of fluids, as well as the abnormal loss of fluids, results in a diminished circulating as well as crush injuries. Both of burns and crush injuries are characterized by cellular injury and release of the cellular metabolic products into the tissues. These products cause changes within the capillaries resulting in a loss of plasma from the capillaries into the surrounding tissue. The total circulating volume decreases, and there is an increase in the percentage of red cell mass. The quantity of blood or plasma loss necessary o cause hypovolemic shock varies between 10% and 20% of the normal circulating volume. The normal physiological response to hypovolemic is increase H.R and arteriolar constriction in an attempt to maintain B.P.

Clinical features of hypovolemic shock: are Apathy, Pallor, cyanosis, Sweating, tachycardia, hypertension, Shallow respiration, Thirst, vomiting, subnormal temperature.

Septic shockAcute or chronic bacterial inflammation as

acute pyenephritis or pancreatitis lead to massive inflammation —> toxemia —> fever and fall in the vascular tone (peripheral resistance) via peripheral vasodilatation -> pooling of the blood —> decrease venous return —> decrease cardiac output -> fall of B.P -> syncope.