Cellular death/hypoxic damage

When blood flow falls below a certain critical level that is required to maintain tissue viability swelling of the area affected will occur. When the occlusion becomes too great blood supply is cut off. Eventually the loss of blood flow reaches a level where tissue viability can no longer be maintained (Edwards 2002b). This damage can occur due to:

All of these and others can lead to hypoxic injury (Table 4.1), which can affect viability of tissue and its surrounding area. The hypoxic damage may either occur inside the body and is invisible to the naked eye or appear on the surface of skin and be visible. Those areas of hypoxic damage that are invisible are generally due to acute tubular necrosis. Hypoxic injury that is visible is due to occlusions of limbs or pressure ulcers, which may lead to the appearance of offensive unsightly necrotic wounds, which do not heal.

Table 4.1 The conditions that lead to cell death, injury and repair

The interrupted supply of oxygenated blood to cells can result in cellular changes, which in turn can stimulate the inflammatory response (IR) (see later). The interrupted supply of oxygenated blood to cells results in anaerobic metabolism and cellular membrane disruption (Fig. 4.1).

Fig. 4.1 The processes of cellular hypoxia and cell death. Intracellular oedema occurs due to a reduction in ATP, the cell membrane can no longer maintain ionic gradients and sodium and water moves into the cell.

Tissue injury: the formation of oedema

Oedema is an abnormal collection of fluid in tissues, which can either collect in interstitial or intracellular spaces (Edwards 2003c). Oedema is a problem of fluid distribution and does not necessarily indicate fluid excess. The causes of oedema are varied (Table 4.1) and include hypoxia (leads to intracellular oedema) (see previous) and the inflammatory response (leads to interstitial oedema) (see later).

Interstitial oedema is usually associated with weight gain, swelling and puffiness, tight-fitting clothes and shoes, limited movement of an effected area, and symptoms associated with an underlying pathological condition. There are generally many different types of interstitial oedema, named due to the mechanisms that cause it and may be localized or generalized. Interstitial oedema is formed in three different ways:

Fig. 4.2 Normal capillary dynamics and pressures allow the normal movement of fluid across a semi-permeable membrane (filtration) to nourish the cell. The majority of the fluid is absorbed (absorption) back into the circulation. The remaining excess is drained by the lymphatic system.

Table 4.2 The conditions that lead to changes in hydrostatic pressure and oedema formation

Table 4.3 The conditions that lead to changes in colloid osmotic pressure and oedema formation

Tissue repair: activation of the inflammatory response

Cellular damage e.g. leg ulcers, surgical procedures, and trauma (Table 4.1) causes stimulation of the IR that ends with repair to damaged cells and tissues (Edwards 2006). Activation of the IR is part of the innate immune system, and represents a major physiological event in the body (Fig. 4.3). Following the damage tissues release mediators, the most important are:

Fig. 4.3 The Inflammatory immune response. An increase in permeability allows protein rich fluid to move out of the extracellular fluid compartment reducing colloidal osmotic pressure, this increases interstitial fluid colloidal osmotic pressure and oedema formation.

(Modified from Marieb 2010)

The list of these chemical mediators is immense and rapidly growing. The mediators are released at the site of injury and will enhance the activity of the body’s own immune and non-specific responses. Release of these mediators is to:

The mediators act as a signalling system (chemotaxis) to attract nutrients, fluids, clotting factors, neutrophils and macrophages to damaged sites. The arrival of macrophages to an area of damaged tissue is central to acute inflammation control, but macrophages can remain at sites of prolonged or chronic inflammation. The mediators cause a localized increase in:

The endothelium is a major contributor to activation of the IR. It is not just an inert barrier between flowing blood and the substructure of blood vessels and tissue, but an active metabolic organ responsible for anticoagulation. Coagulation always accompanies injury, to prevent excessive blood loss and to isolate the injured site. A victim of an acute tissue injury or a patient with a wound that will not heal or is infected, varicose or pressure ulcers could potentially release inflammatory mediators that circulate in the blood stream and could alter endothelial integrity elsewhere. This may incite coagulation abnormalities whereby there is a concomitant activation of coagulation or alterations in the haemostatic balance causing systemic thrombosis or gross haemorrhage known as DIC.

A lack of regulation of the IR can lead to an uncontrolled intravascular inflammation that ultimately harms the body. The mediators become toxic to other cells, damaging tissues, vessels, and organs far away from the initial injury. There are currently no conclusive indicators why some inflammatory processes proceed smoothly to healing while others lead to increase tissue damage. If there were such signs then the serious systemic conditions such as multi-system organ failure (MSOF) and systemic inflammatory response syndrome (SIRS) thought to be caused by over stimulation of the IR could be prevented.

The effect of treatments on the physiological processes

The interventions used to treat the insult/injury can lead to further stimulation of the physiological processes identified above. Some of the interventions used may prevent the physiological processes identified above from causing serious damage and/or complications, treatments such as:

Instigation of these treatments early may stem the IR and neuroendocrine activation and prevent further endothelial damage.

Epilepsy

Epilepsy is a neurological condition when the child has recurrent or unprovoked seizures. A child is usually diagnosed as having epilepsy if they have had two or more seizures that started in the brain. Seizures are caused by abnormal electrical discharges in the brain. In the UK, there are an estimated 58 000 children under 18 with epilepsy. Epilepsy usually begins in childhood and affects 1 out of every 100 children. If seizures are ‘mini’ (petit mal) instead of ‘grand mal’, it may not be obvious that the child is having a seizure.

High temperatures

For in an emergency see Section 1. There are four general states of increased body temperature (Edwards 1998b, 2003b):

Heat cramps, heat exhaustion are generally not life threatening. However, heat stroke, malignant hyperthermia and NMS must be recognized quickly, as, untreated, they may be fatal.

During a high temperature due to an infection the treatment by cooling methods such as tepid sponging or fanning has been criticized. Cooling methods are of no use, as they result in:

The best way to treat a high temperature is by the use of antipyrexial drug therapy, in preference to cooling methods.

Hyperpyrexia due to damage of the hypothalamus results in the body failing to activate compensatory cooling mechanisms. This tends to increase cellular metabolism, oxygen consumption and carbon dioxide production.

Unless the temperature is monitored carefully and cooling methods such as fanning and tepid sponging are instituted, irreversible brain damage and death occur.

Hypothermia

A drastic decrease in body temperature is known as hypothermia, and is characterized by a marked cooling of core temperature, and is defined as a core temperature below 35°C (Edwards 1999). Progressive temperature reduction below this level will result in reduced metabolism and risk of cardiac arrest. At 28–30°C, loss of consciousness will ensue. Low temperatures cause compensatory shivering and vasoconstriction, to shunt the blood to vital organs, and prevent excess heat loss from skin surfaces, causing metabolic and cardio-respiratory stress to ill patients. Hypothermia can be accidental of therapeutic:

The nurse needs to be aware of any patients at risk of hypothermia and take notice of how long the patient has been exposed for in theatre. Rewarming methods are divided into three groups:

The process of re-warming should proceed at no faster than a few degrees per hour. If a patient is rapidly re-warmed oxygen consumption, myocardial demand and vasodilatation increase faster than the heart’s ability to compensate and death can occur.

Diabetes insipidus

This is a disease of the posterior pituitary gland, which is the size of a pea and secretes many vital hormones, important in the control of other endocrine glands, known at the ‘leader’ or ‘master’ endocrine gland.

Diabetes mellitus

This is a common condition characterized by a persistently raised blood glucose level due to a deficiency or lack of insulin. An estimated 1.4 million people in the UK have diabetes (Richards and Edwards 2003).

Asthma

The most common diagnosis for children admitted to hospital is asthma and its related disorders. In the last 20 years, hospitals have dealt with a dramatic increase in both asthma-related admissions and readmissions in the paediatric population. Asthma admission rates are more frequent amongst girls, and the likelihood of readmission is higher amongst children under five years of age. Asthma is an inflammatory condition of the airways mediated by a wide range of stimuli usually the immunoglobulin IgE, the release of chemical mediators, leading to bronchospasm (Fig. 4.4), which is due to an imbalance between:

Fig. 4.4 Sequence of events that lead to asthma.

These actions contributes to plugging mucus and oedema (Fig. 4.5).

Fig. 4.5 Sequence of events leading from asthma to hypoxaemia.

Pneumonia

Pneumonia is an acute inflammation of the substance of the lungs due to:

Aspiration pneumonia

Aspiration of gastric contents, either solids or liquids, can lead to severe illness; this can be fatal as gastric acid contents in the lungs is very destructive. Material enters the right lung more readily because of the wider right bronchus. Infection usually caused by an anaerobic organism.

Pulmonary oedema

Fluid in the interstitial and alveolar spaces of the lungs. The general cause is by an increase in hydrostatic pressure within the pulmonary circulation due to:

Pulmonary embolism (PE)

A PE is an occlusion of pulmonary vascular bed by an embolus or a thrombus, tissue fragments, lipids, fats or an air bubble:

The effect of the embolism depends on the extent of the pulmonary blood flow obstructed, the size of the affected vessels, nature of the embolism and the secondary effect. The size of the pulmonary artery in which the blood clot is logged determines the severity of symptoms and prognosis. If the embolus blocks the pulmonary artery and one of its main branches, immediate death may occur. Patient may complain of:

Pneumothorax

An accumulation of air in the pleural space due to:

Clinical features

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