nursing acutely ill adults, high dependency

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NJ249 NURSING CRITICALLY ILL ADULTS:
HIGH DEPENDANCY

All nurses should possess critical care skills to enable them to impact positively on their patients care (DH 2000). The Higginson and Jones (2009) state, in BJN, that the initial assessment of the critically ill patient vary but should follow a pattern based on assessing A, B, C, D and E, in other words airway, breathing, circulation, disability and environment. This essay is concerned with the altered physiology of Jim’s (for confidentiality a pseudonym has be used, NMC 2008) respiration, due to a spontaneous, non-traumatic subarachnoid hemorrhage and the nursing care he received while in the Intensive Therapy Unit (ITU) will be discussed. The pathophysiology of the haemorrhage Jim suffered will be explored and why it caused Jim’s airway to be altered. His airway and its management will be the priority for nursing staff. In order to maintain a patent airway, suctioning of the airway will be the priority followed by oral care to prevent infection, although other nursing needs such as nutrition and pressure areas will be discussed briefly. Jim was admitted to ITU with an endotrachael tube (ETT) which had been placed in A&E after his consciousness dropped due a subarachnoid haemorrhage, see appendix one. According to Kumar et al (2005) a subarachnoid haemorrhage, which occurs in the subarachnoid space, can usually be attributed to a rupture of a saccular aneurysm, also known as a ‘berry’ aneurysm. Kumar et al (2005) continues to explain that two of the possible predisposing factors contributing to the formation of a saccular aneurysm growth are smoking and hypertension. Although Jim had no past medical history, according to the Stroke Association ‘almost a quarter of people in the UK are unknowingly suffering from undiagnosed high blood pressure.’ Hypertension is one of the single biggest risk factor for causing a stroke and therefore could have, at least contributed to the haemorrhage. Jim’s conscious level was 14 on admission and within three hours had dropped to 8. His conscious was measured by the Glasgow Coma Scale (GCS). GCS is a neurological tool that measures eye, verbal and motor responses. In general, a GCS of 8 or less, as with Jim, is classified as a severe brain injury (Adam, Osbourne 2005), and was caused as a direct result of his subarachnoid haemorrhage which caused his intracranial pressure (ICP) to increase. ICP can be explained with reference to the Monro-Kellie hypothesis, which states that because the cranium is a fixed structure it cannot expand in size. Within this fixed structure are three main components; cerebrospinal fluid (CSF), blood and brain tissue. The hypothesis goes on to explain that if there is an increase in any one of these components then this must be compensated by a decrease in the volume of the other two otherwise ICP will increase. Brain tissue is not easily displaced therefore CSF volume is displaced into the spinal cord and, or the dura can expand slightly to increase absorption and create a downward displacement of venous blood (Book, Porth 2000). These two compensatory mechanisms enable the body to keep ICP within normal range at least in the short term. CSF and blood are therefore able to adjust to some extent to enable ICP to remain normal, when brain tissue is displaced, such as herniation or ‘coning’, damage to the brain occurs and then death. The haemorrhage Jim suffered caused a space occupying lesion, which caused the volume of blood in his brain to increase, which had to be compensated for in order to keep ICP within normal limits. The compensatory mechanism is temporary and maintains a normal ICP, however, when the compensation system has been fully exhausted and if lesion volume continues or secondary injury (swelling) occurs, ICP consequently increases. As Jim’s ICP increased he began to vomit and, caused his conscious level to fall. It also steadily...
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