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| Karen Tapp is a Clinical Nurse Specialist, in the Intensive Therapy Unit at St. Vincent's Hospital, Sydney. |
This is a case study of Mr. Jamieson, a 57 year old man who sustained a massive intraventricular haemorrhage in circumstances unknown.
The anatomy and physiology is described in relation to an intraventricular haemorrhage and the nursing care of the unconscious head injured patient in the Intensive Therapy Unit (ITU) is examined. This includes the use and management of intraventricular drains and the implication of a diagnosis of brain death.
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Missionbeat brought Mr. Jamieson (pseudonym) to the Accident and Emergency Department of St. Vincent's Hospital at 2120 hours on the 29 May 1992. On arrival he was unkempt and covered with vomit and faeces.
He had a patent airway despite a decreased level of consciousness (L.O.C.) and a spontaneous respiratory rate of 12 breaths/minute. A gag and cough reflex were present. Air entry was poor, though equal to both lungs. A large amount of crepitus could be heard over the region between the 8th and 12th rib on the right (R) side, suggesting fractures. His pulse rate was bradycardic, 50/minute and regular. A blood pressure (BP) of 110/80 mmHg was recorded. Due to exposure, Mr. Jamieson was hypothermic with a core body temperature of 34.4°C.
Neurologically, Mr. Jamieson exhibited signs and symptoms consistent with those of a cerebral insult and increased intracranial pressure (I.C.P.). This was determined by the Glasgow Coma Scale (G.C.S.), an internationally recognised tool used to assess changes in level of consciousness. Mr. Jamieson showed nonpurposeful movement with his (R) upper limb only, in response to painful stimuli. He made no verbal response and did not open his eyes. His pupils were small and reacting equally to light. He scored 6 points of a maximum 15 points on the G.C.S.
A laceration and swelling were noted over the occiput. A large bruise covered the (R) hip and multiple small grazes were over both knees and shins. At the time of admission, blood results of significance were potassium 3.3 mmol/L and blood alcohol of 0.36%.
At 2300 hours on 29 May 1992, it was recorded that Mr. Jamieson had deteriorated neurologically. His pupils were mid-sized and not reacting to light. This suggested that neither parasympathetic nor sympathetic innervation were operational (Hickey 1986: 128). An urgent Computerized Tomography (C.T.) scan was attended at 2345 hours.
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C.T. scanning allows highly accurate diagnosis of neurological conditions by computer analysis of horizontal cross sections of the brain (Holloway 1988: 76).
Mr. Jamieson's C.T. scan revealed a large intraventricular haemorrhage completely filling the 4th ventricle, cerebral aqueduct, 3rd ventricle and occipital horns of both lateral ventricles. A blood clot was adherent to both choroid plexuses in the lateral ventricles. Raised intracranial pressure (ICP) and obstructive hydrocephalus were demonstrated by dilatation of the entire ventricular system and effacement of cerebral sulci. Subarachnoid blood was within the left (L) Sylvian fissure and obliterating the basal cisterns. No midline shift and no extra axial collections were observed. Linear fractures through the (R) occipital bone, internal occipital protuberance and mid occiput, and a transverse fracture through the (L) petrous temporal bone were visible.
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The ventricular system of the brain consists of four (4) irregularly shaped interconnected spaces for the production and circulation of cerebrospinal fluid (CSF). There are two lateral ventricles, one in each cerebral hemisphere, extending into each lobe. These contain the major part of the choroid plexus which produces CSF. The third ventricle is posterior to the hypothalamus and the fourth ventricle sits in the brain stem, posterior to the pons. CSF flows throughout these chambers and then via the foramen of Magendie into the subarachnoid space. It bathes the spinal cord and flows over the surface of the cerebral hemispheres to the superior sagittal sinus, where it is reabsorbed.
The rate of CSF production is normally equal to the rate of its absorption (Tortora 1981: 330). However following a cerebral haemorrhage, the arachnoid villi, the small channels that the CSF is absorbed through, can become seriously blocked. This is due to the sudden appearance of large numbers of cells in the CSF (Guyton 1991: 376). Consequently there is an accumulation of fluid within the ventricles of the brain known as hydrocephalus internal (Taber 1981: 676). This increases the intracranial pressure.
The intracranial volume is contained in a tightly closed space. Therefore, an increase of any labile element of its contents - nervous tissue, blood volume, CSF - can take place only at the expense of the other element(s), or by an increase in intracranial pressure (Thompson 1991: 280). Mr Jamieson had increased ICP due to haemorrhage into the CSF compartments.
When all compensatory mechanisms of the brain fail in response to increased ICP, brain damage occurs because of tissue ischaemia and compression (Luckman & Sorenson, 1982: 541). The compression of Mr. Jamieson's brain caused irreversible, ischaemic damage.
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The medical management and nursing care of Mr. Jamieson which follows, aimed to normalise ICP and prevent any further neurological damage occurring.
Mr. Jamieson's condition deteriorated rapidly during the C.T. scan. He was unable to maintain a clear airway, so oral intubation was performed and ventilatory support commenced. Following C.T. scan, he was transferred to the operating theatre for the insertion of an intraventricular drain (I.V.D.). A catheter was passed into the lateral ventricle via a right frontal burr hole to drain C.S.F. and blood from the ventricular system and thus reduce intracranial volume (Sinclair 1992: 21).
Mr. Jamieson arrived in ITU, hypothermic and hypotensive. His haemoglobin (Hb) level was 6.6 g/dl. A blood transfusion totalling six (6) units of packed cells aimed to replace blood loss to maximise tissue oxygen (O2) delivered, by raising available haemoglobin (Skowronski 1990: 373). The post transfusion Hb was 12.8 g/dl, which is within normal limits.
Circulating blood volume was maintained by intravenous colloid and crystalloid solutions. The use of metaraminol, an inotropic drug, was not required until Mr. Jamieson's last hours of care in ITU. Mr. Jamieson received no other significant drug therapy in the management of his neurological condition.
Due to the extensive damage visualised on the cerebral C.T. scan, combined with his clinical presentation, Mr. Jamieson's prognosis was considered poor. His medical management and nursing care were primarily supportive.
The aims, actions and rationale for each action of Mr. Jamieson's nursing care, while in ITU is summarised in Table 1 (Appendix).
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Despite the implementation of all appropriate medical and nursing actions, Mr. Jamieson's condition did not improve. In fact, all evidence suggested he was brain dead. Brain death is the irreversible loss of all brainstem function (OH 1990: 294).
Clinical diagnosis can only be made in a patient who is normothermic, normotensive, free of neuromuscular blocking agents, with normal metabolic and biochemical blood levels (Pearson, 1990: 1).
At 1000 hours on 31 May 1992 these conditions were present in Mr. Jamieson. The following neurological tests and responses were recorded in order to diagnose brain death:
On the 1 June 1992, the same neurological tests were repeated and all tests concluded that Mr. Jamieson had suffered brain death. A cerebral angiogram was conducted to confirm this. The absence of cerebral blood flow is presently considered the most reliable ancillary test in diagnosing brain death (Alvarez et al. 1988: 225). This proved to be the case with Mr. Jamieson.
The possibility of organ donation was discussed. However, in the absence of any traceable relative, permission for organ donation was required from the Clinical Superintendent of St. Vincent's Hospital and the Coroner. In view of a potential criminal act underlying the situation, permission for organ donation was denied by the State Coroner.
Ventilation was ceased at 1800 hours and Mr. Jamieson died soon after.
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Hospitalisation causes psychological and social stress on a patient and his significant others. Those persons who play key roles in a patient's life are significant others (Holloway 1988: 36). Mr. Jamieson had no family and his closest significant friend was his employer. Responsibility for meeting Mr. Jamieson's needs was met by the nurses who cared for him.
Although Mr. Jamieson was unconscious, all nursing staff introduced themselves. They continually orientated him to his surroundings and explained all procedures performed. Unnecessary stimuli were reduced and a pleasant auditory environment was created by soft playing of music at night.
Mr. Jamieson was not left unattended and raised bed rails provided safety at all times.
Nursing staff liaised with the social worker assigned to investigate Mr. Jamieson's specific social circumstances.
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As the cause of Mr Jamieson's injuries remained undetermined, the body of Mr. Jamieson was transferred to the City Coroners' Court Glebe and an autopsy was performed in accordance with legal requirements. The results of the investigations were not available at the time of writing this case study.
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Mr. Jamieson's case history illustrates that the consequence of a massive intraventricular haemorrhage is raised I.C.P., which leads to cerebral compression and ischaemia. An intraventricular drain may be inserted to reduce CSF volume and thus I.C.P. However in the case of Mr. Jamieson, brain damage from such abnormal physiology was irreversible and resulted in brain death.
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| GOAL | NURSING ACTION | RATIONALE | MR JAMIESON'S CASE |
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Table One. Nursing Care Plan
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