Aneurismal Subarachnoid Haemorrhage And Traumatic Brain Injury: Analysis And Management

Overview of ASAH and TBI

SAH commonly known as Aneurismal Subarachnoid Haemorrhage is a disease that is a worldwide health burden. It has high rate of fatality rate and is an incurable disease. The overall projection of the disease includes initial huge amount of bleeding, increase of delayed cerebral ischemia and rebleeding (Yavin et al. 2014). The Pulmonary oedema of Neurology and Cardiac Manifestations signifies the seriousness of Aneurismal Subarachnoid Haemorrhage. The International trial of Subarachnoid Aneurysm indicated favourable outcomes of the procedure of endovascular coiling in contrast to the remedy of surgical clipping towards the end of first year. On the other hand, TBI commonly known as Traumatic Brain Injury is a disease where there is a mild loss of consciousness or disorientation that lasts less than thirty minutes. TBI is commonly known as Concussion, Minor Traumatic Brain Injury, minor head injury, minor brain injury and minor head trauma (Wall et al. 2014).  MBTI is a most prevalent form of Traumatic Brain Injury and 15% of the patients are observed to have the symptoms for more than one year.

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This essay discusses about two patients namely, Leo and Tamara who has been admitted for ASAH and MTBI respectively. The main objective of the essay is to analyse both the concordance of their disease and to suspect that which of the patients shows high-rise of intracranial pressure (Wall et al. 2014).

ICP or the Intracranial Pressure is a pressure that is created in the skull, which creates further pressure to the tissue of the brain and to the cerebrospinal fluid. The intracranial pressure is measured by the mercury level in terms of millimetres (Wall et al. 2014).  There are various mechanisms of human body, which keeps the intracranial pressure in control. The intracranial hypertension commonly known as IH, raised Intracranial Pressure or IICP is the elevation of the pressure in the level of the cranium. The normal pressure range of intracranial pressure is 7 to 15 mm of HG and the upper limit is 20 to 25 mm of HG. The Intracranial pressure is the most damaging facet of brain trauma. The Intracranial pressure raises the level of pressure of the blood in the brain. The constant pressure can rapture the veins of the brain that results in brain haemorrhage. The increase in pressure can lead to intracranial hematoma which results in the shift in the structure of the brain by crushing the tissues of the brain. This phenomenon causes brain herniation and restricts the supply of the blood to the brain. The increase in the intracranial pressure can also be an outcome of the swelling of brain tissues. This swelling can result from any previous injury or some brain disease like meningitis. The common symptoms of Intracranial pressure includes, headache, ocular palsies, back pain, papilledema , altered levels of consciousness and vomiting without any incidence of nausea. Prolonged incidence of papilledema can cause disturbances in the visual fields like optic atrophy and extreme cases can even lead to permanent blindness (Marshall-Bowman, Barratt and Gibson 2013). Papilledema results due to the swelling of the optic disc. It acts as a reliable sign to prove that the intracranial pressure has increased.  The brain is the only body part where the supply of oxygen is limited due to the hypoventilation during the hours of sleep. Cerebral oedema may also worsen due to the lying position in the hours of sleep. The headache can increase due the occurrence of coughing, sneezing or bending. In children, the high rate of heart is the indication of high intracranial pressure (Sekhon et al. 2014). The injury in the brain also degrades the oxygen level in the body that results in irregular breathing.

Symptoms and Diagnosis of Intracranial Pressure

The closure of the sutures and the fontanels of the skull give a structure to the brain that prohibits any further expansion to the volume of the brain. In normal conditions these content can be divided into 3 compartments, 80% of cerebral parenchyma, 10% of cerebrospinal fluid and 10% of blood. The increase in the volume of any three of these aspects will raise the ICT pressure (Lewis et al. 2014). The whole phenomenon is known as the Menro – Kellie doctrine. Therefore, when the buffer mechanisms become unsuccessful, the increase in the intracranial pressure further decreases the CPP (cerebral perfusion pressure). This constant decrease in the level of CPP increases the occurrence of high pressure on the ischemic lesions.

Intracranial Pressure elucidates the pressure inside the vaults of the cranial nerves. It can be assumed that the brain functions normally when the intracranial pressure is between 10 to 20 mmHg in case of adults, 3 to 7mmHg in case of children and 1.5 to 6 mmHg in case of newborns. Intracranial Pressure mainly occurs due to the communication between the cerebrospinal fluids, the brain and the blood of the cerebral system. The water content of cerebral parenchyma ranges from 75 percent to 80 percent. Water levels are found mainly in the intracellular space that consists of grey and white matter and extracellular space that consists of interstitial space. The blood level of the brain refers to CBV, which is commonly known as cerebral blood volume, and CBF. The intracranial pressure changes with posture of the body that generally indicates to the standing and sitting conditions. The changes of ICP are also dependent on the fluctuation levels of pressure of arteries and breathing levels. The constant coughing and sneezing can increase the pressure in the jugular or epidural veins. The venous pressure in the intracranial space results in further raise of the level of pressure of intracranial space (Mangat et al. 2015).

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The review of the report of the patients that are given are analysed in the below discussion. Leo, who is a thirty eight year old man, was taken in the emergency section with the complaint of acute headache. The patient does not have any history of brain injury or do not have any migraine problems.  He works as a Cabinetmaker and is married with a child. The primary survey shows that the patient was detonating day by day; he responded to voices, the airway of the patient was clear. He had irregularity in breathing; the circulation of the capillary return in 2 seconds is HR 110. The patient was detected with slurred voices and pain was localized in the body parts. The body temperature was relatively high and was above the normal range.  The respiratory rate was recorded as sixteen irregular deep ventilation, blood pressure was recorded as 170 by 110 and the headache was rated 9 out of 10. The right eye as droopy and the downward gaze had no reaction. Leo was detected with tonic clonic seizure and a raise in the induction incubation. The patient was diagnosed with the dysfunction in the cerebrospinal fluid. At the initial drainage of cerebrospinal fluid, craniotomy and ventriculostomy was implemented to diminish the intracranial pressure and the drainage of cerebrospinal fluid. However, for implementation of better methods, the patient was taken to the Intensive Care Unit. The following procedures was implemented. The EVD level was aeroed to the Foremen of Munro. The EVD report showed drainage of fresh blood and t was recorded to be 10 ml per hour. Propofol and fentanyl infusions were given to sedate the patients. The infusion of nimodipine was started at 5mls per hours and the dose was increased to 10mls per hour after the hypotension was controlled. The patient was positioned 40 degrees upright on his back. On the third day, the intracranial pressure became more variable, drainage of EVD also increased, and the output of urine increased to 100mls per hour. The core body temperature increased to a huge rate, the right pupil of the patient also became unresponsive and the size of pupil rose to four. The CT scan showed a vasospasm of middle cerebral artery. The vasospasm was treated by the implementation of endovascular angioplasticity and the infusion of verapamil. During his course of stay in the ICU, Leo has gone through three more treatments of endovascular vasospasm (Karic et al. 2016). After the sixth day, percutaneous tracheostomy was implemented and EVD was removed. He was removed from mechanical ventilation when his neurological function improved gradually. He was then allocated to the neurological rehabilitation ward.

Case Studies and Treatment of ASAH and TBI

On the other hand, there was a paediatric minor traumatic brain injury case. She is eight-year-old female named Tamara.  She hit her head while playing with her brother. She had short span of unconsciousness and vomited without nausea. The side of her brain swelled and she gradually developed severe headache. The primary survey observed that she was unresponsive to any voice and rapid breathing was recorded (Hung et al. 2015). She was also unresponsive to any kind of touch. A small haematoma with a minor fracture in the skull was reported. She was given basic medication and was further observed. Eventually the initial stage of seizure which was seen decreased and oral diets and fluids were given to her. The parental supervision was required and before discharge, her family was informed to supervise the patient’s mental and physical health.

The above two cases showed deterioration in the neurological surveillance (Greenberg et al. 2015). The management of the patients diagnosed with ICH cerebral oedema aims to lower level of ICP and a higher level of CPP. From a viewpoint of a therapist, the several measures to be taken are discussed n this essay. Firstly, the promotion of jugular venous outflow is very important. Secondly, the decrease in the metabolism decreases cerebral oxygen consumption. Thirdly, the detection of external ventricular drain is necessary which helps to control the drainage of cerebrospinal fluid and which further decreases the ICP. Fourthly, the implementation of Prophylactic antiepileptic is very important. Lastly, repeated cranial CT scan is also very important to have a good observation on the condition of the brain (D’Souza 2015).

The family care is centred with the shared belief that for the positive development emotional and physical health of the patient, the involvement of the family in the planning delivery and evaluation of care is very important. In several studies, it has been found that the involvement of the family members played a vital role for the detection of the deterioration of the patients. Several implementations have been made effective for the family escalation of the care of the patients. In case of the above two case studies the role of family is of utmost priority.  The two tutorial cases showed the patient is highly dependent on their family, as they have been detected with initial phases of seizures (Stocchetti and Maas 2014). However, the patients are needs the full observation of the family members as well. The constant support and guidance from the members of the family will affect the positive development of the health of the patients.

Management of ICP and Patient Care

Therefore, the essay concludes that for a basic treatment of Intracranial pressure entails a depth of knowledge of the disease. Any medication errors can degrade the health of the patients to a huge extent. The intervention of the family members is of utmost priority. The patients should be diagnosed as early as possible to before it is too late. 

References

D’Souza, S., 2015. Aneurysmal subarachnoid hemorrhage. Journal of neurosurgical anesthesiology, 27(3), p.222.

Greenberg, M.S., Wood, N.E., Spring, J.D., Gurvits, T.V., Nagurney, J.T., Zafonte, R.D. and Pitman, R.K., 2015. Pilot Study of Neurological Soft Signs and Depressive and Postconcussive Symptoms During Recovery From Mild Traumatic Brain Injury (mTBI). The Journal of neuropsychiatry and clinical neurosciences, 27(3), pp.199-205.

Hung, R., Carroll, L., Cancelliere, C., Cote, P., Rumney, P., Keightley, M., Coronado, V., Stålnacke, B.M. and Cassidy, J.D., 2014. A systematic review of the clinical course, natural history and prognosis for pediatric MTBI: Results of the International Collaboration on MTBI Prognosis (ICoMP). Archives of Physical Medicine and Rehabilitation, 95, pp.174-191.

Karic, T., Roe, C., Nordenmark, T.H., Becker, F. and Sorteberg, A., 2016. Impact of Early Mobilization and Rehabilitation on Global Functional Outcome One Year After Aneurysmal Subarachnoid Haemorrhage. Journal of Rehabilitation Medicine, 48(8), pp.676-682.

Lewis, P.M., Smielewski, P., Rosenfeld, J.V., Pickard, J.D. and Czosnyka, M., 2014. A continuous correlation between intracranial pressure and cerebral blood flow velocity reflects cerebral autoregulation impairment during intracranial pressure plateau waves. Neurocritical care, 21(3), pp.514-525.

Mangat, H.S., Chiu, Y.L., Gerber, L.M., Alimi, M., Ghajar, J. and Härtl, R., 2015. Hypertonic saline reduces cumulative and daily intracranial pressure burdens after severe traumatic brain injury. Journal of neurosurgery, 122(1), pp.202-210.

Marshall-Bowman, K., Barratt, M.R. and Gibson, C.R., 2013. Ophthalmic changes and increased intracranial pressure associated with long duration spaceflight: an emerging understanding. Acta Astronautica, 87, pp.77-87.

McAllister, T., McDonald, B., Flashman, L., Ferrell, R. and Saykin, A., 2014, May. Differential Effects of Bromocriptine and Pergolide on Working Memory Performance and Brain Activation Patterns in Individuals with Mild Traumatic Brain Injury (MTBI). In BRAIN INJURY (Vol. 28, No. 5-6, pp. 806-806). TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND: INFORMA HEALTHCARE.

Mensing, L.A., Rinkel, G.J., Vlak, M.H., van der Schaaf, I.C. and Ruigrok, Y.M., 2016. Difference in Aneurysm Characteristics between Patients with Familial and Sporadic Aneurysmal Subarachnoid Haemorrhage. PloS one, 11(4), p.e0154281.

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Stocchetti, N. and Maas, A.I., 2014. Traumatic intracranial hypertension. New England Journal of Medicine, 370(22), pp.2121-2130.

Wall, M., Kupersmith, M.J., Kieburtz, K.D., Corbett, J.J., Feldon, S.E., Friedman, D.I., Katz, D.M., Keltner, J.L., Schron, E.B. and McDermott, M.P., 2014. The idiopathic intracranial hypertension treatment trial: clinical profile at baseline. JAMA neurology, 71(6), pp.693-701.

Wall, M., McDermott, M.P., Kieburtz, K.D., Corbett, J.J., Feldon, S.E., Friedman, D.I., Katz, D.M., Keltner, J.L., Schron, E.B. and Kupersmith, M.J., 2014. Effect of acetazolamide on visual function in patients with idiopathic intracranial hypertension and mild visual loss: the idiopathic intracranial hypertension treatment trial. Jama, 311(16), pp.1641-1651.

Wall, M., McDermott, M.P., Kieburtz, K.D., Corbett, J.J., Feldon, S.E., Friedman, D.I., Katz, D.M., Keltner, J.L., Schron, E.B. and Kupersmith, M.J., 2014. Effect of acetazolamide on visual function in patients with idiopathic intracranial hypertension and mild visual loss: the idiopathic intracranial hypertension treatment trial. Jama, 311(16), pp.1641-1651.

Yavin, D., Luu, J., James, M.T., Roberts, D.J., Sutherland, G.R., Jette, N. and Wiebe, S., 2014. Diagnostic accuracy of intraocular pressure measurement for the detection of raised intracranial pressure: meta-analysis: a systematic review. Journal of neurosurgery, 121(3), pp.680-687.