Response System to Clinical Deterioration
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This document discusses the response system to clinical deterioration in patients with increased intracranial pressure (ICP). It covers the causes, symptoms, and interventions for managing ICP, as well as the assessment of vital signs and pain management. The importance of patient and family education in the care and management of patients with brain injuries is also highlighted.
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Running Head: RESPONSE SYSTEM TO CLINICAL DETERIORATION
RESPONSE SYSTEM TO CLINICAL DETERIORATION
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RESPONSE SYSTEM TO CLINICAL DETERIORATION
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1RESPONSE SYSTEM TO CLINICAL DETERIORATION
Increases intracranial pressure (ICP) refers to the pressure exerted within the cranium
by the combination of the total volume of brain tissue, blood and cerebrospinal fluids (CSF)
in the skull. All these three components exist in a state of dynamic equilibrium. According to
the Monroe-Kellie hypothesis, if there is increase in any of the three components namely
brain tissue, CSF and blood it should be balanced by the decrease in volume of any of the
other three components otherwise, it will result in the elevation of ICP
(Criticalcareontario.ca, 2019). Cushing reflex is a physiological response of the nervous
system due to increase in the ICP. Thus, increase in the ICP triggers the cerebral ischemic
response. Increased ICP also causes other effects such as decrease in the cerebral perfusion
pressure (CPP) as well as CBF. The individual increase in cerebral ischemic response, CPP
and CBF causes an overall increase in the carbon dioxide content (Healthline, 2019). The
increased amount of carbon dioxide causes a sympathetic nervous system response that
ultimately leads to increase in MAP which in turn increases the CPP (Sciencedirect.com,
2019). Reflex bradycardia is occurs independently due to the elevation of MAP which
indicates that the values of ICP can increase so much that it might cause life threatening
conditions. These conditions can lead to aggressive medical conditions such as brain injury,
coma, stroke and even death (Seunggu Han, 2019).
The reasons for increased ICP includes hydrocephalus which means building up of
excess CSF inside the brain ventricles. The other causes are bleeding into the brain, brain
swelling, and aneurysm. Brain injury or brain tumor are the other main reasons behind ICP.
The minor causes of ICP are the brain infections such as meningitis or encephalitis, high
blood pressure or stroke. The symptoms of ICP are headache, nausea, vomiting, and decrease
in mental abilities, vision problems, breathing difficulty and seizures (Cedars-sinai.org,
2019). Leo and Tamara both suffer from ICP and have experienced most of the above
mentioned clinical symptoms such as confusion, seizures, high BP, nausea, vomiting, shallow
Increases intracranial pressure (ICP) refers to the pressure exerted within the cranium
by the combination of the total volume of brain tissue, blood and cerebrospinal fluids (CSF)
in the skull. All these three components exist in a state of dynamic equilibrium. According to
the Monroe-Kellie hypothesis, if there is increase in any of the three components namely
brain tissue, CSF and blood it should be balanced by the decrease in volume of any of the
other three components otherwise, it will result in the elevation of ICP
(Criticalcareontario.ca, 2019). Cushing reflex is a physiological response of the nervous
system due to increase in the ICP. Thus, increase in the ICP triggers the cerebral ischemic
response. Increased ICP also causes other effects such as decrease in the cerebral perfusion
pressure (CPP) as well as CBF. The individual increase in cerebral ischemic response, CPP
and CBF causes an overall increase in the carbon dioxide content (Healthline, 2019). The
increased amount of carbon dioxide causes a sympathetic nervous system response that
ultimately leads to increase in MAP which in turn increases the CPP (Sciencedirect.com,
2019). Reflex bradycardia is occurs independently due to the elevation of MAP which
indicates that the values of ICP can increase so much that it might cause life threatening
conditions. These conditions can lead to aggressive medical conditions such as brain injury,
coma, stroke and even death (Seunggu Han, 2019).
The reasons for increased ICP includes hydrocephalus which means building up of
excess CSF inside the brain ventricles. The other causes are bleeding into the brain, brain
swelling, and aneurysm. Brain injury or brain tumor are the other main reasons behind ICP.
The minor causes of ICP are the brain infections such as meningitis or encephalitis, high
blood pressure or stroke. The symptoms of ICP are headache, nausea, vomiting, and decrease
in mental abilities, vision problems, breathing difficulty and seizures (Cedars-sinai.org,
2019). Leo and Tamara both suffer from ICP and have experienced most of the above
mentioned clinical symptoms such as confusion, seizures, high BP, nausea, vomiting, shallow
2RESPONSE SYSTEM TO CLINICAL DETERIORATION
breathing and headache. The neurological deterioration of Leo is caused by meningitis, high
blood pressure, hydrocephalus, aneurism as he suffered from middle cerebral artery aneurism
and intracranial hemorrhage. On the other hand, Tamara’s case of neurological deterioration
is caused by seizures and intracranial hemorrhage. The frequent neurological observations
can help the nurses in recognizing the patient condition and thus, the patient condition can be
improved with interventions from early treatment. GCS or Glassgow Coma Scale assessment
is the most common technique to score the level of consciousness. Leo had a GCS score of 12
which has been classified as having a moderate brain injury while Tamara’s GCS score of 9
that was assessed post seizure has also been classified as moderate although Tamara was
sedated (). Another useful technique is Hunt and Hess grading system. It is a useful clinical
tool as it calculates the severity of SAH or subarachnoid hemorrhage. Leo’s survival
percentage according to the system is approximately 50%.World Federation of Neurological
Surgeons and Fisher scale are also used to analyze the condition of the patient. Fisher scale is
used to predict the risk of cerebral vasopasm after SAH while WFNS is used to classify
patients on the scale of SAH damage using GCS in combination with the absence or presence
of vision problems as examining the pupil size and the ability of the patient to response to
light help the physicians in determining the rate of patient deterioration
(Aci.health.nsw.gov.au, 2019). Leo had a vision problem as his right eye was droopy and had
downward gaze which might be due to increased ICP. The assessment of patient’s limbs can
also determine the neurovascular changes of the patient.
The condition of hypoxia and prophylactic hyperventilation can further cause damage
to critically reduced cerebral perfusion. As, it is known that brain represents just 2% of the
total body weight, it uses approximately 20% of the body’s oxygen supply. The neurons in
brain derive their energy for performing certain conscious functions that planning and
thinking as well as certain unconscious functions like heart rate and digestion from the
breathing and headache. The neurological deterioration of Leo is caused by meningitis, high
blood pressure, hydrocephalus, aneurism as he suffered from middle cerebral artery aneurism
and intracranial hemorrhage. On the other hand, Tamara’s case of neurological deterioration
is caused by seizures and intracranial hemorrhage. The frequent neurological observations
can help the nurses in recognizing the patient condition and thus, the patient condition can be
improved with interventions from early treatment. GCS or Glassgow Coma Scale assessment
is the most common technique to score the level of consciousness. Leo had a GCS score of 12
which has been classified as having a moderate brain injury while Tamara’s GCS score of 9
that was assessed post seizure has also been classified as moderate although Tamara was
sedated (). Another useful technique is Hunt and Hess grading system. It is a useful clinical
tool as it calculates the severity of SAH or subarachnoid hemorrhage. Leo’s survival
percentage according to the system is approximately 50%.World Federation of Neurological
Surgeons and Fisher scale are also used to analyze the condition of the patient. Fisher scale is
used to predict the risk of cerebral vasopasm after SAH while WFNS is used to classify
patients on the scale of SAH damage using GCS in combination with the absence or presence
of vision problems as examining the pupil size and the ability of the patient to response to
light help the physicians in determining the rate of patient deterioration
(Aci.health.nsw.gov.au, 2019). Leo had a vision problem as his right eye was droopy and had
downward gaze which might be due to increased ICP. The assessment of patient’s limbs can
also determine the neurovascular changes of the patient.
The condition of hypoxia and prophylactic hyperventilation can further cause damage
to critically reduced cerebral perfusion. As, it is known that brain represents just 2% of the
total body weight, it uses approximately 20% of the body’s oxygen supply. The neurons in
brain derive their energy for performing certain conscious functions that planning and
thinking as well as certain unconscious functions like heart rate and digestion from the
3RESPONSE SYSTEM TO CLINICAL DETERIORATION
oxidation of glucose. Thus, in the absence of oxygen, brain cells cannot metabolize glucose
and the neurons do not get enough energy. The brain ultimately gets deprived of oxygen that
causes brain death (Alzheimer's Disease and Dementia, 2019). In Leo’s case the SpO2 was
98% on 4L/min of oxygen provided via nasal spec. It becomes unacceptable when the level is
dropped to 85%. The clinical interventions that can be taken by the nurses in order to
improve the condition of Leo is to disconnect him from the transport ventilator and
ventilating him with 100% oxygen will clear the secretions. Along with this the change in the
HME filter will also help Leo to maintain adequate perfusion thereby providing systemic
oxygenation to the brain. The nurses can incubate him and attach him to the transport
ventilator. The ventilation can be done on SIMV 12x600 and the carbon dioxide level of Leo
can be monitored that will help in maintaining and observing the open airway as well as
carbon monoxide levels. Leo had a respiratory rate of 16 with deep ventilation system which
is quite unacceptable and shows the signs of impaired brainstem function. In case of Tamara,
the SpO2 was 100% post her seizure which had been achieved by the protecting her airway
and keeping her on oxygen of 8L per minute via an oxygen mask. She had a respiratory rate
of 20 which is within the normal range and thus, no such management is required other than
continuous monitoring of respiration.
The assessment of the patient’s blood pressure is also very useful for the calculation
of the cerebral perfusion pressure and for measuring of blood pressure in the artery. As the
auto regulatory functions are impaired this increases systemic blood pressure that might cause
increased regional cerebral blood flow and there is disruption of the blood brain barrier that
causes cerebral edema. The patients who have a brain injury their cerebrovascular auto
regulatory mechanisms are often impaired that largely increases their systemic blood pressure
which is in turn directly related to their cerebral capillaries hat ultimately results in the
breakdown of the blood brain barrier. This worsens the condition of cerebral edema and thus
oxidation of glucose. Thus, in the absence of oxygen, brain cells cannot metabolize glucose
and the neurons do not get enough energy. The brain ultimately gets deprived of oxygen that
causes brain death (Alzheimer's Disease and Dementia, 2019). In Leo’s case the SpO2 was
98% on 4L/min of oxygen provided via nasal spec. It becomes unacceptable when the level is
dropped to 85%. The clinical interventions that can be taken by the nurses in order to
improve the condition of Leo is to disconnect him from the transport ventilator and
ventilating him with 100% oxygen will clear the secretions. Along with this the change in the
HME filter will also help Leo to maintain adequate perfusion thereby providing systemic
oxygenation to the brain. The nurses can incubate him and attach him to the transport
ventilator. The ventilation can be done on SIMV 12x600 and the carbon dioxide level of Leo
can be monitored that will help in maintaining and observing the open airway as well as
carbon monoxide levels. Leo had a respiratory rate of 16 with deep ventilation system which
is quite unacceptable and shows the signs of impaired brainstem function. In case of Tamara,
the SpO2 was 100% post her seizure which had been achieved by the protecting her airway
and keeping her on oxygen of 8L per minute via an oxygen mask. She had a respiratory rate
of 20 which is within the normal range and thus, no such management is required other than
continuous monitoring of respiration.
The assessment of the patient’s blood pressure is also very useful for the calculation
of the cerebral perfusion pressure and for measuring of blood pressure in the artery. As the
auto regulatory functions are impaired this increases systemic blood pressure that might cause
increased regional cerebral blood flow and there is disruption of the blood brain barrier that
causes cerebral edema. The patients who have a brain injury their cerebrovascular auto
regulatory mechanisms are often impaired that largely increases their systemic blood pressure
which is in turn directly related to their cerebral capillaries hat ultimately results in the
breakdown of the blood brain barrier. This worsens the condition of cerebral edema and thus
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4RESPONSE SYSTEM TO CLINICAL DETERIORATION
causes elevation in ICP (Betterhealth.vic.gov.au, 2019; Alzheimer's Disease and Dementia,
2019). The increase in cerebral edema and elevated ICP also impair cerebral perfusion and
might also result in cerebral ischemia (Shi et al., 2013). Now, in case of Leo, his blood
pressure was 170/110, that falls into the high range of BP which is a classical sign of
increased ICP. In Tamara’s case, her diastolic pressure of 98 was within the range however,
her diastolic pressure that falls under 45 is below the normal range. This is a sign that her
systolic blood pressure is differentiating from her diastolic pressure that alters her respiratory
pattern resulting in the quick breathing so that enough oxygen is reaching the brain. This
situation can be managed if the patient’s pulse rate is checked so that the regularity of the
heart rate can be determined. It also indicates about the strength of heart contraction. The
patient who have a brain injury, the arterial pressure exceeds the intracranial pressure,
thereby restoring the flow of blood to the brain. The CNS ischemic response usually causes
the increased arterial blood pressure that stimulates the baroreceptors in the carotid bodies,
that drastically slows the heart rate often leading to bradycardia. In Leo’s case, his heart rate
was 116 and his headache pain might be related to rhythm sinus bradycardia. On the other
hand, Tamara had a heart rate of 90 that falls under the normal range.
Another way of assessing the neural abnormalities is theis the detection of patient’s
body temperature. The damage caused to hypothalamus due to head trauma, hydrocephalus or
any other injury like infection, hemorrhage or dehydration is related to hyperthermia. When
the body suffers from hyperthermia, it increases the body’s metabolic expenditure, glutamate
release and neutrophil activity to a level that is higher than those patients with brain injury
who are normothermic. This additional effect may further compromise the injured brain that
will enhance the vulnerability to secondary pathogenic events that will accelerate the
neuronal damage. The decrease in body temperature to about 35 to 35.5 degrees can reduce
the intracranial pressure while maintaining sufficient cerebral perfusion pressure without ny
causes elevation in ICP (Betterhealth.vic.gov.au, 2019; Alzheimer's Disease and Dementia,
2019). The increase in cerebral edema and elevated ICP also impair cerebral perfusion and
might also result in cerebral ischemia (Shi et al., 2013). Now, in case of Leo, his blood
pressure was 170/110, that falls into the high range of BP which is a classical sign of
increased ICP. In Tamara’s case, her diastolic pressure of 98 was within the range however,
her diastolic pressure that falls under 45 is below the normal range. This is a sign that her
systolic blood pressure is differentiating from her diastolic pressure that alters her respiratory
pattern resulting in the quick breathing so that enough oxygen is reaching the brain. This
situation can be managed if the patient’s pulse rate is checked so that the regularity of the
heart rate can be determined. It also indicates about the strength of heart contraction. The
patient who have a brain injury, the arterial pressure exceeds the intracranial pressure,
thereby restoring the flow of blood to the brain. The CNS ischemic response usually causes
the increased arterial blood pressure that stimulates the baroreceptors in the carotid bodies,
that drastically slows the heart rate often leading to bradycardia. In Leo’s case, his heart rate
was 116 and his headache pain might be related to rhythm sinus bradycardia. On the other
hand, Tamara had a heart rate of 90 that falls under the normal range.
Another way of assessing the neural abnormalities is theis the detection of patient’s
body temperature. The damage caused to hypothalamus due to head trauma, hydrocephalus or
any other injury like infection, hemorrhage or dehydration is related to hyperthermia. When
the body suffers from hyperthermia, it increases the body’s metabolic expenditure, glutamate
release and neutrophil activity to a level that is higher than those patients with brain injury
who are normothermic. This additional effect may further compromise the injured brain that
will enhance the vulnerability to secondary pathogenic events that will accelerate the
neuronal damage. The decrease in body temperature to about 35 to 35.5 degrees can reduce
the intracranial pressure while maintaining sufficient cerebral perfusion pressure without ny
5RESPONSE SYSTEM TO CLINICAL DETERIORATION
cardiac dysfunction or less oxygen level. Thus, the patients with severe traumatic brain injury
can be treated within an optimal temperature of 35 to 35.5 degrees. Leo, had a body
temperature of about 36.7 degrees which is within the normal range despite the fact that he
was suffering from meningitis. While Tamara’s primary diagnosis shows that she was not
suffering from any fever and thus, she had normal body temperature.
The assessment of the blood glucose level (BGL) of the patient can minimize the
deterioration rate as the brain continuously needs oxygen as well as glucose. In case of Leo,
the blood glucose level is of 11 which is classified as hyperglycemic. This condition had
occurred due to lactic acidosis, electrolyte disturbances, inflammation, vessel disorders,
rupture of the blood brain barrier and hyper-permeability (Krishnamoorthy et al., 2017).
Thus, it becomes important to monitor his BGL and to notify the physician so that
hyperglycemia can be controlled. In case of Tamara, her BGL was 4 mmol that falls within
the normal range.
In order to relieve the patient from distress assessing the level of pain can be a useful
tool. Leo’s pain protocol showed that a dose of 100 μg fentanyl should aid in the surgical
pain as he had craniotomy and ventriculostomy that has been elevated by headache. There
was also a decrease in his blood pressure and heart rate. The infusion of propofol and bolus
dose of IV Rocuronium will decrease his consciousness and he will not have the memory of
his seizures along with relaxing his muscles. The drugs thiopentene and suxamethnium
during the incubation period will reduce his pain as thiopentene is a short acting barbiturate
while suxamenthnium causes short term paralysis. He can be saved from repeated infusion by
the double dose of IV cannula and it will also give the nurses an intravenous access in case of
emergency. Tamara can be treated with the intranasal administration of the midazolam 7.5μg
that will sedate her and she will not remember anything. It is also very necessary to create
cardiac dysfunction or less oxygen level. Thus, the patients with severe traumatic brain injury
can be treated within an optimal temperature of 35 to 35.5 degrees. Leo, had a body
temperature of about 36.7 degrees which is within the normal range despite the fact that he
was suffering from meningitis. While Tamara’s primary diagnosis shows that she was not
suffering from any fever and thus, she had normal body temperature.
The assessment of the blood glucose level (BGL) of the patient can minimize the
deterioration rate as the brain continuously needs oxygen as well as glucose. In case of Leo,
the blood glucose level is of 11 which is classified as hyperglycemic. This condition had
occurred due to lactic acidosis, electrolyte disturbances, inflammation, vessel disorders,
rupture of the blood brain barrier and hyper-permeability (Krishnamoorthy et al., 2017).
Thus, it becomes important to monitor his BGL and to notify the physician so that
hyperglycemia can be controlled. In case of Tamara, her BGL was 4 mmol that falls within
the normal range.
In order to relieve the patient from distress assessing the level of pain can be a useful
tool. Leo’s pain protocol showed that a dose of 100 μg fentanyl should aid in the surgical
pain as he had craniotomy and ventriculostomy that has been elevated by headache. There
was also a decrease in his blood pressure and heart rate. The infusion of propofol and bolus
dose of IV Rocuronium will decrease his consciousness and he will not have the memory of
his seizures along with relaxing his muscles. The drugs thiopentene and suxamethnium
during the incubation period will reduce his pain as thiopentene is a short acting barbiturate
while suxamenthnium causes short term paralysis. He can be saved from repeated infusion by
the double dose of IV cannula and it will also give the nurses an intravenous access in case of
emergency. Tamara can be treated with the intranasal administration of the midazolam 7.5μg
that will sedate her and she will not remember anything. It is also very necessary to create
6RESPONSE SYSTEM TO CLINICAL DETERIORATION
awareness among both the patients that the pain might not subside unless the fluid inside the
skull is drained completely.
Next assessment can be that of patient’s bladder as vital brain injury can laed to
incontinence when the systems involved with the function are compromised
(Betterhealth.vic.gov.au, 2019). In case of Leo, it is evident that he was suffering from urine
problems due to the inconsistency of the hydrocephalus and this can be managed by inserting
urinary catheter. Tamara’s urine problem can be due to damage in the brain controlling the
bladder. The other assessment might include the checking of ECG that reflects that Leo had a
positive TnT level due to sympathetic over- activity induced by subarachnoid hemorrhage.
The photophobia and nuchal rigidity of Leo can also be important for the diagnosis of the
patient.
The most important part in generating response to the patient is to instruct their
families about the patient care and management especially when the patient is unable to
recognize the family members, cause of injury, develops headache or blurry vision
(Betterhealth.vic.gov.au, 2019). It is also important to make sure that the family understands
that attending the appointments and tests. The patients should attend the rehabilitation as they
might feel great distress or emotional outbursts.
awareness among both the patients that the pain might not subside unless the fluid inside the
skull is drained completely.
Next assessment can be that of patient’s bladder as vital brain injury can laed to
incontinence when the systems involved with the function are compromised
(Betterhealth.vic.gov.au, 2019). In case of Leo, it is evident that he was suffering from urine
problems due to the inconsistency of the hydrocephalus and this can be managed by inserting
urinary catheter. Tamara’s urine problem can be due to damage in the brain controlling the
bladder. The other assessment might include the checking of ECG that reflects that Leo had a
positive TnT level due to sympathetic over- activity induced by subarachnoid hemorrhage.
The photophobia and nuchal rigidity of Leo can also be important for the diagnosis of the
patient.
The most important part in generating response to the patient is to instruct their
families about the patient care and management especially when the patient is unable to
recognize the family members, cause of injury, develops headache or blurry vision
(Betterhealth.vic.gov.au, 2019). It is also important to make sure that the family understands
that attending the appointments and tests. The patients should attend the rehabilitation as they
might feel great distress or emotional outbursts.
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7RESPONSE SYSTEM TO CLINICAL DETERIORATION
8RESPONSE SYSTEM TO CLINICAL DETERIORATION
References
Aci.health.nsw.gov.au. (2019). Subarachnoid Haemorrhage (SAH) | Emergency Care
Institute. Retrieved from
https://www.aci.health.nsw.gov.au/networks/eci/clinical/clinical-resources/clinical-
tools/neurology/headache/subarachnoid-heamorrhage
Alzheimer's Disease and Dementia. (2019). Traumatic Brain Injury (TBI). Retrieved from
https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/
traumatic-brain-injury
Betterhealth.vic.gov.au. (2019). Acquired brain injury. Retrieved from
https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/acquired-brain-
injury
Cedars-sinai.org. (2019). Increased Intracranial Pressure (ICP) | Cedars-Sinai. Retrieved from
https://www.cedars-sinai.org/health-library/diseases-and-conditions/i/increased-
intracranial-pressure-icp-headache.html
Criticalcareontario.ca. (2019). Retrieved from
https://www.criticalcareontario.ca/EN/Neurosurgical%20Care/FINAL%20ICP
%20Presentation-Final-Nov30_2016.pdf
Healthline. (2019). Increased Intracranial Pressure (ICP): Symptoms and Treatments.
Retrieved from https://www.healthline.com/health/increased-intracranial-
pressure#symptoms
Krishnamoorthy, V., Chaikittisilpa, N., Kiatchai, T., & Vavilala, M. (2017). Hypertension
After Severe Traumatic Brain Injury: Friend or Foe?. Journal of neurosurgical
anesthesiology, 29(4), 382–387. doi:10.1097/ANA.0000000000000370
References
Aci.health.nsw.gov.au. (2019). Subarachnoid Haemorrhage (SAH) | Emergency Care
Institute. Retrieved from
https://www.aci.health.nsw.gov.au/networks/eci/clinical/clinical-resources/clinical-
tools/neurology/headache/subarachnoid-heamorrhage
Alzheimer's Disease and Dementia. (2019). Traumatic Brain Injury (TBI). Retrieved from
https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/
traumatic-brain-injury
Betterhealth.vic.gov.au. (2019). Acquired brain injury. Retrieved from
https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/acquired-brain-
injury
Cedars-sinai.org. (2019). Increased Intracranial Pressure (ICP) | Cedars-Sinai. Retrieved from
https://www.cedars-sinai.org/health-library/diseases-and-conditions/i/increased-
intracranial-pressure-icp-headache.html
Criticalcareontario.ca. (2019). Retrieved from
https://www.criticalcareontario.ca/EN/Neurosurgical%20Care/FINAL%20ICP
%20Presentation-Final-Nov30_2016.pdf
Healthline. (2019). Increased Intracranial Pressure (ICP): Symptoms and Treatments.
Retrieved from https://www.healthline.com/health/increased-intracranial-
pressure#symptoms
Krishnamoorthy, V., Chaikittisilpa, N., Kiatchai, T., & Vavilala, M. (2017). Hypertension
After Severe Traumatic Brain Injury: Friend or Foe?. Journal of neurosurgical
anesthesiology, 29(4), 382–387. doi:10.1097/ANA.0000000000000370
9RESPONSE SYSTEM TO CLINICAL DETERIORATION
Sciencedirect.com. (2019). Cerebral Perfusion Pressure - an overview | ScienceDirect Topics.
Retrieved from https://www.sciencedirect.com/topics/agricultural-and-biological-
sciences/cerebral-perfusion-pressure
Seunggu Han, M. (2019). Increased intracranial pressure (ICP): Symptoms, causes, and
treatment. Retrieved from https://www.medicalnewstoday.com/articles/324165.php
Shi, J., Dong, B., Mao, Y., Guan, W., Cao, J., Zhu, R., & Wang, S. (2013). Review:
Traumatic brain injury and hyperglycemia, a potentially modifiable risk
factor. Oncotarget, 7(43), 71052–71061. doi:10.18632/oncotarget.11958
Sciencedirect.com. (2019). Cerebral Perfusion Pressure - an overview | ScienceDirect Topics.
Retrieved from https://www.sciencedirect.com/topics/agricultural-and-biological-
sciences/cerebral-perfusion-pressure
Seunggu Han, M. (2019). Increased intracranial pressure (ICP): Symptoms, causes, and
treatment. Retrieved from https://www.medicalnewstoday.com/articles/324165.php
Shi, J., Dong, B., Mao, Y., Guan, W., Cao, J., Zhu, R., & Wang, S. (2013). Review:
Traumatic brain injury and hyperglycemia, a potentially modifiable risk
factor. Oncotarget, 7(43), 71052–71061. doi:10.18632/oncotarget.11958
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