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Problem-Solving Approach for Patient with Raised Intracranial Pressures

Info: 4167 words (17 pages) Reflective Nursing Essay
Published: 3rd Dec 2020

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This reflection is based on a 40-year-old, designated by S., admitted to the Intensive Care Unit (ICU) for management of traumatic brain injury (TBI). S. had fallen from a flight of stairs and after taken to the emergency department, she dropped her Glasgow Coma Scale from 15 to 7 (E2, V1, M4). She was then intubated and mechanically ventilated and taken to computed tomographic (CT) scan and angiogram. Their results revealed contusions and a subdural haematoma affecting the right frontal and temporal lobe. Considering this, S. was taken to the operating theatres for emergency hematoma evacuation and insertion of an ICP bolt. S. was admitted to the critical care setting for neuroprotective management.

I took over S. care on the first 48 hours of admission. During my shift, a sudden raise in ICP was noted from a pattern of 5-14 mmHg. No changes to care or stimulus have been provoked.

John’s (1993) model of reflection is used through this case study where possible alternative actions and implications for practice are also considered.

On assessment, the following was found:


Arterial Blood Gas (ABG)

Heart rate: 115 beats/minute

pH: 7.31

Blood pressure: 110/54mmHg (MAP: 73mmHg)

Supported with noradrenaline  (0.1 mcg/kg/min)

CVP: 5 mmHg

pCO2: 6.5kPa

SpO2: 98%

pO2: 12.2kPa

Temperature: 36.3

HCO3: 22

ICP: 38mmHg     CPP: 35mmHg

BE: -3.2

Pupils: Size 4, equal and reactive to light

Lactate: 2.2

RASS: -4, sedated with maximum dose of Propofol and fentanyl for weight


Ventilated on Bilevel (Ideal TV: 420ml)


Pinsp: 14     PS: 14


PEEP: 10


FiO2: 0.40


Respiratory rate: 22


Peak pressure: 21


TV: 360ml      MV: 9.3/minute



ICP is defined as the cerebrospinal fluid (CSF) pressure within the ventricles and its monitoring is advocated for the management of severe head injury although its use is increasing also for subarachnoid haemorrhage and for postoperative control after several neurosurgical procedures (Stocchetti et al, 2003). Raised ICP contributes to reduced cerebral blood flow (CBF), derangement of cerebral metabolism and cerebral ischemic deficits leading to secondary brain injury (Lv et al, 2015) also associated with oxygen supply / demand imbalance and ultimately disrupt normal cellular function as described by Hallman and Joffe (2013).

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Current treatment is directed at reducing ICP and achieving optimal levels for cerebral perfusion pressure (CPP) so the primary aim of this ICP/CPP directed therapy to limit further damage to brain tissue (Mestecky, 2011) and improve cerebral oxygenation (Orliaguet et al., 2008). CPP is the driving force for delivery of blood to the brain and therefore a marker of adequacy of cerebral circulation (Adam et al., 2017) and it can be calculated by the difference of mean arterial pressure (MAP) minus the ICP.

According to current guidelines from Brain Trauma Foundation (BTF) (2017), it is recommended placement of an ICP monitor in all salvageable patients with a GCS score of 3 to 8 and an abnormal CT scan, treatment of ICP >22 mmHg and maintenance of  CPP of 50 to 70 mmHg, depending on the status of cerebral autoregulation. It is now well established that CPP<50mmHg results in ischaemia (Mestecky, 2011) and that raised ICPs is strongly associated with increased morbidity and mortality (Adam et al., 2017).

As the ICPs of my patient started to rise to undesirable values, I assessed its possible causes. The initial evaluation was to verify the head rotation and neck flexion. These are factors associated with increased ICP, decreased jugular venous return and localised changes in CBF (Adam et al, 2017).  Another non-invasive physical intervention is head bed elevation performed with the intention of improving venous return and CSF distribution to the subarachnoid space (Fan 2004; Magnaes 1978 cited by Alarcon et al., 2017). On the other hand, head elevation greater than 30° has been observed to decrease systemic arterial pressure, cardiac output, central venous pressure and CPP suggesting detrimental effects on cerebral perfusion (Hung et al., 2000). Nevertheless, a more recent Cochrane review suggests that the optimum angle of the head-of-bed elevation needs to be decided individually after an analysis of the response of ICP, CPP and CBF in each backrest position. This relationship may need to be analysed daily, keeping in mind what clinical goal is desirable (decrease of ICP or maintenance/increase in CPP) for each person (Alarcon et al, 2017). The patient showed a neutral head and neck positioning with no signs of flexion and the head of bed was elevated to 300. The tube ties were not exerting pressure so therefore I continued with the assessment.

I have then evaluated the patient’s pupillary response as this remains a fundamental part of the patient neurological testing. Dilated pupils, having a sluggish or no reaction to light may indicate dysfunction of the III cranial nerve (oculomotor) due to tentorial or tonsillar herniation and brain stem compression in which ipsilateral dilation of the pupils may occur (Mcgloin and Mcleod, 2010). The Neurological Pupil index, which requires an automated pupilometer to assess pupil size and reactivity, is other method which does not require specialized skills to perform or interpret the findings, and may add additional objectivity to the clinical examination as the degree of pupil reactivity was associated with ICPs, with less reactivity corresponding to higher ICPs as demonstrated by Chen et al.(2011). S.’s pupils were equal in size and reactive to light indicating the preservation of the III cranial nerves and no brain stem compression.

As stated by Spitzfaden et al. (1999), control of agitation and excessive patient movement are key components in the management of ICP so as my patients ICP rose, it was important to access the sedation provided. S. was sedated with propofol and fentanyl, both at maximum dose for her weight. According to Kotani (2018), propofol has been reported to have many pharmacological effects: it reduces CBF, cerebral metabolic rate, and ICP, inhibits glutamate receptors and it reduces ischemic neuronal injury. Fentanyl is administered to limit pain, facilitate mechanical ventilation and potentiate the effect of sedation (Adam et al, 2017) decreasing brain metabolism and ICP. After assessing her sedation through the Richmond Agitation Sedation Scale (RASS), it has been made clear the rise in ICP would not be likely provoked by inefficiency of sedation as shown by the score of -4 (deeply sedated).

I have also considered my patients temperature. Hyperthermia has been associated with increased ICP (Elf et al., 2018) and ICP rises 3–4 mmHg for every 1o Celsius of temperature elevation as stated by Cooper and Golfinos (2000), cited by Elf et al., (2008). For the same increase in temperature cerebral metabolic requirements increase by 10% (Mcgloin and Mcleod, 2010). Cooling methods such as paracetamol and cooling blankets should be started to reduce any temperature above 37 o Celsius (Grande (2006), cited by Mcgloin and Mcleod (2010). However, S.’s temperature was 36.3o Celsius and therefore not originating the rise in ICP.

Another aspect took in consideration with the rise in ICP was the decrease in CPP to 38mmHg. My patient was in the hypoperfusion phase (72hours post injury) meaning CBF is reduced by both extrinsic and intrinsic factors resulting in global and regional ischaemia. Pressure autoregulation is impaired due to deranged myogenic responses making CBF pressure passive which can lead to cytotoxic oedema so cerebral perfusion should be protected as suggested by Mcgloin and Mcleod (2010). This protection will occur by maintaining CPP≥70 mmHg as suggested by Myburgh (2003), cited by Mcgloin and Mcleod (2010) and in view of this the rate of noradrenaline was increased to meet the desired targets and normovolaemia corrected.

At the time of these interventions, the result of an arterial blood gas became available for the patient as shown on the descriptive part of this case study.

I noted the PaO2 was within range. Hypoxaemia is associated with poorer outcomes: when the oxygen content of the blood falls, the cerebral blood flow increases in an effort to maintain cerebral oxygenation (Mcleod, 2006).

There was a significant respiratory acidosis due to hypercapnia and this was likely the cause of raised ICP. Adam et al., (2017) state carbon dioxide is a potent regulator of CBF and its response to changes in PaCO2 is dramatic. Hypercapnia will increase CBF and cerebral blood volume causing vasodilation and inverse occurs with hypocapnia contributing in changes to ICP. NICE (2007), cited by Mcgloin and Mcleod (2010), recommends the pCO2 should be maintained at 4.5-5 kPa in accordance with the parameters set by the unit where patient care took place. An increase in the respiratory rate was made to manage hypercapnia. The patient’s minute volume (tidal volume x respiratory rate) was increased and therefore so the carbon dioxide excretion. Minutes after this intervention, a drop in S.’s ICP was noted to 15 mmHg.


In view of the control of pCO2, the mode of ventilation chosen has a significant importance. It should allow a better control of the expired minute volume as it is what controls the expired pCO2 as stated by Mcgloin and Mcleod (2017). If the intervention performed would not be sufficient, I would suggest a change in the ventilation mode to volume cycled mode reflecting this could lead to raised intrathoracic pressures and reduced the cardiac output (Macleod, 2006) and subsequently the CPP.

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I could also suggest hyperventilating the patient. Hyperventilation induced arterial hypocapnia (HV) has been used for decades in in the management of patients with elevated intracranial pressure (ICP) as stated by Brandi et al. (2019) although nowadays it should only be used as temporary measure as it can develop iatrogenic cerebral oedema (BTF (2007), cited by Mcgloin and Mcleod, 2010). Increased alveolar ventilation induces a dose-response decrease in arterial partial pressure of carbon dioxide (PaCO2), resulting in vasoconstriction of the cerebral arterioles and consequently, CBF, volume and ICP decrease. (Brandi et al, 2019). Hyperventilation should be avoided during the first 24 h after injury when CBF often is reduced critically (Carney et al., 2017).

If there was still a rise in ICPs although the management was optimal, the team could consider administering mannitol or hypertonic solutions as these fluids will increase the osmolality of blood and create an osmotic gradient so water is drawn from the brain to the blood reducing ICP (Mcgloin and Mcleod, 2010).

A barbituric coma may be induced to control raised ICP in severe TBI as it reduces brain metabolic demands although its use is reserved for refractory intracranial hypertension unresponsive to medical management as noted by Adam et al. (2017).

Seizures will result in an increase in CBF which could further increase ICP so prophylactic anti - epileptic drugs (AEDs) may be used in the short term following TBI (BTF, 2007). If seizure activity occurs, rapid control is required to prevent ischaemic damage which can rapidly increase metabolic demands of the brain (Mestecky, 2011).


The goals of management for raised intracranial pressure are to protect the brain from further insult by maintaining optimal cerebral perfusion pressure and reducing ICP. This case study has highlighted many of the aspects involved in managing ICP in a TBI patient. Care of these patients should be timely, well-coordinated and incorporate a vast knowledge of intracranial physiology associated with the best evidence-based included in recent guidelines. Nursing interventions should rationalize and prioritise care in order to prevent the risks of cerebral ischemia and further insult. I will advocate and institute appropriate management of this group of patients, detect early complications of care and make decisions on individual patient basis and be able to justify those decisions in light of evidence based care. Overall, this case study has equipped me with necessary knowledge and skills to respond and manage changes in the context of raised ICPs.


Adam, S., Osborne, S., Welch, J. (2017) Critical Care Nursing Science and Practice. Oxford: Oxford University Press.

Alarcon, Jose D et al. “Elevation of the head during intensive care management in people with severe traumatic brain injury.” The Cochrane database of systematic reviews vol. 12,12 CD009986. 28 Dec. 2017, doi:10.1002/14651858.CD009986.pub2

Brandi, G. et al. (2019) ‘Cerebral metabolism is not affected by moderate hyperventilation in patients with traumatic brain injury’, Critical Care, 23(1), pp. 1–7. Available at: http://0-search.ebscohost.com.wam.city.ac.uk/login.aspx?direct=true&db=eoah&AN=48473640&site=ehost-live (Accessed: 21 December 2019).

Carney, N. et al. (2017) ‘Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition’, Neurosurgery, 80(1), pp. 6–15. doi: 10.1227/NEU.0000000000001432.

Chen, J. W. et al. (2011) ‘Pupillary reactivity as an early indicator of increased intracranial pressure: The introduction of the Neurological Pupil index’, Surgical Neurology International, 2, p. 82. doi: 10.4103/2152-7806.82248.

Elf, K. et al. (2008) ‘Temperature disturbances in traumatic brain injury: relationship to secondary insults, barbiturate treatment and outcome’, Neurological Research, 30(10), pp. 1097–1105. doi: 10.1179/174313208X319125.

Hallman, M. and Joffe, A. (2013) ‘ICU Management of Traumatic Brain Injury’, Current Anesthesiology Reports, 3(2), pp. 89–97. Available at: http://0-search.ebscohost.com.wam.city.ac.uk/login.aspx?direct=true&db=eoah&AN=30286673&site=ehost-live (Accessed: 22 December 2019).

Hung, O. R., Hare, G. M. and Brien, S. (2000) ‘Head elevation reduces head-rotation associated increased ICP in patients with intracranial tumours’, Canadian Journal Of Anaesthesia = Journal Canadien D’anesthesie, 47(5), pp. 415–420. Available at: http://0-search.ebscohost.com.wam.city.ac.uk/login.aspx?direct=true&db=mdc&AN=10831197&site=ehost-live (Accessed: 22 December 2019).

Kim, J. Y., & Bae, H. J. (2017). Spontaneous Intracerebral Hemorrhage: Management. Journal of stroke19(1), 28–39. doi:10.5853/jos.2016.01935

Kotani, Y. et al. (2008) ‘The Experimental and Clinical Pharmacology of Propofol, an Anesthetic Agent with Neuroprotective Properties’, CNS Neuroscience & Therapeutics, 14(2), pp. 95–106. doi: 10.1111/j.1527-3458.2008.00043.x.

Lv, Y. et al. (2015) ‘Clinical observation of the time course of raised intracranial pressure after subarachnoid hemorrhage’, Neurological Sciences, 36(7), pp. 1203–1210. doi: 10.1007/s10072-015-2073-9.

McLeod, A. (2006) ‘Mechanical ventilation for raised intracranial pressure in the patient with cerebral insult’, British Journal of Neuroscience Nursing, 2(7), pp. 338–344. doi: 10.12968/bjnn.2006.2.7.21819.

Mestecky, A. (2011) Assessment and Management of Raised Intracranial Pressure In: Woodward, S. and Mestecky, A. (eds.) Neuroscience Nursing: Evidence-Based Practice. 1 st ed. Chichester: Blackwell Publishing.

Orliaguet, G. et al. (2008) ‘Management of critically ill children with traumatic brain injury’, Pediatric Anesthesia, 18(6), pp. 455–461. Available at: http://0-search.ebscohost.com.wam.city.ac.uk/login.aspx?direct=true&db=eoah&AN=14179758&site=ehost-live (Accessed: 21 December 2019).

Spitzfaden, A. C., Jimenez, D. F. and Tobias, J. D. (1999) ‘Propofol for Sedation and Control of Intracranial Pressure in Children’, Pediatric Neurosurgery, 31(4), pp. 194–200. Available at:http://0search.ebscohost.com.wam.city.ac.uk/login.aspx?direct=true&db=eoah&AN=30997973&site=ehost-live (Accessed: 22 December 2019).

Stocchetti, N. et al. (2003) ‘Head injury, subarachnoid haemorrhage and intracranial pressure monitoring in Italy’, Acta Neurochirurgica, 145(9), pp. 761–765. doi: 10.1007/s00701-003-0092-4.


According to the Brain Trauma Foundation (2017), Traumatic brain injury (TBI) is associated with elevated ICP, primarily as a result of cerebral oedema, and can lead to a decrease of cerebral blood flow and brain stem herniation, and is the most common cause of death and disability after severe TBI.

Adam at al. (2017) state patients who do not have an operable lesion but who have progressive intracranial hypertension that is unresponsive to standard medical management should be consider for decompressive craniectomy to lower ICP.

The rationale for decompressive craniectomy (DC) for cases experiencing increased ICP, is to allow for the oedematous brain tissue to herniate outwards, avoiding compression of vital brain structures thus acting as a possible life-saving intervention (Moussa and Khedr, 2017), The technical aspects of DC involve removing a section of skull and opening the underlying dura. The bone flap is placed into the patient’s abdominal subcutaneous space or in a tissue bank and the cranium is later reconstructed, weeks to months later. (Khan et al.,2017).

DC can reduce ICP and increase CPP, but its use and timing remain controversial as stated by Kolias et al. (2013), cited by Wang et al. (2015).  DC has generally been used as a last resort to control ICP when medical therapies failed, is at the discretion of the neurosurgeon and involves multiple factors. DC remains a highly-debated topic and the 21th century is marked by efforts to gather the evidenced-based indications, optimal time and effects of DC following TBI (Kolias et al. 2013, Carney et al., 2016).

According to the evidence available, there are two main RCT (Randomised Controlled Trials) that provide an overview of DC following TBI: The DECRA (Decompressive Craniectomy in Patients with Severe Traumatic Brain Injury) trial performed from 2002 to 2010 in Australia, New Zealand and Australia and it recruited 155 patients; The RESCUEicp (Randomised Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intracranial Pressure) which enrolled 408 patients from 2004 to 2014 and was performed to assess the effectiveness of craniectomy as a last-tier intervention in patients with TBI and refractory intracranial hypertension.

Although both trials access the use of DC for high ICPs there are a few diffrences to note. The DECRA trial aimed to assess the effectiveness of early craniectomy — offered as a stage 2 treatment within 72 hours after injury — for moderate intracranial hypertension (intracranial pressure, >20 mm Hg for 15 minutes within a 1-hour period [continuous or cumulative]) in patients with diffuse TBI. The RESCUEicp trial aimed to assess the effectiveness of decompressive craniectomy offered as a last-tier treatment. In the DECRA trial, adults with severe diffuse TBI and intracranial hypertension refractory to first-tier medical management were randomized to receive either standard care or bifrontotemporoparietal DC.  Wang et al., (2015) meta- analysis showed patients in the DC group had shorter duration with ICP above the treatment threshold, fewer interventions needed to reduce ICP, and fewer days in the intensive care unit; the DC group had worse extended GOS scores (95% CI, p = 0.03), and a greater risk of an unfavourable outcome (95% CI , p = 0.02). Rates of death at 6 months were similar in the DC (19%) and standard-care groups (18%).  The DECRA authors concluded that DC lead to lower ICPs and shorter ICU stays, but also to an increased rate of unfavourable outcomes, specifically, they found that those undergoing DC were more likely to be severely disabled, in a vegetative state, or dead (Khan et al,2017)

In conclusion, at 6 months, decompressive craniectomy for severe and refractory intracranial hypertension after TBI resulted in mortality that was 22 percentage points lower than that with medical management. Surgery also was associated with higher rates of vegetative state, lower severe disability, and upper severe disability than medical management. The rates of moderate disability and good recovery with surgery were similar to those with medical management.

Two recent trials have led to mixed, or even conflicting, results. One concluded that patients undergoing DC had a higher rate of adverse outcomes despite shorter intensive care unit (ICU) stays and lower ICPs. The other found that patients undergoing DC had a lower mortality, had a higher rate of favourable functional outcomes but were more likely to be in a vegetative state.

In view of the currently available evidence, and owing to the number of potential complications with DC, indiscriminate use of DC for patients with TBI is not appropriate.


More investigation is needed before a true set of prognostic factors can be established and the question of the utility of DC has not been adequately answered.

Moussa, WMM & Khedr, W 2017, ‘Decompressive craniectomy and expansive duraplasty with evacuation of hypertensive intracerebral hematoma, a randomized controlled trial’, Neurosurgical Review, vol. 40, no. 1, pp. 115–127, viewed 30 December 2019, .

Brain Trauma Foundation Guidelines for the management of severe traumatic brain injury. J Neurotrauma. 2007;24 (Suppl 1):1–106.

Wang et al. (2015) ‘Outcomes of Early Decompressive Craniectomy Versus Conventional Medical Management After Severe Traumatic Brain Injury: A Systematic Review and Meta-Analysis’, Medicine, 94(43), pp. 1–9. doi: 10.1097/MD.0000000000001733.

Cooper, D. J. et al. (2011) ‘Decompressive craniectomy in diffuse traumatic brain injury’, The New England Journal of Medicine, 364(16), pp. 1493–1502. doi: 10.1056/NEJMoa1102077.

Rush, B. et al. (2016) ‘Craniotomy Versus Craniectomy for Acute Traumatic Subdural Hematoma in the United States: A National Retrospective Cohort Analysis’, World Neurosurgery, 88, pp. 25–31. doi: 10.1016/j.wneu.2015.12.034.

Khan, A. D. et al. (2017) ‘Indicators of Survival and Favorable Functional Outcomes after Decompressive Craniectomy: A Multi-Institutional Retrospective Study’, The American Surgeon, 83(8), pp. 836–841. Available at: http://0-search.ebscohost.com.wam.city.ac.uk/login.aspx?direct=true&db=mdc&AN=28822387&site=ehost-live (Accessed: 1 January 2020).


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