Blood, number of things, these can be: either
Blood, cerebrospinal fluid (CSF) and brain tissue are all constituents of the cranium. The pressure within the cranium is known as intracranial pressure (ICP); it is the same as that found in the brain tissue and CSF. (2) The pressure-volume relationship between ICP, brain tissue, blood, volume of CSF, and cerebral perfusion pressure (CPP) is known as the Monro-Kellie hypothesis. 12) This hypothesis states that the cranial compartment is considered as an enclosed and inelastic container, which has a fixed volume; if an increase of any one of the components occurs, it must be accompanied with a decrease in another in order to maintain a state of equilibrium, if this does not occur it will eventually lead to an increase in ICP. (13) The normal values for ICP are dependent on the age of the patient, their body posture and clinical conditions. In adults normal range is considered 40mm Hg. 7) ICP hypertension can be caused by a number of things, these can be: either intracranial (primary) – brain tumour, trauma, non-traumatic intracerebral haemorrhage, ischemic stroke or hydrocephalus.
Or it may be extracranial (secondary) – airway obstruction, hypoxia, hypertension, seizures, posture, drug intoxication, or it may be postoperative- mass lesions, increased cerebral volume or disturbances of CSF. (14) ICP hypertension signs and symptoms vary relying on etiology.Common symptoms that suggest a rise in ICP include headache, nausea, vomiting, ocular palsies, back pain, progressive mental status decline and papilledema. (17) In regards to the boy in our case study, it is clear that he most probably has elevated ICP due to traumatic brain injury (TBI)- which is a primary cause of elevated ICP; this is evident from the symptoms that he was experiencing. In order to get a definitive diagnosis it is crucial that further tests be carried out. Sustained elevated levels of ICP will lead to reduced cerebral blood flow and hence brain herniation.
Pressure will arise from the herniation, causing brain injury and may possibly lead to death. (17) Hence, it is vital to identify patients with elevated ICP. ICP monitoring may be crucial in some patients, but care should be taken as it is an invasive technique and may cause unwanted risks. Therefore monitoring should only be used in patients that will benefit from it; these include patients with severe TBI with a Glasgow Coma Scale (GCS) < 8, post craniotomy, hematomas, abscesses or tumours that occlude the CSF pathway, intracranial hemmorrhage, cerebral oedema, encephalopathy from ypertensivecrisis, and meningitis/encephalitis that causes malabsorption of CSF. (9) Utilisation of an ICP monitoring device is important in the above mentioned patients; it is also the only way to reliably diagnose a patient with an elevated ICP.
The three devices used to monitor ICP include: • The subarachnoid screw- which is a hollow screw that is inserted into the Dura matter through a hole drilled in the skull; the screw is connected to an external traducer via tubing.CSF fills the screw and allows the sensor to record from within the subdural space. Advantages of this method include the decreased risk of infection and haemorrhage, and the disadvantages include misplacement of the screw, errors in ICP readings leading to underestimation and occlusion by debris. (11) • The Subdural/Epidural Catheter- which is inserted between the skull and dural tissue. The epidural sensor is placed through a burr hole drilled in the skull.
It is less invasive but also less accurate and can’t be used to drain CSF; it also has a lower risk of infection or hemorrhage (19). • Ventriculostomy which is the most commonly used device and also the most accurate way to receive and monitor ICP. (19). A burr hole is drilled into the lateral ventricle of the brain (which contains CSF) and a catheter is inserted. This catheter is connected to a standard transducer set which is never pressurized. In addition to monitoring ICP the ventriculostomy is also used for the therapeutic drainage of CSF.Generally, the catheter stays within the patient for two weeks, but the length of time varies depending on the patients condition, it must be noted that the longer the dwelling time within a patient, the greater the increase in risk factors.
(10) A disadvantage of using a ventriculostomy to monitor ICP is that debris, such as tissue fragments or blood clots can lead to obstruction of the catheter; this will lead to inaccurate ICP monitoring and alteration in CSF drainage. 8) Another disadvantage is the increase in the risk of infection and an associated risk of bleeding due to the fact that ventriculostomy is such an invasive technique. (9). In addition to the above complications, other unwanted risks may include CSF leakage, over drainage of CSF which may result in ventricular collapse and herniation, and air leakage into the subarachnoid space or ventricle (14) The goals of ICP therapy include: (15) • Maintaining ICP at < 20-25 mm Hg • Maintain cerebral perfusion pressure between 60 and 75 mm Hg • Avoid factors that lead to elevated ICP.Treatments of elevated ICP include: • Positioning of bed head- Elevating the head of the bed to 30 degrees will lead to a decrease in jugular venous outflow pressure and hence will decrease ICP. Care must be taken in patients who are hypovolemic or hypotensive, due to the fact that it may be associated with a decrease in blood pressure and an overall decrease in CPP. (2) • Hyperventilation- Carbon dioxide dilates the cerebral blood vessels which leads to an increase in the volume of blood in the intracranial vault consequently increasing ICP.
Hence, decreasing the PCO2 will lead to vasoconstriction which in turn leads to a decrease in intracranial volume resulting in a decrease in ICP. (6) Consequences of hyperventilation include a reduction in cerebral blood flow which results in increased risk for ischemic injury. For this reason hyperventilation should only be used when necessary and for a short period, ensuring that PCO2 doesn’t fall below 30mm Hg. (16) • Oxygenation- oxygen saturation should be kept at about 95% in order to keep the brain well oxygenated and prevent ischemia. 18) • Intravenous fluids- patients with elevated ICP should be kept normovolaemic with the use of hypertonic or isotonic IV fluids including: normal saline, lactated ringers and albumin. (4) • Osmotic diuretics- Mannitol is used to remove extra cellular fluid by creating an osmotic gradient across the capillary gradient; it decreases blood viscosity and is only used temporarily until surgery can be performed.
Mannitol use leads to an increase in urine output and systemic acidosis. (13) Serum osmolality should be kept below 320 mOsm/kg otherwise it will lead to acute renal failure.Other osmotic diuretics that have been used include hypertonic saline. (4) • Steroids- e. g.
dexamethasone, are used to decrease inflammation and oedema, it not used in TBI, usually reserved for use in patients with intracranial tumours. (5) • Anti-convulsants- are used to decrease patients probability of having a seizure, should use high doses as sub-therapeutic levels do not protect a patient from having seizures; close monitoring for therapeutic drug levels should be performed to decrease toxicity . 2) • Hypothermia- the aim is to lower bladder temperature to 35-36 degrees for 48 hours following trauma or haemorrhage as this will lead to decrease in overall metabolic demand and hence decrease in ICP.
Shivering is controlled with use of desflurane and pethidine. (1) • Barbiturate coma- this is only used when other measures have failed; when patient is in a barbiturate coma, the rate of the body’s metabolic process, oxygen consumption and CO2 production is lowered hence lowering ICP. (3) • Sedatives- propofol is commonly used because of its short half life, benzodiazepines are also used.Sedating patients will lead to decrease in metabolic rate and hence decrease in ICP. (1) • Drainage- Ventriculostomy is used to drain CSF through the ventricles and is considered to be gold standard treatment in elevated ICP. (10) • Decompressive craniectomy- is used when conventional medical therapy has failed; this operation expands the dura with a graft and increases the volume available for brain swelling by removal of a large bone flap from the cranium, hence leading to an overall decrease in ICP.
3) According to our case study, the best treatment approach for our patient will be by making sure he is well hydrated, his bed should be elevated to 30 degrees hyperventilation should be avoided and osmotic diuretics should be used. He most probably will not require barbiturates or craniectomy procedure. Some therapies that may be employed in the near future include: Ketamine, Tris-hydroxymethyl-aminomethane, Etomidate and Lobectomy/ removal of contusion but all require further studies to determine their future role as a definitive treatment for intracranial hypertension.
1,16) Case summary: Our case study was about a 6 year old child who weighed 45 kg. He ran into a goal post while playing football with his siblings; on impact he shook his head and walked away, then collapsed when he reached his mother. When he was brought into the emergency department it was found that he had a contusion on his head, but the skin wasn’t broken or bruised, he had lost consciousness for about 5 minutes and when he woke up was confused and couldn’t remember anything, he felt very irritated and wanted to be with his mother.On examination, it was found that his electrolytes and renal function were normal, but he had a slight increase in ALT and GGT, which may indicate some mild, sub-clinical liver dysfunction. The Glasgow Coma Scale (GCS) was used in order to determine his level of consciousness, this was found to be 10- meaning that it was moderate; but since he has alteration in GCS and he is under 16 years old, it is crucial that a CT or MRI are performed; will expect to find a hematoma. U & E’s should be repeated over time to monitor for changes in liver and we also need to screen for toxins and drugs to see if they are the cause.References: 1.
Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical anagement of severe traumatic brain injury in infants, children, and adolescents. Chapter 16. The use of corticosteroids in the treatment of severe pediatric traumatic brain injury. Pediatr Crit Care Med 2003;4:S60-4.
2. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, et al: Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring.
J Neurotrauma 2007; 24: 37-44 3.Bullock R, Chesnut RM, Clifton G, et al. Guidelines for the management of severe traumatic brain injury.
J Neurotrauma 2000; 17:451-553. 4. Doorman, H. , Sondheimer, J. , & Cadnapaphornchai, P. Mannitol-induced acute renal failure. Medicine,1990;69:153.
5. Fanconi S, Kloti J, Meuli M, et al. Dexamethasone therapy and endogenous cortisol production in severe pediatric head injury. Intens Care Med 1988;14:163-6.
6. Figaji AA, Zwane E, Thompson C, et al. Brain tissue oxygen tension monitoring in pediatric severe traumatic brain injury: Part 1:Relationship with outcome.
Childs Nervous System. 2009; 25: 1325-1333 7. Lang, E.
, & Chestnut, R. Intracranial pressure and cerebral perfusion pressure in severe head injury. New Horizon. 1995; 3: 400-409. 8.
Lavin, P. Management of hypertension in patients with acute stroke. Archives of Internal Medicine, 1986;146: 66. 9. Lozier AP, Sciacca RR, Romanoli M et al. Ventriculostomy-related infection: a critical review of the literature. Neurosurgery 2002; 51: 170–182.
10. Mayhall, C. , Archer, N. , & Lamb, V. , et. Al. Ventriculostomy-related infections.
A prospective epidemiologic study. New England Journal of Medicine, 1984;310:9: 553-559. 11. Miller, J. , Bobo, H. , & Kapp, J.
Inaccurate Pressure Readings From Subarachnoid Bolts. Neurosurgery, 1986;19:2: 253-250. 12. Mokri B, The Monro-Kellie hypothesis: applications in CSF volume depletion. Neurology. 2001;56 12: 1746–8. 13.
Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg1991;75:731–9.
14. National Institute of Health. 2000). Intracranial Pressure Monitoring.
Warren G. Magnuson Clinical Center. Retrieved 22/10/2011 http://clinicalcenter. nih.
gov/ccmd/pdf_doc/Clinical%20Monitoring/04-Intracranial%20Pressure%20Mo. pdf/ 15. NSG. (2003). Breif Summary of Traumatic Brain Injury.
National Guideline Clearinghouse. Retrieved 22/10/2011from: http://www. guideline. gov/summary/summary.
aspx? ss=15&doc_id=3794&nbr=3020#s23 16. Raichle ME, Posner JB, Plum F: Cerebral blood flow during and after hyperventilation. Arch Neurol 23:394-403,1970 17.
Saatman KE, Duhaime AC, Bullock R, et al. Classification of traumatic brain injury for targeted therapies. J Neurotrauma 2008; 25: 719-738. 18. Zwane E, Fieggen AG, et al. Pressure auto regulation, intracranial pressure, and brain tissue oxygenation in children with severe traumatic brain injury. J Neurosurg Pediatr 2009;4: 420-428.
19. Zhong, J. (2003). Advances in ICP Monitoring Techniques. Maney Publishing.
Retrieved 21/10/2011from http://www. ingentaconnect. com/content/maney/nres/2003/00000025/00000004/art00005picpicpic