Monitoring and interpretation of intracranial pressure

M Czosnyka; J D Pickard

doi:10.1136/jnnp.2003.033126

Responses

Neuroscience for neurologists

Monitoring and interpretation of intracranial pressure

Compose a Response to This Article

Compose Response

Title *

Author Information

Contributors
First Name and Middle Initial * First or given name, e.g. 'Peter'. Last Name * Your last, or family, name, e.g. 'MacMoody'. Email Address * Your email address, e.g. higgs-boson@gmail.com Occupation * Your role and/or occupation, e.g. 'Orthopedic Surgeon'. Affiliation * Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.

Statement of Competing Interests

Competing interests? *

Yes

Please describe the competing interests

PLEASE NOTE:

A rapid response is a moderated but not peer reviewed online response to a published article in a BMJ journal; it will not receive a DOI and will not be indexed unless it is also republished as a Letter, Correspondence or as other content. Find out more about rapid responses.
We intend to post all responses which are approved by the Editor, within 14 days (BMJ Journals) or 24 hours (The BMJ), however timeframes cannot be guaranteed. Responses must comply with our requirements and should contribute substantially to the topic, but it is at our absolute discretion whether we publish a response, and we reserve the right to edit or remove responses before and after publication and also republish some or all in other BMJ publications, including third party local editions in other countries and languages
Our requirements are stated in our rapid response terms and conditions and must be read. These include ensuring that: i) you do not include any illustrative content including tables and graphs, ii) you do not include any information that includes specifics about any patients,iii) you do not include any original data, unless it has already been published in a peer reviewed journal and you have included a reference, iv) your response is lawful, not defamatory, original and accurate, v) you declare any competing interests, vi) you understand that your name and other personal details set out in our rapid response terms and conditions will be published with any responses we publish and vii) you understand that once a response is published, we may continue to publish your response and/or edit or remove it in the future.
By submitting this rapid response you are agreeing to our terms and conditions for rapid responses and understand that your personal data will be processed in accordance with those terms and our privacy notice.

I agree to and have read the terms and conditions for rapid responses and BMJ Privacy Notice *

CAPTCHA

This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.

Vertical Tabs

Other responses

Jump to comment:

Intracranial metabolic monitoring: why is it not being exploited?
Richard G Fiddian-Green
Published on: 13 April 2016
ICP and cerebral oedema at high altitude.
Richard G Fiddian-Green
Published on: 13 April 2016
Might intracranial pressure be a passive reflection of intracranial pH?
Richard G Fiddian-Green
Published on: 13 April 2016

Published on: 13 April 2016
Intracranial metabolic monitoring: why is it not being exploited?
- Richard G Fiddian-Green, FRCS, FACS
Dear Editor
This review confirms that ICP monitoring provides no information about intracerebral tissue energetiics except by inference in extremis.[1]
This informtion is vital if the management of the disorders listed in this review and many others is to be significantly improved beyond optimal care today. There is an opportunity to obtain this information in conjunction with the ICP with the same ease and...
Show More

Dear Editor
This review confirms that ICP monitoring provides no information about intracerebral tissue energetiics except by inference in extremis.[1]
This informtion is vital if the management of the disorders listed in this review and many others is to be significantly improved beyond optimal care today. There is an opportunity to obtain this information in conjunction with the ICP with the same ease and risks. The opportunity is readily available but, despite the relevant parties in the US having been informed of these opportunities more than 10 years ago, has been exploited in ways that raise significant questions about the quality of the data obtained. This would seem to be because of a lack of appreciation of the relevant technical considerations and metabolic determinants of cellular dysfunction, apoptosis and necrosis.
Further information may be obtained from a review I had published on a popular Canadian medical website last year.[2] My insight into the relevant issues has been refined considerably since then [3] and will no doubt continue to be refined.
References
1. M Czosnyka and J D Pickard Monitoring and interpretation of intracranial pressure J Neurol Neurosurg Psychiatry 2004; 75: 813-821
2. www.redflagsweekly.com/conferences/damaged_brains/ oct05_Fiddian_3.html 12k
3. Fiddian-Green TG. Rapid responses to: Vipin Zamvar, David Williams, Judith Hall, Nicola Payne, Clare Cann, Karen Young, S Karthikeyan, and John Dunne Assessment of neurocognitive impairment after off-pump and on-pump techniques for coronary artery bypass graft surgery: prospective randomised controlled trial BMJ 2002; 325: 1268
Show Less

Conflict of Interest:
None declared.
- Back to top
Published on: 13 April 2016
ICP and cerebral oedema at high altitude.
- Richard G Fiddian-Green, FRCS, FACS
Dear Editor,
In my earlier eLetter I wrote, "Increasing blood flow to the brain by increasing pCO2 may do much more metabolic harm than good. Indeed in upregulating oxidative phosphorylation and down regulating ATP-dependent enzymatic activity... keeping the intracerebral pH abnormally low could reduce the need for blood flow to abnormally low levels". Is this statement compatible with the effects of high altitud...
Show More

Dear Editor,
In my earlier eLetter I wrote, "Increasing blood flow to the brain by increasing pCO2 may do much more metabolic harm than good. Indeed in upregulating oxidative phosphorylation and down regulating ATP-dependent enzymatic activity... keeping the intracerebral pH abnormally low could reduce the need for blood flow to abnormally low levels". Is this statement compatible with the effects of high altitude on pH and intracranial pressure? A rise in intracranial pressure caused by acute cerebral oedema is one of the more feared complications of high altitude afflicting climbers.
Acute ascent is accompanied 5 days later by a respiratory alkalosis suggested to have been caused by "a fall in the chemoreflex threshold and .. corrected by an elevation in the concentration of weakly dissociated protein anions" [1]. Bicarbonate was not significantly changed. In another study of blood gases a significant increase in arterial pH from 7.34 to 7.43 (p <0.01) was observed with a prolonged stay at 3500 m that remained significantly increased at 5800 m [2]. The effective renal plasma flow reduced significantly (p <0.01) from 615.6 at sea level (SL) to 381.5 ml x min(-1) x 1.73 m(-2) at 5800 m. Cerebral blood flow (CBF) is also reduced at high altitude.
Chronic changes in CBF was studied by 133Xe inhalation dynamic single photon emission computer tomography in 8 members of a climbing expedition to the Himalayas. "With one exception they had all previously climbed at high altitudes. All stayed above 6,500 m for approximately 3 weeks, and 5 reached the summit of Mt. Everest. One year after the completion of the expedition the average CBF in climbers was still more than 15% lower than in the reference group. The climbers had higher relative CBF increase after injection of the carbonic anhydrase inhibitor acetazolamide [which causes a metabolic acidosis] than the reference subjects" [3].
In 12 subjects, ascending from 150 to 3,475 m, CBF was 24% increased at 24 h [45.1 to 55.9 initial slope index (ISI) units] and 4% increased at 6 days (47.1 ISI units). Increases in CBF were similar in subjects with or without acute mountain sickness (AMS) and acetazolamide-provoked increases of CBF in AMS subjects caused no acute change in symptoms [4]. (Presumably this effect is short-lived and son replaced by a decline in blood flow).
In a randomized, double-blind cross-over study 10 subjects were exposed to a simulated altitude of 4500 m for 10 h after administration of placebo, acetozolamide (250 mg bid) or theophylline (250 mg bid). Almost all subjects showed a decrease in inner cerebrospinal fluid (iCSF) volumes (placebo - 10.3%, P= 0.02; acetazolamide - 13.2%, P= 0.008, theophylline - 12.2%, n.s.). There was no correlation between AMS symptoms and fluid shift [5].
The influence of acetazolamide (ACZ) upon the ability to perform and sustain maximal and submaximal exercise bouts under normoxic and hypoxic conditions was examined in four groups of healthy male subjects (N = 27). ACZ (500 mg) or inert placebo (Pla) was administered prior to exercise in a quasi-randomized, double-blind, crossover fashion. ACZ was shown to lower venous pH (ACZ, 7.31 +/- 0.01, vs Pla, 7.35 +/- 0.08) and bicarbonate (ACZ, 22.4 +/- 0.27 mM, vs Pla, 25.4 +/- 0.6 mM) and to elevate urine pH (ACZ, 7.36 +/- 0.06, vs Pla, 5.84 +/- 0.19).
No significant effect of ACZ upon VO2, VCO2, RER, or heart rate (HR) was observed during submaximal exercise (75% of peak VO2) although VE was increased by 14% and time to exhaustion (EXHt) was reduced by 29%. Prior to exercise, venous pH (ACZ, 7.39 +/- 0.04, vs Pla, 7.44 +/- 0.007) and bicarbonate were lower with ACZ (ACZ, 21.6 +/- 0.46 mM, vs Pla, 24.2 +/- 0.25 mM), while urine pH was higher (ACZ, 7.6 +/- 0.07, vs Pla, 5.9 +/- 0.25). Other than a higher PCO2 (increased ox-phos) and lower venous lactate (decreased anaerobuc glycolysis) with ACZ, no significant differences were identified at peak VO2 [6].
Might then the respiratory alkalosis that develops at high altitude reduce blood flow with prolonged exposure by upregulating oxidative phosporylation and down regulating anaerobic glycolysis, the antithesis of the metabolic effects of acute liver failure [7]? The decline in paCO2 might have achieved this by a mass action on oxidative phosporylation [8]. What then of the benedicial effects of ACZ in AMS? Might the metabolic acidosis it induces have a similar effect on oxidative phosporylation and the symptomatic benefits be due to improved efficiency of ATP resynthesis?
Might then ACZ have reduced the efficiency of oxidative phosporylation by decreasing the availability of lactate normally generated in muscles during exercise for ATP resynthesis by oxidative phosporyation in accordance with the lactate shuttle hypothesis [9] even though ox;phos might have been upregulatd by hypocarbia? What then of the cerebral oedema which may develop at high altitude?
If upregulating oxidative phoporylation decreases the need for cerebral blood flow, as proposed in my earlier Letter, might it also decrease intracraniail pressure by decreasing intracerebral capillary density and hence blood volumes? If so upregulating anaerobic glycolysis could have the opposite effects. (The acute decline in CSF might have been a cytoprotective response to the acute and apparently transient increase in CBF). If so the capacity for cytoprotectve responses mounted to accommodate cellular stesses might also be compromised. Hence the reduced time to exhaustion from exercise caused by ACZ. The critical determinants of cerebral oedema might well be the pathologic changes that might be induced by a critical decline in ability of the liver and other organs to recyle anarobic metabolities from the brain and the conversion of xanthine dehydrogenase to xanthine oxidase with accelerated free radical release [10].
ACZ and supplmentary oxygen at high altitude delivered by face mask might both be double edged swords benefittting climbers by increasing by mass action both the capacity for ATP resynthesis by oxidative phoporylation at rest and the potential for exceeding the anaerobic threshold and generating free radicals during acute rductive stresses such as exercise. It might be safer and more effective for climbers to rely upon physiological acclimatiation to avoid AMS and to deliver supplementary oxygen intraperitoneally via a chronically implanted system should the need ever arise [11]. Viagra, which has become a popular substitute for ACZ, might also be a double-edged sword.
The statement I made in my earlir eLetter appears to be compatible with the effects of high altitude on pH and intracranial pressure.
References
1. Somogyi RB, Preiss D, Vesely A, Fisher JA, Duffin J. Changes in respiratory control after 5 days at altitude. Respir Physiol Neurobiol. 2005 Jan 15;145(1):41-52.
2. Singh MV, Salhan AK, Rawal SB, Tyagi AK, Kumar N, Verma SS, Selvamurthy W. Blood gases, hematology, and renal blood flow during prolonged mountain sojourns at 3500 and 5800 m. Aviat Space Environ Med. 2003 May;74(5):533-6.
3. Rootwelt K, Stokke KT, Nyberg-Hansen R, Russell D, Dybevold S. Reduced cerebral blood flow in high altitude climbers. Scand J Clin Lab Invest Suppl. 1986;184:107-12.
4. Jensen JB, Wright AD, Lassen NA, Harvey TC, Winterborn MH, Raichle ME, Bradwell AR. Cerebral blood flow in acute mountain sickness. J Appl Physiol. 1990 Aug;69(2):430-3.
5. Fischer R, Vollmar C, Thiere M, Born C, Leitl M, Pfluger T, Huber RM. No evidence of cerebral oedema in severe acute mountain sickness. Cephalalgia. 2004 Jan;24(1):66-71.
6. Stager JM, Tucker A, Cordain L, Engebretsen BJ, Brechue WF, Matulich CC. Normoxic and acute hypoxic exercise tolerance in man following acetazolamide. Med Sci Sports Exerc. 1990 Apr;22(2):178-84.
7. Anaerobic glycolysis in acute liver failure Richard G Fiddian-Green (9 March 2005) eLetter re: J G O’Grady Acute liver failure Postgrad Med J 2005; 81: 148-154.
8. pCO2, pH and the regulation of aerobic / anaerobic glycolysis. Richard G Fiddian-Green (15 March 2005) eLetter re: Jerry Yee and Irawan Susanto Sublingual Capnometry : In Search of Its Holy Grail Chest 2000; 118: 894-896.
9. Dienel GA, Cruz NF. Nutrition during brain activation: does cell- to-cell lactate shuttling contribute significantly to sweet and sour food for thought? Neurochem Int. 2004 Jul-Aug;45(2-3):321-51.
10. Is increasing FiO2 above 0.2 always harmful? Richard G Fiddian-Green (23 March 2005) eLetter re: K. S. Khaw, C. C. Wang, W. D. Ngan Kee, C. P. Pang, and M. S. Rogers Effects of high inspired oxygen fraction during elective Caesarean section under spinal anaesthesia on maternal and fetal oxygenation and lipid peroxidation Br. J. Anaesth. 2002; 88: 18-23.
11. Might enteric or intraperitoneal oxygen improve performance? Richard G Fiddian-Green BJSM Online, 29 Jun 2004 eLetter re: G Neumayr, R Pfister, G Mitterbauer, A Maurer, and H Hoertnagl Effect of ultramarathon cycling on the heart rate in elite cyclists Br J Sports Med 2004; 38: 55-59.
Show Less

Conflict of Interest:
None declared.
- Back to top
Published on: 13 April 2016
Might intracranial pressure be a passive reflection of intracranial pH?
- Richard G Fiddian-Green, FRCS, FACS
Dear Editor,
Where does fluid accumulate in intracerebral oedema, extracellulary, intracellularly or both? The distinction is important for it has a direct bearing on treatment of the intracranial compartment syndrome [1].
If the fluid accumulates intracellularly then clamping the intra- arterial pH, using the Radiometer pH-stat automatic titrator or its equivalent[2], at an abnormally low level might r...
Show More

Dear Editor,
Where does fluid accumulate in intracerebral oedema, extracellulary, intracellularly or both? The distinction is important for it has a direct bearing on treatment of the intracranial compartment syndrome [1].
If the fluid accumulates intracellularly then clamping the intra- arterial pH, using the Radiometer pH-stat automatic titrator or its equivalent[2], at an abnormally low level might reverse the oedema very efficiently by promoting the exit of Na+ and its osmotic equivalent of water [3]. Success should be revealed in a reduction or elimination of any abnormal gap between arterial blood and intacranial interstitial fluid pCO2 and a decrease in intracranial pressure.
Additional advantages of keeping the intracranial pH abnormally low is that oxidative phosphorylation should be upregulated and anaerobic glycolysis downregulated thereby greatly decreasing the metabolic need for intracerebral blood flow [4].
The pH-clamping might be better accomplished by reducing arterial [HCO3-] than by increasing arterial pCO2, as done in the pH-stat protocol used in cardiac surgery, for a rise in pCO2 has the potential to inhibit oxidative phosphorylation by mass action. In so doing anaerobic glycolysis could become the principle if not the sole source of ATP resynthesis. As the demand for nutrient delivery to sustain the same rate of ATP resynthesis is so much greater in these metabolic circumstances a nutrient supply/demand imbalance could easily be precipitated. This might even be the mechanism by which an elevation in pCO2 increases intracranial blood flow.
Increasing blood flow to the brain by increasing pCO2 may do much more metabolic harm than good. Indeed in upregulating oxidative phosphorylation and down regulating ATP-dependent enzymatic activity, in accordance with the Daniel Atkinson energy charge hypothesis [5], keeping the intracerebral pH abnormally low could reduce the need for blood flow to abnormally low levels. Blood flow and intracranial pressure are simply incapable of measuring the adequacy of tissue energetics except by inference when flow stops and intracranial pressure rises to extrmely high levels.
References
(1). Intracranial compartment syndrome Richard G Fiddian-Green bmj.com, 3 Oct 2002 eLetter re: Jonathan Wasserberg Treating head injuries BMJ 2002; 325: 454-455
(2). Fiddian-Green RG, Silen W Mechanisms of disposal of acid and alkali in rabbit duodenum. Am J Physiol. 1975 Dec;229(6):1641-8.
(3). pH-dependence of [Na+] and fluid shifts. Richard G Fiddian-Green (16 August 2004) eLetter re: Karen E. Yeates, Michael Singer, and A. Ross Morton Salt and water: a simple approach to hyponatremia CMAJ 2004; 170: 365-369
(4).Successful evolutionary adaptation to environmental stress? Richard G Fiddian-Green Heart Online, 14 Jul 2004 eLetter re: D A Lawlor, G Davey Smith, R Mitchell, and S Ebrahim Temperature at birth, coronary heart disease, and insulin resistance: cross sectional analyses of the British women’s heart and health study Heart 2004; 90: 381-388
(5). Hardie DG, Hawley SA. AMP-activated protein kinase: the energy charge hypothesis revisited. Bioessays. 2001 Dec;23(12):1112-9.
Show Less

Conflict of Interest:
None declared.
- Back to top

Main menu

Plain text

PLEASE NOTE:

Vertical Tabs

Other responses

Jump to comment:

Log in using your username and password

Main menu

Log in using your username and password

You are here

Plain text

PLEASE NOTE:

Vertical Tabs

Other responses

Jump to comment:

Read the full text or download the PDF:

Log in using your username and password