Decrease in white blood cell counts after thiopentone barbiturate therapy for refractory intracranial hypertension: A common complication

Shin Yi Ng; Ki Jinn Chin; Tong Kiat Kwek

doi:10.4103/0976-3147.116441

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Original Article

4 (

Supp 1

); S31-S34

doi:

10.4103/0976-3147.116441

Decrease in white blood cell counts after thiopentone barbiturate therapy for refractory intracranial hypertension: A common complication

Shin Yi Ng, Ki Jinn Chin^,, Tong Kiat Kwek

Departments of Anaesthesiology, Singapore General Hospital,Canada

1 Department of Anaesthesia, University of Toronto, Toronto Western Hospital, Ontario, Canada

2 Departments of Tan Tock Seng Hospital, Singapore, Republic of Singapore,Canada

Dr. Shin Yi Ng Consultant, Department of Anaesthesiology, Singapore General Hospital Outram Road, Singapore . 169 608 Singapore ng.shin.yi@sgh.com.sg

Journal of Neurosciences in Rural Practice

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This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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This article was originally published by Thieme Medical and Scientific Publishers Private Ltd. and was migrated to Scientific Scholar after the change of Publisher.

Abstract

ABSTRACT

Background: Leucopenia has been reported after induction of thiopentone barbiturate therapy for refractory intracranial hypertension. However, the incidence and characterisitics are not well described. Aims: We performed a retrospective review to describe the incidence and characteristics of leucopenia after induction of thiopentone barbiturate therapy. Setting and Design: Our centre is a national referral centre for neurotrauma and surgery in a tertiary medical institution.Materials and Methods: We performed a retrospective review of all patients who received thiopentone barbiturate therapy for refractory intracranial hypertension during an 18 month period from January 2004 to June 2005 in our neurosurgical intensive care unit. Statistical Analysis Used: Statistical analysis was performed using SPSS version 15.0. All data are reported as mean ± standard deviation or median (interquartile range). The Chi square test was used to analyze categorical data and student t test done for comparison of means. For paired data, the paired t?test was used.-test was used. Results: Thirty eight (80.9%) out of 47 patients developed a decrease in white blood cell (WBC) count after induction of thiopentone barbiturate coma. The mean decrease in WBC from baseline to the nadir was 6.4 × 10 ⁹ /L (P <lt; 0.001) and occurred 57 (3-147) h after induction. The mean nadir WBC was 8.6 < 3.6 × 10 ⁹ /L. Three (6.4%) patients were leucopenic, with a WBC count of 2.8, 3.1, and 3.6 < 10 ⁹ /L. None of them were neutropenic. We did not find an association between decrease in WBC count and clinical diagnosis of infection. We did not find any association between possible risk factors such as admission GCS, maximum ICP prior to induction of barbiturate coma, APACHE II score, total duration and dose of thiopentone given, and decrease in WBC count. Conclusions: Decrease in WBC count is common, while development of leucopenia is rare after thiopentone barbiturate coma. Regular monitoring of WBC counts is recommended.

Keywords

traumatic brain injury

leucopenia

Barbiturate coma

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Conflict of Interest

None declared

References

Brain trauma foundation , American association of neurological surgeons, congress of neurological surgeons , . Guidelines for management of severe traumatic brain injury. J Neurotrauma. 2007;24:S1-106. suppl 1
[Google Scholar]
Schalen W, Messeter K, Nordstrom C. H., . Complications and side effects during thiopentone therapy in patients with severe head injuries. Acta Anaesthesiol Scand. 1992;36:369-77.
[Google Scholar]
Ng S. Y., Chin K. J., Kwek T. K., . Dyskalaemia associated with thiopentone barbiturate coma for refractory intracranial hypertension: A case series. Intensive Care Med. 2011;37:1285-9.
[Google Scholar]
Stover J. F., Stocker R, . Barbiturate coma may promote reversible bone marrow suppression in patients with severe isolated traumatic brain injury. Eur J Clin Pharmacol. 1998;54:529-34.
[Google Scholar]
Frenette A. J., Perreault M. M., Lam S, Williamson D. R., . Thiopental-induced neutropenia in two patients with severe head trauma. Pharmacotherapy. 2007;27:464-71.
[Google Scholar]
Loop T, Liu Z, Humar M, Hoetzel A, Benzing A, Pahl H. L., et al . Thiopental inhibits the activation of nuclear factor kappa B. Anesthesiology. 2002;96:1202-13.
[Google Scholar]
Ward C, Chilvers E. R., Lawson M. F., Pryde J. G., Fujihara S, Farrow S. N., et al . NF-kappa B activation is a critical regulator of human granulocyte apoptosis in vitro. J Bio Chem. 1999;274:4309-18.
[Google Scholar]
Humar M, Pischke S. E., Loop T, Hoetzel A, Schmidt R, Klaas C, et al . Barbiturates directly inhibit the calmodulin/calcineurin complex: A novel mechanism of inhibition of nuclear factor of activated T cells. Mol Pharmacol. 2004;65:350-61.
[Google Scholar]
Keskil S, Baykaner M. K., Ceviker N, Aykol S, . Head trauma and leukocytosis. Acta Neurochir (Wien). 1994;131:211-4.
[Google Scholar]
Campbell S. J., Perry V. H., Pitossi F. J., Butchart A. G., Chertoff M, Waters S, et al . Central nervous system injury triggers hepatic CC and CXC chemokine expression that is associated with leukocyte mobilization and recruitment to both the central nervous system and the liver. Am J Pathol. 2005;166:1487-97.
[Google Scholar]
Pelosi P, Barassi A, Severgnini P, Gomiero B, Finazzi S, Merlini G, et al . Prognostic role of clinical and laboratory criteria to identify early ventilator-associated pneumonia in brain injury. Chest. 2008;134:101-8.
[Google Scholar]
Neuwelt E. A., Kikuchi K, Hill S. A., Lipsky P, Frenkel E, . Barbiturate inhibition of lymphocyte function: Differing effects of various barbiturates used to induce coma. J Neurosurg. 1982;56:254-9.
[Google Scholar]
Eberhardt K. E., Thimm B. M., Spring A, Masos W. R., . Dose dependent rate of nosocomial pulmonary infection in mechanically ventilated patients with brain edema receiving barbiturates: A prospective case study. Infection. 1992;20:12-8.
[Google Scholar]

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[1] Brain trauma foundation , American association of neurological surgeons, congress of neurological surgeons , . Guidelines for management of severe traumatic brain injury. J Neurotrauma. 2007;24:S1-106. suppl 1
[Google Scholar]

[2] Schalen W, Messeter K, Nordstrom C. H., . Complications and side effects during thiopentone therapy in patients with severe head injuries. Acta Anaesthesiol Scand. 1992;36:369-77.
[Google Scholar]

[3] Ng S. Y., Chin K. J., Kwek T. K., . Dyskalaemia associated with thiopentone barbiturate coma for refractory intracranial hypertension: A case series. Intensive Care Med. 2011;37:1285-9.
[Google Scholar]

[4] Stover J. F., Stocker R, . Barbiturate coma may promote reversible bone marrow suppression in patients with severe isolated traumatic brain injury. Eur J Clin Pharmacol. 1998;54:529-34.
[Google Scholar]

[5] Frenette A. J., Perreault M. M., Lam S, Williamson D. R., . Thiopental-induced neutropenia in two patients with severe head trauma. Pharmacotherapy. 2007;27:464-71.
[Google Scholar]

[6] Loop T, Liu Z, Humar M, Hoetzel A, Benzing A, Pahl H. L., et al . Thiopental inhibits the activation of nuclear factor kappa B. Anesthesiology. 2002;96:1202-13.
[Google Scholar]

[7] Ward C, Chilvers E. R., Lawson M. F., Pryde J. G., Fujihara S, Farrow S. N., et al . NF-kappa B activation is a critical regulator of human granulocyte apoptosis in vitro. J Bio Chem. 1999;274:4309-18.
[Google Scholar]

[8] Humar M, Pischke S. E., Loop T, Hoetzel A, Schmidt R, Klaas C, et al . Barbiturates directly inhibit the calmodulin/calcineurin complex: A novel mechanism of inhibition of nuclear factor of activated T cells. Mol Pharmacol. 2004;65:350-61.
[Google Scholar]

[9] Keskil S, Baykaner M. K., Ceviker N, Aykol S, . Head trauma and leukocytosis. Acta Neurochir (Wien). 1994;131:211-4.
[Google Scholar]

[10] Campbell S. J., Perry V. H., Pitossi F. J., Butchart A. G., Chertoff M, Waters S, et al . Central nervous system injury triggers hepatic CC and CXC chemokine expression that is associated with leukocyte mobilization and recruitment to both the central nervous system and the liver. Am J Pathol. 2005;166:1487-97.
[Google Scholar]

[11] Pelosi P, Barassi A, Severgnini P, Gomiero B, Finazzi S, Merlini G, et al . Prognostic role of clinical and laboratory criteria to identify early ventilator-associated pneumonia in brain injury. Chest. 2008;134:101-8.
[Google Scholar]

[12] Neuwelt E. A., Kikuchi K, Hill S. A., Lipsky P, Frenkel E, . Barbiturate inhibition of lymphocyte function: Differing effects of various barbiturates used to induce coma. J Neurosurg. 1982;56:254-9.
[Google Scholar]

[13] Eberhardt K. E., Thimm B. M., Spring A, Masos W. R., . Dose dependent rate of nosocomial pulmonary infection in mechanically ventilated patients with brain edema receiving barbiturates: A prospective case study. Infection. 1992;20:12-8.
[Google Scholar]

Decrease in white blood cell counts after thiopentone barbiturate therapy for refractory intracranial hypertension: A common complication

Abstract

ABSTRACT

Keywords

traumatic brain injury

leucopenia

Barbiturate coma

Conflict of Interest

References

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