Intracranial hypertension

Timing of Intracranial Hypertension Following Severe Traumatic Brain Injury

Authors: Stein DM, Brenner M, Hu PF, Yang S, Hall EC, Stansbury LG, Menaker J, Scalea TM.

BACKGROUND: We asked whether continuous intracranial pressure (ICP) monitoring data could provide objective measures of the degree and timing of intracranial hypertension (ICH) in the first week of neurotrauma critical care and whether such data could be linked to outcome.
METHODS: We enrolled adult (>17 years old) patients admitted to our Level I trauma center within 6 h of severe TBI. ICP data were automatically captured and ICP 5-minute means were grouped into 12-hour time periods from admission (hour 0) to >7 days (hour 180). Means, maximum, percent time (% time), and pressure-times-time dose (PTD, mmHg h) of ICP >20 mmHg and >30 mmHg were calculated for each time period.
RESULTS: From 2008 to 2010, we enrolled 191 patients. Only 2.1 % had no episodes of ICH. The timing of maximum PTD20 was relatively equally distributed across the 15 time periods. Median ICP, PTD20, %time20, and %time30 were all significantly higher in the 84-180 h time period than the 0-84 h time period. Stratified by functional outcome, those with poor functional outcome had significantly more ICH in hours 84-180. Multivariate analysis revealed that, after 84 h of monitoring, every 5 % increase in PTD20 was independently associated with 21 % higher odds of having a poor functional outcome (adjusted odds ratio = 1.21, 95 % CI 1.02-1.42, p = 0.03).
CONCLUSIONS: Although early elevations in ICP occur, ICPs are the highest later in the hospital course than previously understood, and temporal patterns of ICP elevation are associated with functional outcome. Understanding this temporal nature of secondary insults has significant implications for management.

Idiopathic intracranial hypertension is a rare cause of headache in children

Authors: Viuff AC, Hansen JK, Møller HU.

Idiopathic intracranial hypertension is often believed to be an illness exclusively occurring in obese women in their twenties and thirties. This case describes a four-year-old boy presenting with headache, vomiting photophobia and double vision for six days. He did not have a fever; and all exams and tests, including a magnetic resonance imaging of the brain showed normal values. During the eye examination, he was found to have bilateral papilloedema and when undergoing lumbar puncture an elevated pressure of 230 mm water was discovered. The patient was diagnosed with idiopathic intracranial hypertension and treated with azetazolamide. Within few days, his symptoms disappeared.

Refractory intracranial hypertension due to fentanyl administration following closed head injury

Authors: Hocker SE, Fogelson J, Rabinstein AA.

Background: Although the effects of opioids on intracranial pressure (ICP) have long been a subject of controversy, they are frequently administered to patients with severe head trauma. We present a patient with an uncommon paradoxical response to opioids.Case Report: A patient with refractory intracranial hypertension after closed head injury was managed with standard medical therapy with only transient decreases in the ICP. Only after discontinuation of opiates did the ICP become manageable without metabolic suppression and rescue osmotic therapy, implicating opiates as the etiology of refractory intracranial hypertension in this patient.Conclusion: Clinicians should consider opioids as a contributing factor in malignant intracranial hypertension when findings on neuroimaging do not explain persistent and refractory intracranial hypertension.

High-Dose Barbiturates for Refractory Intracranial Hypertension in Children With Severe Traumatic Brain Injury

Authors: Mellion SA, Bennett KS, Ellsworth GL, Moore K, Riva-Cambrin J, Metzger RR, Bratton SL.

OBJECTIVES:: To evaluate high-dose barbiturates as a second-tier therapy for pediatric refractory intracranial hypertension complicating severe traumatic brain injury. DESIGN:: This is a retrospective cohort study of children with refractory intracranial hypertension treated with high-dose barbiturates. SETTING:: A single center level I pediatric trauma from 2001 to 2010. PATIENTS:: Thirty-six children with refractory intracranial hypertension defined as intracranial pressure greater than 20 mm Hg despite standard management treated with high-dose barbiturates after severe traumatic brain injury. INTERVENTIONS:: High-dose barbiturates were administered for refractory intracranial hypertension for a minimum duration of 6 hrs and monitored by continuous electroencephalography. MEASUREMENTS AND MAIN RESULTS:: Exposure was control of refractory intracranial hypertension defined as > 20 mm Hg within 6 hrs after starting barbiturates. Pediatric cerebral performance category scores at hospital discharge and at 3 months (or longer) follow-up were the primary outcomes. Ten (28%) of 36 patients had control of refractory intracranial hypertension. Neither demographic nor injury characteristics were associated with refractory intracranial hypertension control. Children who responded received barbiturates significantly later after injury (76 vs. 29 median hours). Overall, 14 children died, 13 without control of intracranial pressure. Survival was more common in those who responded compared with those who did not respond to high-dose barbiturates, although this did not reach statistical significance (relative risk of death 0.2; 95% confidence interval; ). Of the 22 survivors, 19 had an acceptable survival (pediatric cerebral performance category less than 3) at 3 months or longer after injury; however, only three returned to normal function. Among survivors, control of refractory intracranial hypertension was associated with significantly better pediatric cerebral performance category scores and over two-fold likelihood of acceptable long-term outcome (relative risk 2.3; 95% confidence interval ) compared with uncontrolled refractory intracranial hypertension despite high-dose barbiturates. CONCLUSIONS:: Addition of high-dose barbiturates achieved control of refractory intracranial hypertension in almost 30% of treated children. Control of refractory intracranial hypertension was associated with increased likelihood of an acceptable long-term outcome.

Idiopathic intracranial hypertension as the initial presentation of systemic lupus erythematosus

Authors: Rajasekharan C, Renjith SW, Marzook A, Parvathy R.

A 14-year-old girl was referred for evaluation of headache with episodes of transient blurring of vision, and intermittent fever for 4 weeks. On examination she was conscious and febrile, with multiple annular purpuric skin lesions present over the face and back. Neurological examination revealed a bilaterally extensor plantar response, with bilateral papilloedema. Lumbar puncture yielded clear spinal fluid with a very high opening pressure with a normal biochemistry and cytology. Neuroimaging showed evidence of raised intracranial tension. She was provisionally diagnosed to have idiopathic intracranial hypertension (IIH) and started on anticerebral oedema measures. Despite medication, she continued to be symptomatic. On the sixth day of admission, her antinuclear antibody and antidouble-stranded DNA registered positively in high titres. She was diagnosed with systemic lupus erythematosus (SLE) with IIH and was started on corticosteroids, with dramatic recovery of her symptoms and clinical signs. Reports of SLE, the maiden presentation of which is IIH, are rare in the literature.

Nocturnal carbon dioxide monitoring in patients with idiopathic intracranial hypertension

Authors: Abraham A, Peled N, Khlebtovsky A, Benninger F, Steiner I, Stiebel-Kalish H, Djaldetti R.

BACKGROUND: Idiopathic intracranial hypertension may be associated with sleep apnea. This study evaluated the incidence of sleep breathing disorders in patients with idiopathic intracranial hypertension.
MATERIALS AND METHODS: Overnight respiratory monitoring was performed in 22 untreated patients with idiopathic intracranial pressure diagnosed at a tertiary medical center over a two-year period and 12 sex- and age-matched control subjects. Breathing measures included heart rate, respiratory rate,oxygen saturation, and continuous end-tidal capnography. Sleep quality and daily fatigue were assessed by self-report questionnaires.
RESULTS: Mean age of the study group was 32.6±12.2 years and of the control group, 37.0±12.9 years. Neither group had significant findings of hypoxia or hypercarbia during sleep, and there were no between-group differences in mean carbon dioxide level (patients, 35.8±4.41 mmHg; controls, 37.6±4.38 mmHg; p>0.02) or minimal oxygen saturation (96.35±1.99% and 5.69±1.71%, respectively; p>0.02). The study group had significantly more events of apnea (CO(2)) per hour of sleep than the control group (1.21±1.38 and 0.92±0.56, respectively; p=0.02), although values were still within normal range (<5/hr).
CONCLUSION: Idiopathic intracranial hypertension is not associated with a clinically significant nocturnal breathing abnormality, and hypercarbia is apparently not involved in the pathogenesis. However, it is possible that a subtle increase in paroxysmal sleep apnea (CO(2)) events might be sufficient to cause vasodilatation of the cerebral blood vessels, thereby increasing intracranial pressure. Screening for sleep apnea may be appropriate in idiopathic intracranial hypertension patients, and further studies are needed to clarify this issue.


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