Evidence map›Paper›PMID 16960299›Full record

ReviewNeurocritical care2006

Endocrine failure after traumatic brain injury in adults.

David J Powner, Cristina Boccalandro, M Serdar Alp, Dennis G Vollmer

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Neurocritical care, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 104 citations in OpenAlex.

  1. Traumatic brain injury and prolactin.Reviews in endocrine & metabolic disorders · 2024
    Review
  2. Hypothalamic Injury and Clinical Outcomes in Patients with Post-Traumatic Hyponatremia: A Diffusion Tensor Imaging Case-Control Study.Medical science monitor : international medical journal of experimental and clinical research · 2023
    Article
  3. Neurosteroid Receptor Modulators for Treating Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
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  15. Brain death and true patient care.The Linacre quarterly · 2016
    Article
  16. Article
  17. Review
  18. Diabetes Insipidus after Traumatic Brain Injury.Journal of clinical medicine · 2015
    Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

David J PownerDepartment of Neurosurgery, University of Texas Health Science Center at Houston, Houston, TX 77030, USA. david.j.powner@uth.tmc.edu
Cristina Boccalandro
M Serdar Alp
Dennis G Vollmer
The University of Texas Health Science Center at Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo review histopathological and clinical data linking endocrine failure to traumatic brain injury (TBI) during acute neurosurgical treatment and rehabilitation.

methodsA focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publications.

resultsEndocrine failure may produce clinically important consequences during acute and convalescent care after TBI, and may be caused by direct injury to the hypothalamic- pituitary axis (HPA), neuroendocrinological effects from catecholamines and cytokines, or from systemic infection/inflammation that produces primary gland failure. Autopsy evidence of hemorrhage or ischemia in the HPA is common soon after TBI. The estimated incidence of acute hormone reduction is adrenal 15%, thyroid 5 - 15%, growth hormone 18%, vasopressin 3 - 37%, and gonadal (25 - 80%). Hyperprolactinemia occurs in more than 50% of patients. Inappropriate secretion of antidiuretic hormone (SIADH) and the euthyroid sick syndrome are common. Acute adrenal failure, central hypothyroidism, SIADH, and diabetes insipidus (DI) may cause poor neurological outcomes including death, hypo/hypernatremia, hypotension, and increased vasoactive drug requirements. Treatment of those conditions is warranted. Delayed diagnosis of hypopituitarism is often mistaken for symptoms of residual head injury. Some chronic hormone deficiency occurs in 30 - 40% of selected patients after TBI, more than one deficiency in 10 - 15%, growth hormone in 15 - 20%, gonadal hormones in 15%, and hypothyroidism in 10 - 30%. Chronic adrenal failure and DI are reported over a wide incidence. Prolactin is elevated in 30%. All clinical symptoms respond favorably to replacement therapy.

conclusionsSevere TBI associated with basilar skull fracture, hypothalamic edema, prolonged unresponsiveness, hyponatremia, and/or hypotension is associated with a higher occurrence of endocrinopathy. Greater awareness of this possible complication of TBI and appropriate testing are encouraged.

Indexed as

Adrenal InsufficiencyAdultBrain InjuriesDiagnosis, DifferentialEuthyroid Sick SyndromesHumansHyperprolactinemiaHypopituitarismHypothalamo-Hypophyseal SystemInappropriate ADH SyndromePituitary-Adrenal System

Identifiers

PMID16960299
OpenAlexW2005196522

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.