Evidence map›Paper›PMID 30334138›Full record

ReviewPituitary2019

Posterior pituitary dysfunction following traumatic brain injury: review.

Roxana Maria Tudor, Christopher J Thompson

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pituitary, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Arginine Vasopressin Deficiency and Oxytocin Deficiency in the Endocrine Clinic.The Journal of clinical endocrinology and metabolism · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. 'Un-thirsty' hypernatremia.Endocrinology, diabetes & metabolism case reports · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Traumatic brain injury inducing swift transition from syndrome of inappropriate antidiuretic hormone secretion to central diabetes insipidus: a case report.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2024
    Article
  15. Review
  16. Article
  17. Diagnosis and Management of Central Diabetes Insipidus in Adults.The Journal of clinical endocrinology and metabolism · 2022
    Review
  18. Review
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

Roxana Maria TudorAcademic Department of Endocrinology, Beaumont Hospital/RCSI Medical School, Dublin, Ireland. roxanamariatudor@beaumont.ie.ORCID http://orcid.org/0000-0002-4538-6010
Christopher J ThompsonAcademic Department of Endocrinology, Beaumont Hospital/RCSI Medical School, Dublin, Ireland.
Beaumont Hospital · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurohypophysial dysfunction is common in the first days following traumatic brain injury (TBI), manifesting as dysnatremia in approximately 1 in 4 patients. Both hyponatremia and hypernatremia can impair recovery from TBI and in the case of hypernatremia, there is a significant association with excess mortality. Hyponatremia secondary to syndrome of inappropriate antidiuretic hormone secretion (SIAD) is the commonest electrolyte disturbance following TBI. Acute adrenocorticotropic hormone (ACTH)/cortisol deficiency occurs in 10-15% of TBI patients and can present with a biochemical picture identical to SIAD. For this reason, exclusion of glucocorticoid deficiency is of particular importance in post-TBI SIAD. Cerebral salt wasting is a rare cause of hyponatremia following TBI. Hyponatremia predisposes to seizures, reduced consciousness, and prolonged hospital stay. Diabetes insipidus (DI) occurs in 20% of cases following TBI; where diminished consciousness is present, appropriate fluid replacement of renal water losses is occasionally inadequate, leading to hypernatremia. Hypernatremia is strongly predictive of mortality following TBI. Most cases of DI are transient, but persistent DI is also predictive of mortality, irrespective of plasma sodium concentration. Persistent DI may herald rising intracranial pressure due to coning. True adipsic DI is rare following TBI, but patients are vulnerable to severe hypernatremic dehydration, exacerbation of neurologic deficits and hypothalamic complications, therefore clinicians should be aware of this possible variant of DI.

Indexed as

AnimalsBrain Injuries, TraumaticDiabetes InsipidusHumansHypothalamic DiseasesPituitary Gland, PosteriorAdipsic diabetes insipidusDiabetes insipidus (DI)HyponatremiaPosterior pituitary dysfunctionSyndrome of inappropriate antidiuretic hormone secretion (SIAD/SIADH)Traumatic brain injury (TBI)

Identifiers

PMID30334138
OpenAlexW2896784210

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.