DIABETES INSIPIDUS FOLLOWING CRANIO-FACIAL TRAUMA: REVIEW
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Romanian Journal of Oral Rehabilitation
Vol. 12, No. 4, October - December 2020
DIABETES INSIPIDUS FOLLOWING CRANIO-FACIAL TRAUMA:
REVIEW
Otilia Boișteanu1, Andrei Ionuț Cucu2, Liviu Vlad Hârtie3*, Anton Nicoleta4*
Florin Sava1, Andrei Nicolau1, Cristina Ungureanu5, Victor-Vlad Costan1
1. Department of Oral and Maxillo-Facial Surgery, Faculty of Medical Dentistry, “Grigore T.
Popa” University of Medicine and Pharmacy, Iasi
2. Department of Neurosurgery, “Nicolae Oblu” Neurosurgical Hospital, Iasi
3. Department of Anesthesiology, “Nicolae Oblu” Neurosurgical Hospital, Iasi
4. Department of Ophthalmology, Faculty of Medicine, “Grigore T. Popa” University of
Medicine and Pharmacy, Iasi
5. Department of Endocrinology, Faculty of Medicine, “Grigore T. Popa” University of
Medicine and Pharmacy, Iasi
Corresponding authors* nicolofta@gmail.com
* hartievlad@gmail.com
Abstract:
Post-traumatic diabetes insipidus (PTDI) is now well recognized after head trauma, and although rare, it can have
severe consequences. Although PTDI occurs especially in traumatic brain injuries (TBIs), a number of cases have
been reported in literature in which it can also occur in craniofacial trauma or mild TBIs. Accurate evaluation and
long-term follow-up of all cranio-facial injuries are necessary to detect the occurrence of PTDI. Furthermore, future
research should focus more on clinical and experimental studies to elucidate the exact mechanisms involved in post-
traumatic pituitary damage, particularly in the onset of PTDI.
Key words: post-traumatic diabetes insipidus, cranio-facial injuries, posterior pituitary
dysfunction.
Introduction (3), neuroendocrine dysfunctions can also
TBIs have been recognized to cause occur after mild TBIs, with much lower rates
posterior pituitary dysfunction for many of occurrence (4,5). Moreover, repetitive
years (1). PTDI can occur in any type of mild TBIs can disrupt hormone secretion (6)
head injury, although it most commonly and from this point of view athletes are the
occurs in severe and moderate trauma, in most exposed (3). Maxillo-facial injuries can
which case it is accompanied by skull also produce PTDI and literature reports
fracture and neurological deficits (2). several cases (7-9).
Although severe TBIs most commonly cause Posterior pituitary dysfunction
disorders of the hypothalamic-pituitary axis secondary to head trauma is much rarer than
125Romanian Journal of Oral Rehabilitation
Vol. 12, No. 4, October - December 2020
anterior pituitary dysfunction (3). This can of Pergamon (129-c.200/216 AD), he later
also be explained by the fact that the called it the pituitary gland, inspired by the
posterior pituitary gland obtains its blood Latin word pituita (glairy mucus), based on
supply via the inferior pituitary artery and his beliefs that waste products from the
vascular lesions do not usually appear after activity of the brain are discharged through
the transection of the stalk. Instead, PTDI this sella turcica of sphenoid bone as phlegm
may occur as a result of rupture of the neural (15,16).
connections between the hypothalamus and The pituitary gland can be divided
the posterior pituitary (3). into adenohypophysis (anterior pituitary)
The actual prevalence of PTDI is and neurohypophysis (posterior pituitary),
difficult to estimate due to the heterogeneity which represents approximately 20% of the
between studies in terms of the diagnostic total volume of the gland. The
criteria used, the characteristics of the neurohypophysis can also be divided into
population studied, the different three portions: the median eminence, the
classification grades of TBIs and the time of pituitary stalk and the posterior lobe. These
evaluation (10). Thus, in literature, the structures derived from the outgrowth of
prevalence of PTDI varies very widely, diencephalic neuroectoderm and come into
between 2.9% and 51% (10-12), especially contact with the anterior lobe (17).
since the evaluation of posterior pituitary The median eminence is a
function in survivors of TBIs remains an component of the hypothalamus, and it
insufficiently investigated chapter (13). spreads from the optic chiasm to the
In this article we will discuss the mammillary bodies. The hypothalamus
pathophysiology, mechanisms of production consists of multiple nuclei that play a role in
and anatomo-pathological characteristics of regulation of important functions for the
diabetes insipidus secondary to human body; regarding central (neurogenic)
craniocerebral and maxillofacial trauma, DI, two of these hypothalamic nuclei are
endocrine dysfunction rarely encountered relevant, namely supraoptic and
but possibly life threatening. paraventricular nuclei. They lie in the
supraoptic region and above the optic
Anatomy of a "leader of the endocrine chiasm and secrete oxytocin, antidiuretic
orchestra" hormone (ADH) and corticotrophin
The hypophysis or pituitary gland releasing hormone. Of these, ADH and
lies in the sella turcica, a median concavity oxytocin are transported from the
in the sphenoid bone that protects it (14). It hypothalamus along the axons of the
is bordered anteriorly by the tuberculum supraoptic and paraventricular nuclei in the
sellae and anterior clinoid processes of the infundibulum to the posterior pituitary
sphenoid bone, inferior by the sphenoid gland. Here, hormones are stored in
sinus, and posterior by the dorsum sella and secretory granules and are released into the
posterior clinoid processes of the sphenoid circulation when are stimulated by increased
bone (2). Identified and described by Galen plasma osmolality or by decreased arterial
126Romanian Journal of Oral Rehabilitation
Vol. 12, No. 4, October - December 2020
blood pressure (osmoregulation and ADH is thus highly dependent on the
baroregulation) (10). integrity of the pituitary stalk and the
Organ of millimetric size, the hypothalamus, diabetes insipidus can occur
pituitary stalk is a structure that arises from as a result of a defect in one or more sites
the ventromedial hypothalamus and is involving hypothalamic osmoreceptors,
contiguous with the infundibular recess of supraoptic or paraventricular nuclei of the
the third ventricle (18,19). It has a complex hypothalamus, median eminence,
histological structure, containing tanycites infundibulum or posterior pituitary gland
and pituicytes, two types of modified glial (2).
cells that have a supporting role for the
axons of neurons that produce ADH and Pathophysiology of posttraumatic
oxytocin (19). diabetes insipidus
As mentioned above, the pituitary The first research in pituitary damage
gland consists of two lobes (anterior and after TBIs was reported in 1918 by Cyran
posterior), distinct both in terms of (23), followed a few decades later by
embryological origin and physiology. If Holborn (24) and Porter et al. (25) which
Rathke’s pouch or hypophysial is the suggested that changes in the rotational
embryological precursor of the anterior velocity of the head represent the main
pituitary wich arises from the primitive oral mechanism of damage of the hypothalamo-
cavity, in the case of the posterior pituitary, pituitary unit. The two considered that this
it derives from the neurohypophyseal bud rotational velocity of the head leads to
which arises from the neuroectoderm of the stretching or tearing of small vessels or
diencephalon (2,20). The posterior lobe of neuronal structures (24,25). Bondanelli et al.
the pituitary gland occupies the central considers that shearing axonal injury, which
portion of the sella turcica (15) and is more frequently involves the midline
surrounded anterolaterally by the anterior structures, could also induce hypothalamic-
lobe (21). pituitary axis dysfunction (26).
Unfortunately, such changes are not visible
Antidiuretic hormone – from the by means of CT scans and even MR imaging
hypothalamus to the nephron in the early stages, this explaining the lack of
ADH is a hormone produced by the radiological findings in these patients with
paraventricular and supraoptic nuclei of the head trauma and disorders of the
hypothalamus, which is then transported hypothalamic-pituitary axis (27).
down along the pituitary stalk to the In lesions of the hypothalamic-
posterior pituitary by neurosecretory fibers neurohypophyseal axis, PTDI may also
and released by exocytosis into the posterior occur and manifests as diabetes insipidus of
lobe. ADH acts on several specific receptors other origin through polyuria, polydipsia and
(vasopressin receptors), of which three the passage of large amounts of diluted
subtypes have been identified: V1a, V1b and urine. Specifically, the diabetes insipidus
V2 (22). Although the functional state of the criteria are: (1) urine volume >2ml/kg/h or>
127Romanian Journal of Oral Rehabilitation
Vol. 12, No. 4, October - December 2020
300ml/h in two consecutive hours (polyuria), A role of autoimmunity has also been
(2) urine osmolality 300mOsm/kg (1). Central or PTDI (30). In this regard, in patients with
neurogenic diabetes insipidus occurs due to TBIs increased levels of anti-pituitary
deficiency in the synthesis or secretion of antibodies and also anti-hypothalamic
ADH, also known as arginine vasopressin antibodies were observed at three and five
peptide, and affected patients may years post-injury, respectively, compared to
experience severe dehydration and the control groups (32,33). Elevated levels
hypernatraemia. of these antibodies were also identified in
In the case of diabetes insipidus of boxers who had chronic and repeated brain
central origin, it occurs most frequently from injuries (46.2%) compared to control groups
lesions in the hypothalamic- who had less than 10.4% (32,34).
neurohypophyseal axis (17). Its injury
depends primarily on the severity of the Pathological findings in post-traumatic
trauma, and can occur either from the direct diabetes insipidus
impact, the acceleration-deceleration effect, Anatomical data from necropsy of
traumatic vascular consequences such as patients with TBIs indicated that hemorrhage
ischemia or hypoxia, increased intracranial or necrosis occurred in 22% of cases in the
pressure or altered cerebral blood flow posterior pituitary, 21% in the anterior
(10,12,28). Although the exact mechanism pituitary, and 16% in the pituitary stalk (35-
of hypothalamic-pituitary dysfunction in 38). Peripituitary vascular damage also
TBIs with PTDI is not known, there are occurred in one-third of cases (36-38). Other
several theories (29), the most common autopsy studies performed on patients who
being direct trauma to the hypophsis, did not survive severe head trauma showed
disruption or transection of the pituitary hemorrhages in the hypothalamic nuclei or
stalk or damage of the hypophyseal portal the infundibular region, or stalk hemorrhage
veins (30). or infarction (39,40).
Frequently, PTDI has been observed Another study performed on 106
in patients with cranial fractures, especially consecutive autopsies of some patients with
with fractures of the skull base, as they have fatal closed head injuries found
a higher risk of developing posterior hypothalamus lesions in 42.5% of cases.
pituitary dysfunction (26). Also, in a study These have been identified especially in the
among soldiers with pituitary dysfunctions, anterior hypothalamus, being represented by
the prevalence of skull and facial fractures ischemia or infarction (35). The authors of
was 50% compared to those without (0%) the study believe that in such cases, ischemia
(31). This is due to the fact that the pituitary occurs due to shearing of small perforating
gland, by its location at the base of the skull vessels or venous engorgement secondary to
is susceptible to injuries involving fractures intracranial hypertension syndrome. In 28%
of the skull base (30). of cases, these lesions of the hypothalamus
128Romanian Journal of Oral Rehabilitation
Vol. 12, No. 4, October - December 2020
were accompanied by fractures of the middle central DI, as intact hypothalamic nuclei will
cerebral fossa (35). Moreover, in patients produce ADH and release it into the
with permanent DI after TBIs, pathological peripheral circulation via the portal
findings reported a fibrotic posterior lobe capillaries in the median eminence (10,40).
and pituitary stalk and also a reduction in Transection of pituitary stalk
cells in the paraventricular and supraoptic produces a triphasic response characterized
nuclei in the hypothalamus (41,42). by initially diabetes insipidus, followed by
On the other hand, neuroimaging several days of transient inappropriate
studies observed that 30% of TBIs had focal secretion of ADH and later recurrence of
lesions of the hypothalamic pituitary axis diabetes that may be transient or permanent
when examined by MR imaging (43). Other (10). This three-phase response is due to the
findings can include infundibular transection initial shock of the trauma, followed by the
or hematoma, pituitary hemorrhage or release of the pre-synthesized ADH.
infarction, or loss of normal posterior Subsequently, ADH deficiency reappears
pituitary bright spot (2). In 6% of cases with due to damage to neural structures that lead
PTDI, CT and MR imaging studies to impaired synthesis of the hormone.
identified diffuse axonal injury or hypoxic Although very well described, this three-
damage (2). Another imaging study that phase clinical presentation is rare in clinical
followed the MRI scan of 41 moderate- practice (10,47).
severe TBIs patients identified a pituitary PTDI can be with immediate onset,
enlargement in the acute phase of trauma in which occurs through direct injury to the
the first 7 days (28). posterior lobe or with late onset, which
occurs after transection of the stalk. In the
The pattern of endocrine abnormalities latter case, due to the fact that ADH is stored
secondary to head trauma in the posterior lobe of the pituitary gland,
The pattern of endocrine its functions can be maintained for several
abnormalities secondary to TBIs depends on days (2,48).
the location of the lesion in the
hypothalamic-pituitary axis (10). Thus, the Natural history of post-traumatic diabetes
predominant damage of the hypothalamus insipidus
will lead to anterior hypopituitarism, PTDI In most cases, PTDI occurs in the
or inappropriate secretion of ADH (44). The first days after trauma, from 2-3 days (49) to
severity of the clinical picture in the central 4-10 days (11), and is usually transient
DI also depends on the extent of the (10,12,28). Most cases of acute PTDI are
neuronal injury (45), typically requiring the transient, and permanent diabetes insipidus
destruction of 80-90% of the magnocellular after head injuries is rare (50), especially
neurons of the hypothalamus before since diabetes insipidus itself is a rare
symptoms become apparent (46). Lesions disease. The combined incidence of cranial
below the median eminence of the and nephrogenic diabetes insipidus is
hypothalamus rarely cause permanent estimated at 1/25.000 (51). In 2004, Agha et
129Romanian Journal of Oral Rehabilitation
Vol. 12, No. 4, October - December 2020
al. reported a prevalence of permanent considering that there is no causal
diabetes of 6.9% at 6-36 months after head relationship between GCS score on
trauma (13). admission and post-traumatic
Since in most cases PTDI is hypopituitarism (59-62). Although the most
transient, several authors have tried to common PTDI is associated with severe
identify the causes, considering that it trauma (49), it can also occur in mild head
subsides due to slow involution of the injury (56,58,63).
edema, as well as due to regeneration of the
vessels in the affected areas (10). Other Post-traumatic diabetes insipidus
authors have explained that in some cases associated with maxillofacial fractures
the transient nature of diabetes insipidus is Until now, several cases of PTDI
due to the presence of regenerating nerve following maxillofacial fractures have been
fibers in the stump of the pituitary stalk (52). reported in literature (7-9) (Table 1). In
some cases, there was a significant cerebral
Risk factors for post-traumatic diabetes involvement (7), and as a common feature,
insipidus patients with PTDI following maxillofacial
Risk factors identified for PTDI are fractures also had sphenoid bone fractures
the presence of cerebral edema, a low GCS (Table 1). However, the authors presented
score on admission and severe trauma maxillofacial fractures more as an
(13,53). A number of studies have shown association with craniocerebral lesions in the
that the initial GCS score is a predictor of context of PTDI. From studies in literature,
the occurrence of hypopituitarism, including only in one case it was suspected that the
PTDI (26,54-57). Furthermore, a meta- occurrence of PTDI was secondary to
analysis of 14 studies concluded that severe maxillofacial trauma. The case was of an 18-
TBIs (GCS scoreRomanian Journal of Oral Rehabilitation
Vol. 12, No. 4, October - December 2020
Case 17 Motor md Frontal Comminution of F bones Le Fort 13 12+ 6.28 Good
3 (9) cycle and bilaterally involving F III
accident face sinuses, fracture of anterior
clinoid process and mandible
Case 24 Motor Comatose All Left F bone, left orbit at the md 20 md 7.5 Good
4 (7) bike (16 days) head SOF, the palate, the right
body of the mandible
Case 18 High- Disoriented Face Blowout fracture of the left Le FortRomanian Journal of Oral Rehabilitation
Vol. 12, No. 4, October - December 2020
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