Posterior Pituitary Dysfunction after Traumatic Brain Injury

Abstract

Disorders of water balance are well recognized after traumatic brain injury (TBI), but there are no reliable data on their true prevalence in post-TBI patients. We aimed to evaluate the prevalence of posterior pituitary dysfunction in a large cohort of survivors of TBI. One hundred two consecutive patients (85 males) who suffered severe or moderate TBI were evaluated for diabetes insipidus (DI) at a median of 17 months (range 6-36 months) after the event, using the 8-h water deprivation test (WDT). Their results were compared against normative data obtained from 27 matched, healthy controls. Patients' medical records were retrospectively reviewed for the presence of abnormalities of salt and water balance in the immediate post-TBI period. Twenty-two patients (21.6%) developed DI in the immediate post-TBI period (acute DI group), of whom five had abnormal WDT on later testing. In total, seven patients (6.9%) had abnormal WDT (permanent DI group), five of whom had partial DI. Patients in the acute and permanent DI groups were more likely to have more severe TBI, compared with the rest of the cohort (P < 0.05). In the immediate post-TBI period, 13 patients (12.9%) had syndrome of inappropriate secretion of antidiuretic hormone, which persisted in one patient, and one other patient developed cerebral salt wasting. Diabetes insipidus and syndrome of inappropriate secretion of antidiuretic hormone were common in the immediate post-TBI period. Permanent DI was present in 6.9% of patients who survived severe or moderate TBI, which is higher than traditionally thought. Identification of patients with partial posttraumatic DI is important because appropriate treatment may reduce morbidity and optimize the potential for recovery.

Hypopituitarism after traumatic brain injury

“…Diabetes insipidus was present in 2.7% of patients with PTHP (Table 6). In a recent series of 85 patients who had suffered severe or moderate TBI, studied by the water deprivation test, permanent diabetes insipidus was detected in 6.9% of patients (69). The higher frequency of permanent diabetes insipidus as compared with other studies (5, 6, 9, 30) could be explained by the presence, in five out of seven patients, of a partial defect discovered through the water deprivation test.…”

“…A recent retrospective review confirmed the low prevalence (2.9%) of diabetes insipidus in TBI patients admitted to the intensive care unit, and underlined that patients who developed the disease within the first 3 days after injury had a high mortality rate (68). By contrast, other authors demonstrated a high prevalence of diabetes insipidus during the acute phase post-TBI in patients admitted to a neurosurgical center (22 -26%) (49,69) and in patients with head injury damaging the chiasm (37%) (70). However, diabetes insipidus is frequently transient and can spontaneously disappear within a few days or up to 1 month (66,70,71) after the acute event, as confirmed by its low prevalence (0 -6.9%) in patients evaluated after months or years following TBI (5,6,69).…”

Hypopituitarism in childhood and adolescence following traumatic brain injury: the case for prospective endocrine investigation

“…In adults, recent prospective data suggest that the incidence of DI may be as high as 26% in the acute phase immediately following TBI, although in up to 70% of cases complete recovery from DI was achieved within 12 months (43). Overall, the incidence of DI persisting beyond 3-12 months after TBI appears to be in the region of 7-8% in adult survivors, with many cases exhibiting a partial form of DI with mild, subclincial symptoms, which are at risk of being overlooked and undiagnosed (6,44). Post-TBI related DI may also be related to the severity of head injury event, with those patients the lower GCS ratings being more likely to develop permanent DI (44,45).…”

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

“…Other signaling mechanisms could include trans-synaptic (Koliatsos et al, 2004) as well as anterograde and retrograde neuronal degeneration from the site of injury to the more distal sites (Sorensen et al, 1996;Bechmann and Nitsch, 1997), also eventually affecting some of the endocrine functions. While we know something about the effects of TBI on endocrine function based on human studies (Ceballos, 1966;Agha et al, 2004aAgha et al, , 2004bAgha et al, , 2005aAgha et al, , 2005bAimaretti et al, 2004Aimaretti et al, , 2005bBondanelli et al, 2004;Herrmann et al, 2006;Powner et al, 2006;Schneider et al, 2006;Tanriverdi et al, 2006), there is still some uncertainty about the mechanisms by which long-term alterations in the endocrine system (like suppression of serum GH in TBI subjects) evolve over time, and whether such changes could be prevented by therapeutic interventions.…”