Acute and Chronic Posterior Pituitary Insufficiency Among Traumatic Brain Injury Patients at a Tertiary Care Center

Abstract Background: Traumatic brain injury (TBI) is the leading cause of death and disability in young adults. Disorders of salt and water balance are the most commonly recognized medical complications in the immediate post-TBI period and contribute to early morbidity and mortality. Objective: We aimed to evaluate the prevalence of acute (during hospital stay) and chronic posterior pituitary dysfunction in patients of head injury admitted at our tertiary care hospital. Study Design: Prospective, Observational study. Participants: 136 patients, attending tertiary care in North India with TBI with radiological evidence of head injury. Methodology: The severity of brain injury was assessed by the Glasgow Coma Scale (GCS), and Modified Rankin Scale (MRS) score at the time of admission. Lab measurements, apart from routine CBC and biochemical tests, included tests of serum and urinary osmolality, serum sodium, cortisol, and thyroid function test during the hospital stay. All patients were monitored closely during the hospital stay. Surviving patients were evaluated at 3, 6, and 12 months of follow-up. Urinary output and water deprivation tests were done to determine chronic posterior pituitary dysfunction. The results were compared against normative data obtained from 25 matched, healthy controls. Serum & urinary osmolality was measure by the freezing point method. Diabetes insipidus (DI) and Syndrome of inappropriate ADH secretion (SIADH) were diagnosed according to standard criteria. Results: Of 136 patients admitted, 61 (44.85%) had a mild head injury (GCS, ≤8), 47 (35.55%) had a moderate injury (GCS, 9-12), and 27 (19.85%) had a severe injury (GCS, 13-15). DI occurred in 10 patients (7.4%), while SIADH was observed in 4 patients in the immediate TBI period. Risk factors for diabetes insipidus were GCS of ≤ 8 at admission, midline shift, and surgical intervention. DI was an independent risk factor for death. There was a negative correlation between the presence of DI and GCS score (r, -0.367). Most of the patients with DI (8 out of 10) died during the hospital stay. One patient persisted to have partial diabetes insipidus and another one SIADH at three months post-TBI; both patients had recovered at six months of follow-up. No new case of DI or SIADH occurred on the follow up to 12 months. Conclusion: The incidence of acute DI in severe head injury (GCS ≤ 8) could be an indicator of the severity of TBI, and associated with increased mortality as most of our patients died during the hospital stay.

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Long Term Symptoms and Limitations of Activity of People with Traumatic Brain Injury: A Ten-Year Follow-up

Psychological Reports ◽

10.2466/pr0.97.1.169-179 ◽

2005 ◽

Vol 97 (1) ◽

pp. 169-179 ◽

Cited By ~ 52

Author(s):

C. O'Connor ◽

A. Colantonio ◽

H. Polatajko

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Head Injury ◽

Care Center ◽

Tertiary Care ◽

Consecutive Series ◽

Post Injury ◽

What Is Said

This study examined the effect of Traumatic Brain Injury 10 years post-injury. Frequencies of head injury symptoms and activity limitation by level of severity were measured in a consecutive series of 61 adults who were admitted to a tertiary-care center for traumatic brain injury. Irritability and Anxiety were the most frequently reported symptoms from the Head Injury Symptom Checklist. Bothered by noise and Bothered by light were the least frequently reported. Trouble hearing what is said in a group conversation and Trouble hearing what is said in a one-to-one conversation were the most commonly reported limitations of activity from the Health and Activity Limitations Survey. Overall, this study illustrates that symptoms remain many years following brain injury, irrespective of the injury's severity.

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#3104 Is dipsogenic diabetes insipidus the same condition as psychogenic polydipsia?

Journal of Neurology Neurosurgery & Psychiatry ◽

10.1136/jnnp-2021-bnpa.27 ◽

2021 ◽

Vol 92 (8) ◽

pp. A11.2-A11

Author(s):

Ewelina de Leon ◽

Graeme Yorston

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Head Injury ◽

Literature Review ◽

Diabetes Insipidus ◽

Endocrine Disruption ◽

Psychiatric Disease ◽

List Type ◽

Psychogenic Polydipsia

Objectives/AimsTraumatic brain injury is a common cause of permanent or long-term disability,1 and up to 80% of people with moderate to severe brain injury have some degree of pituitary insufficiency. Endocrine disruption has been documented in medical literature since the 1940s,2-4 where central diabetes insipidus has been described as a common transient complication which causes polydipsia (insatiable thirst). However, polydipsia can be caused by other conditions. It is classified into dipsogenic, in a syndrome of disordered thirst-regulating mechanism in patients without psychiatric disease called dipsogenic diabetes insipidus, psychogenic, as a compulsive water drinking in patients with psychiatric conditions referred to as psychogenic polydipsia or psychogenic diabetes insipidus and iatrogenic where large quantities of water are consumed for health benefits. All of which are referred to as primary polydipsia if these conditions cannot be distinguished. Dipsogenic diabetes insipidus and psychogenic polydipsia can be easily mixed up, misdiagnosed or even unrecognised, mainly because their pathophysiology is still unclear. Are these conditions different, or is there anything that can relate them to each other? With this literature review, we are aiming to find the link between subsets of polydipsia after brain trauma, to compare proposed differential diagnosis and their functionality in clinical settings.MethodA literature review was conducted following a search of MEDLINE, CINAHL Plus, APA PsycArticles, APA PsycBooks, APA PsycInfo databases from 1858 onwards.ResultsWe will present our findings from the literature review.ConclusionPolydipsia is a common clinical problem and requires careful evaluation and management to prevent long term neurological sequelae, and there are no evidence-based treatment guidelines.References National Institute of Health and Care Excellence (NICE). (2019). Head Injury. CG176. Retrieved from: https://www.nice.org.uk/guidance/cg176 Escamilla RF, Lisser H. Simmonds disease: A clinical study with revie of the literature; Differentiation from anorexia nervosa by statistical analysis of 595 cases, 101 of which were provided pathologically. The Journal of Clinical Endocrinology & Metabolism 1942;2(2):6596. Porter RJ, Miller RA. Diabetes insipidus following closed head injury. Journal of Neurology, Neurosurgery, and Psychiatry 1946;11:528562. Webb NE, Little B, Loupee-Wilson S, Power EM. Traumatic brain injury and neuro-endocrine disruption: medical and psychosocial rehabilitation. NeuroRehabilitation (Reading, Mass.) 2014;34(4):625636.

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Pengelolaan Central Diabetes Insipidus Pasca Cedera Kepala Berat

Jurnal Neuroanestesi Indonesia ◽

10.24244/jni.v8i2.219 ◽

2019 ◽

Vol 8 (2) ◽

pp. 99-104

Author(s):

Bona Akhmad Fithrah ◽

Marsudi Rasman ◽

Siti Chasnak Saleh

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Diabetes Insipidus ◽

Antidiuretic Hormone ◽

Central Diabetes Insipidus ◽

Young Generation ◽

Posterior Pituitary ◽

Challenging Problem ◽

Mortality And Morbidity ◽

Post Traumatic

Cedera otak traumatika adalah salah satu penyebab kematian dan kesakitan tersering pada kelompok masyarakat muda. Hasil akhir dari cedera kepala berat dapat menyebabkan gangguan kognitif, perilaku, psikologi dan sosial. Salah satu konsekuensi dari cedera kepala berat adalah terjadinya disfungsi hormonal baik dari hipofise anterior maupun posterior. Angka kejadian disfungsi hormonal ini sekitar 20-50%. Salah satu yang paling menantang dan sering terjadi adalah diabetes insipidus (DI) dan Syndrome inappropriate antidiuretic hormone (SIADH). Angka kejadian diabetes insipidus pasca cedera kepala diduga sebesar 1-2,9% dengan berbagai tingkatannya. Pada beberapa kasus bersifat sementara tapi beberapa kasus terjadi bersifat menetap. Pada laporan kasus ini akan dibawakan sebuah kasus diabetes insipidus pasca cedera kepala berat. Pasien mengalami cedera kepala berat, hingga dilakukan decompressive craniectomi dan trakeostomi. Untuk perawatan lanjutan pasien dirujuk ke Jakarta. Saat menjalani terapi lanjutan ini pasien terdiagnosis diabetes insipidus Pada kasus ini diabetes insipidus tidak timbul langsung setelah cedera kepala tetapi baru timbul lebih kurang satu bulan setelah cedera kepala. Diabetes insipidus dikelola dengan menggunakan desmopressin spray dan oral disamping mengganti cairan yang hilang. Pada kasus ini desmopressin sempat di stop sebelum akhirnya diberikan terus menerus dan pasien diterapi sebagai diabetes insipidus yang menetap. Managing Central Diabetes Insipidus in Post Severe Head Injury PatientAbstractTraumatic brain injury is the cause of mortality and morbidity in society mostly in male-young generation. The last outcome of traumatic brain injury might be deficit in cognitive, behavioral, psychological and social. the consequences of traumatic brain injury might be hormonal disfunction from anterior and posterior pituitary. The incidence around 20-50%. The most challenging problem is diabetes insipidus (DI) and syndrome of inappropriate antidiuretic hormone (SIADH). The incident of post traumatic diabetes insipidus around 1-2,9% with several degree. In certain case its only occurred transiently but some report it could be permanent. In this case report will find one case post traumatic diabetes insipidus. This pasien had severe traumatic brain injury and underwent decompressive craniectomy and tracheostomy. For further therapy patient was referred to Jakarta. In this further treatment patient diagnosed with diabetes insipidus. Diabetes insipidus doesn’t occurred since the first day of injury but occurred almost one month after. Diabetes insipidus managed with desmopressin spray and oral beside replace water loss. For a few days desmopressin stop but diabetes insipidus occurred again so desmopressin given daily both spray and oral and the patient had therapy as diabetes insipidus permanent.

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Posterior pituitary dysfunction following traumatic brain injury: review

Pituitary ◽

10.1007/s11102-018-0917-z ◽

2018 ◽

Vol 22 (3) ◽

pp. 296-304 ◽

Cited By ~ 9

Author(s):

Roxana Maria Tudor ◽

Christopher J. Thompson

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Posterior Pituitary ◽

Pituitary Dysfunction

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Clinico-radiologic Profile of Pediatric Traumatic Brain Injury in Western Rajasthan

Journal of Neurosciences in Rural Practice ◽

10.4103/jnrp.jnrp_269_17 ◽

2018 ◽

Vol 09 (02) ◽

pp. 226-231 ◽

Cited By ~ 2

Author(s):

Pawan Kumar Dara ◽

Manish Parakh ◽

Shyama Choudhary ◽

Hemant Jangid ◽

Priyanka Kumari ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Hospital Stay ◽

Road Traffic ◽

Tertiary Care ◽

Care Hospital ◽

Pediatric Traumatic Brain Injury ◽

Csf Rhinorrhea ◽

Temporal Bone Fracture ◽

Fall From Height

ABSTRACTObjective: The aim of this study was to evaluate clinico-radiological profile and outcome of pediatric traumatic brain injury (TBI). Design: Prospective observational study Setting: Intensive Care Unit, ward and OPD of Pediatrics, Dr. S. N. Medical College, Jodhpur (tertiary care hospital). Participants: A total of 188 children (1 month–18 years) were enrolled and 108 admitted. Intervention: TBI classified as mild, moderate, or severe TBI. Neuroimaging was done and managed as per protocol. Demographic profile, mode of transport, and injury were recorded. Outcome: Measured as hospital stay duration, focal deficits, mortality, and effect of early physiotherapy. Results: Males slightly outnumbered females mean age was 5.41 ± 4.20 years. Fall from height was the main cause of TBI (61.11%) followed by road traffic accident (RTA) (27.78%). Majority (56.56%) reached hospital within 6 h of injury, out of which 27% of patients were unconscious. Mild, moderate, and severe grade of TBI was seen in 50%, 27.78%, and 22.22% of cases, respectively. About 12.96% of cases required ventilator support. The average duration of hospital stay was 11.81 ± 12.9 days and was lesser when physiotherapy and rehabilitation were started early. In all children with temporal bone fracture, magnetic resonance imaging (MRI) brain revealed a temporal lobe hematoma and contusion in spite of initial computed tomography (CT) head normal. Children who have cerebrospinal fluid (CSF) rhinorrhea/otorrhea had a high chance of fracture of base of skull and contusion of the basal part of the brain. Conclusion: In India, fall from height is common setting for pediatric TBI besides RTA. Early initiation of physiotherapy results in good outcome. MRI detects basal brain contusions in children presenting with CSF rhinorrhea/otorrhea even if initial CT brain is normal.

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Pituitary dysfunction after traumatic brain injury: are there definitive data in children?

Archives of Disease in Childhood ◽

10.1136/archdischild-2016-311609 ◽

2016 ◽

Vol 102 (6) ◽

pp. 572-577 ◽

Cited By ~ 13

Author(s):

Paula Casano-Sancho

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Paediatric Population ◽

Thyroid Stimulating Hormone ◽

Medical Community ◽

International Consensus ◽

Hormonal Replacement ◽

Pituitary Dysfunction ◽

International Consensus Statement

In the past decade, several studies in adults and children have described the risk of pituitary dysfunction after traumatic brain injury (TBI). As a result, an international consensus statement recommended follow-up on the survivors. This paper reviews published studies regarding hypopituitarism after TBI in children and compares their results. The prevalence of hypopituitarism ranges from 5% to 57%. Growth hormone (GH) and ACTH deficiency are the most common, followed by gonadotropins and thyroid-stimulating hormone. Paediatric studies have failed to identify risk factors for developing hypopituitarism, and therefore we have no tools to restrict screening in severe TBI. In addition, the present review highlights the lack of a unified follow-up and the fact that unrecognised pituitary dysfunction is frequent in paediatric population. The effect of hormonal replacement in patient recovery is important enough to consider baseline screening and reassessment between 6 and 12 months after TBI. Medical community should be aware of the risk of pituitary dysfunction in these patients, given the high prevalence of endocrine dysfunction already reported in the studies. Longer prospective studies are needed to uncover the natural course of pituitary dysfunction, and new studies should be designed to test the benefit of hormonal replacement in metabolic, cognitive and functional outcome in these patients.

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Pituitary deficiency and precocious puberty after childhood severe traumatic brain injury: a long-term follow-up prospective study

Acta Endocrinologica ◽

10.1530/eje-19-0034 ◽

2019 ◽

Vol 180 (5) ◽

pp. 281-290 ◽

Cited By ~ 7

Author(s):

Yamina Dassa ◽

Hélène Crosnier ◽

Mathilde Chevignard ◽

Magali Viaud ◽

Claire Personnier ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Precocious Puberty ◽

Central Precocious Puberty ◽

Height Velocity ◽

Prospective Longitudinal Study ◽

Pituitary Dysfunction ◽

Severe Tbi ◽

Prospective Longitudinal

Objectives Childhood traumatic brain injury (TBI) is a public health issue. Our objectives were to determine the prevalence of permanent pituitary hormone deficiency and to detect the emergence of other pituitary dysfunctions or central precocious puberty several years after severe TBI. Design Follow-up at least 5 years post severe TBI of a prospective longitudinal study. Patients Overall, 66/87 children, who had endocrine evaluation 1 year post severe TBI, were included (24 with pituitary dysfunction 1 year post TBI). Main outcome measures In all children, the pituitary hormones basal levels were assessed at least 5 years post TBI. Growth hormone (GH) stimulation tests were performed 3–4 years post TBI in children with GH deficiency (GHD) 1 year post TBI and in all children with low height velocity (<−1 DS) or low IGF-1 (<−2 DS). Central precocious puberty (CPP) was confirmed by GnRH stimulation test. Results Overall, 61/66 children were followed up 7 (5–10) years post TBI (median; (range)); 17/61 children had GHD 1 year post TBI, and GHD was confirmed in 5/17 patients. For one boy, with normal pituitary function 1 year post TBI, GHD was diagnosed 6.5 years post TBI. 4/61 patients developed CPP, 5.7 (2.4–6.1) years post-TBI. Having a pituitary dysfunction 1 year post TBI was significantly associated with pituitary dysfunction or CPP more than 5 years post TBI. Conclusion Severe TBI in childhood can lead to permanent pituitary dysfunction; GHD and CPP may appear after many years. We recommend systematic hormonal assessment in children 1 year after severe TBI and a prolonged monitoring of growth and pubertal maturation. Recommendations should be elaborated for the families and treating physicians.

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Decompressive craniectomy and postoperative complication management in infants and toddlers with severe traumatic brain injuries

Journal of Neurosurgery Pediatrics ◽

10.3171/2008.12.peds08310 ◽

2009 ◽

Vol 3 (4) ◽

pp. 334-339 ◽

Cited By ~ 37

Author(s):

Matthew A. Adamo ◽

Doniel Drazin ◽

John B. Waldman

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Head Injury ◽

Physical Examination ◽

Decompressive Craniectomy ◽

Severe Traumatic Brain Injury ◽

Brain Injuries ◽

Brain Lesion ◽

High Rate

Object Infants with severe traumatic brain injury represent a therapeutic challenge. The internal absence of open space within the infant cranial vault makes volume increases poorly tolerated. This report presents 7 cases of decompressive craniectomy in infants with cerebral edema. Methods The authors reviewed the medical charts of infants with brain injuries who presented to Albany Medical Center Hospital between January 2004 and July 2007. Variables that were examined included patient age, physical examination results at admission, positive imaging findings, surgery performed, complications, requirement of permanent CSF diversion, and physical examination results at discharge and outpatient follow-up using the King's Outcome Scale for Childhood Head Injury. Seven infants met the inclusion criteria for the study. Six infants experienced nonaccidental trauma, and 1 had a large infarction of the middle cerebral artery territory secondary to a carotid dissection. At admission, all patients were minimally responsive, 4 had equal and minimally reactive pupils, 3 had anisocoria with the enlarged pupil on the same side as the brain lesion, and all had right-sided hemiparesis. Six patients received a left hemicraniectomy, whereas 1 received a left frontal craniectomy. In all cases, bone was cultured and stored at the bone bank. Results Postoperatively, 3 patients who developed draining CSF fistulas needed insertions of external ventricular drains, with incisions oversewn using nylon sutures and a liquid bonding agent. After prolonged CSF drainage and wound care, these patients all developed epidural and subdural empyemas necessitating surgical drainage and debridement. Methicillin-resistant Staphylococcus aureus was found in 2 patients and Enterococcus in the third. All patients developed hydrocephalus necessitating the insertion of a ventriculoperitoneal shunt, and all had bone replaced within 1–6 months from the time of the original operation. Two patients required reoperation due to bone resorption. At outpatient follow-up visits, all had scores of 3 or 4 on the King's Outcome Scale for Childhood Head Injury. Each patient was awake, interactive, and could sit, as well as either crawl or walk with assistance. All had persistent, improving right-sided hemiparesis and spasticity. Conclusions Despite poor initial examination results, infants with severe traumatic brain injury can safely undergo decompressive craniectomy with reasonable neurological recovery. Postoperative complications must be anticipated and treated appropriately. Due to the high rate of CSF fistulas encountered in this study, it appears reasonable to recommend both the suturing in of a dural augmentation graft and the placement of either a subdural drain or a ventriculostomy catheter to relieve pressure on the healing surgical incision. Also, one might want to consider using a T-shaped incision as opposed to the traditional reverse question mark-shaped incision because wound healing may be compromised due to the potential interruption of the circulation to the posterior and inferior limb with this latter incision.

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Emotional reserve and prolonged post-concussive symptoms and disability: a Swedish prospective 1-year mild traumatic brain injury cohort study

BMJ Open ◽

10.1136/bmjopen-2017-020884 ◽

2018 ◽

Vol 8 (7) ◽

pp. e020884 ◽

Cited By ~ 3

Author(s):

Christian Oldenburg ◽

Anders Lundin ◽

Gunnar Edman ◽

Catharina Nygren Deboussard ◽

Aniko Bartfai

Keyword(s):

Traumatic Brain Injury ◽

Cohort Study ◽

Brain Injury ◽

Head Injury ◽

Emergency Departments ◽

Psychological Resilience ◽

Psychiatric Assessment ◽

Post Traumatic ◽

Traumatic Symptoms

ObjectiveProlonged post-concussive symptoms (PCS) affect a significant minority of patients withmild traumatic brain injury (mTBI). The aetiology is multifactorial depending on preinjury as well as peri-injury and postinjury factors. In this study, we examine outcome from an emotional reserve perspective.DesignProspective cohort study.SettingPatients were recruited from three emergency departments in major university hospitals in Stockholm, Sweden. Follow-up data were collected in an outpatient setting at one of the recruiting hospitals.Participants122 patients with a history of blunt head trauma (aged 15–65 years; admitted for mTBI within 24 hours after trauma (Glasgow Coma Scale score of 14–15, loss of consciousness <30 min and/or post-traumatic amnesia <24 hours). Exclusion criteria were other significant physical injury and other major neurological disorder, including previous significant head injury.ProcedureRecruitment in three emergency departments. Initial assessments were made within 1 week after the injury. Patients were mailed the follow-up questionnaires 1 year postinjury.Outcome measuresA psychiatric assessment was performed at 1 week post injury. The participants also completed a personality inventory, measures of psychological resilience, depression, anxiety and post-traumatic symptoms. One-year outcome was measured by the Rivermead Post Concussion Symptoms and the Rivermead Head Injury Follow-Up questionnaires.ResultsThe psychiatric assessment revealed more symptoms of anxiety, depression and post-traumatic symptoms in the acute stage for patients who later developed PCS.After 1 year, 94 participants were still in the programme (male/female 57/37) and 12% matched the extended criteria for PCS (≥3 symptoms and ≥2 disabilities). PCS patients reported more preinjury and concurrent psychiatric problems, lower level of functioning before the injury and experienced more stress. They showed higher somatic trait anxiety, embitterment, mistrust and lower level of psychological resilience than recovered participants.ConclusionIntrapersonal emotional reserve shape the emergence and persistence of PCS after mTBI.

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SAT-235 Young Male with Persistent Central Diabetes Insipidus After a Car Accident

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.548 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Liudmila Yesaulava ◽

Caroline Houston ◽

Sanjeda Sultana

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Specific Gravity ◽

Diabetes Insipidus ◽

Intracranial Hypertension ◽

Serum Sodium ◽

Mass Effect ◽

Midline Shift ◽

Pituitary Dysfunction ◽

Ct Head

Abstract BACKGROUND: Central diabetes insipidus (CDI) occurs in 20% of cases of traumatic brain injury (TBI). Most cases of post-TBI CDI resolve within 2–5 days. Only 6% of long-term survivors of TBI have evidence of persistent CDI.1 We report a patient with persistent CDI after TBI. Clinical Case: A 27 year old male was referred for polyuria. Three months prior he was in a rollover motor vehicle accident. At that time, CT head revealed frontal and occipital contusions with scattered subarachnoid, subdural, and intraventricular blood. There was no evidence of skull fracture, mass-effect, or midline shift. On hospital day 4, his urine output increased to > 3L/day, with serum sodium of 146 mEq/L (n 135–145) and urine specific gravity of 1.015 (n 1.005–1.030). Repeat head CT revealed bilateral subdural hematomas causing mild mass effect. During the rest of his 2-month hospitalization, he continued to have polyuria with specific gravity as low as 1.005, and occasional hypernatremia, with a peak serum sodium of 149 mEq/L. Serum sodium on discharge was 144 mEq/L. On presentation to our clinic, his family and caretakers reported polydipsia, polyuria and nocturia. He had no history of diabetes mellitus or lithium use. On exam he was tachycardic but normotensive with no signs of dehydration. Neurologic exam was normal except for distractibility and impaired long- and short-term memory. After 3 hours of water deprivation, laboratory testing revealed serum sodium 150 mEq/L, serum osmolality 307 mOsmol/kg (n 270–295), urine osmolality 119 mOsmol/kg (n 300–900), and ADH 3 pmol/L (n </= 14); consistent with CDI. Oral desmopressin led to resolution of polydipsia and polyuria. Evaluation of anterior pituitary function was normal. Six months post TBI, CT head revealed increased left frontal subdural hematoma with effacement of the right lateral ventricle and 1cm left-to-right midline shift. A burr hole procedure was performed but CDI persisted. Conclusion: Animal studies have shown that neurohypophyseal apoptosis occurs by inducing intracranial hypertension lasting 12 hours or more.2 Persistent DI may herald rising intracranial pressure (ICP), as reflected by our patient’s case.1 Clinicians should be aware of the reciprocal association between increased ICP and persistent CDI following TBI. References: (1) Tudor R. M., Thompson C. J. Posterior pituitary dysfunction following traumatic brain injury: review. Pituitary. 2019 Jun; 22(3):296–304. (2) Tan H., et al. Assessment of the role of intracranial hypertension and stress on hippocampal cell apoptosis and hypothalamic-pituitary dysfunction after TBI. Sci Rep. 2017 Jun; 7(1):3805.

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