Provocative hypothalamopituitary axis tests in severe head injury

Corte, Francesco Della; Mancini, Antonio; Valle, Domenico; Gallizzi, Francesca; Carducci, P; Mignani, Vittorio; Marinis, Laura De

doi:10.1097/00003246-199808000-00030

Cited by 89 publications

(13 citation statements)

References 32 publications

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“…Hyponatremia was previously thought to be primarily due to SIADH [7,49], with acute ACTH deficiency felt to be a relatively rare entity. However, almost all previous studies relied on assessment of cortisol dynamics at a single time point, providing only a “snapshot” of patients’ pituitary function [50,51,52,53,54,55,56]. Plasma cortisol levels are highly dynamic in the days following TBI [51,52], so protocols with only a single time point for testing may underestimate the true incidence of pituitary dysfunction immediately following TBI.…”

Section: Hyponatremia Following Traumatic Brain Injurymentioning

confidence: 99%

Neurosurgical Hyponatremia

Hannon

Thompson

2014

JCM

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Hyponatremia is a frequent electrolyte imbalance in hospital inpatients. Acute onset hyponatremia is particularly common in patients who have undergone any type of brain insult, including traumatic brain injury, subarachnoid hemorrhage and brain tumors, and is a frequent complication of intracranial procedures. Acute hyponatremia is more clinically dangerous than chronic hyponatremia, as it creates an osmotic gradient between the brain and the plasma, which promotes the movement of water from the plasma into brain cells, causing cerebral edema and neurological compromise. Unless acute hyponatremia is corrected promptly and effectively, cerebral edema may manifest through impaired consciousness level, seizures, elevated intracranial pressure, and, potentially, death due to cerebral herniation. The pathophysiology of hyponatremia in neurotrauma is multifactorial, but most cases appear to be due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Classical treatment of SIADH with fluid restriction is frequently ineffective, and in some circumstances, such as following subarachnoid hemorrhage, contraindicated. However, the recently developed vasopressin receptor antagonist class of drugs provides a very useful tool in the management of neurosurgical SIADH. In this review, we summarize the existing literature on the clinical features, causes, and management of hyponatremia in the neurosurgical patient.

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Section: Hyponatremia Following Traumatic Brain Injurymentioning

confidence: 99%

Neurosurgical Hyponatremia

Hannon

Thompson

2014

JCM

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“…In contrast, patients with severe penetrating head injury may manifest hypocortisolaemia early after trauma (22). Random serum GH concentrations were reported to be elevated after TBI (25), with an exaggerated response to GHRH (26). However, impaired GH response to arginine has also been reported in patients with very severe TBI, with high mortality (27).…”

Section: Anterior Pituitarymentioning

confidence: 99%

“…Other workers have demonstrated low TSH and T3 concentrations after TBI, which seem to be adaptive changes rather than pituitary failure (22). Some studies have linked hypothyroidism to poor outcome from TBI (22,31), though this association is not universally shared (26) and remains unproven.…”

Section: Anterior Pituitarymentioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: Neuroendocrine surveillance and management of neurosurgical patients

Garrahy

Sherlock

Thompson

2017

European Journal of Endocrinology

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Advances in the management of traumatic brain injury, subarachnoid haemorrhage and intracranial tumours have led to improved survival rates and an increased focus on quality of life of survivors. Endocrine sequelae of the acute brain insult and subsequent neurosurgery, peri-operative fluid administration and/or cranial irradiation are now well described. Unrecognised acute hypopituitarism, particularly ACTH/cortisol deficiency and diabetes insipidus, can be life threatening. Although hypopituitarism may be transient, up to 30% of survivors of TBI have chronic hypopituitarism, which can diminish quality of life and hamper rehabilitation. Patients who survive SAH may also develop hypopituitarism, though it is less common than after TBI. The growth hormone axis is most frequently affected. There is also accumulating evidence that survivors of intracranial malignancy, who have required cranial irradiation, may develop hypopituitarism. The time course of the development of hormone deficits is varied, and predictors of pituitary dysfunction are unreliable. Furthermore, diagnosis of GH and ACTH deficiency require dynamic testing that can be resource intensive. Thus the surveillance and management of neuroendocrine dysfunction in neurosurgical patients poses significant logistic challenges to endocrine services. However, diagnosis and management of pituitary dysfunction can be rewarding. Appropriate hormone replacement can improve quality of life, prevent complications such as muscle atrophy, infection and osteoporosis and improve engagement with physiotherapy and rehabilitation.

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“…For example, a blunted GH response to GHRH or arginine (ARG) stimulation test has been found in patients with severe TBI and very poor outcome [148]. By contrast, a normal GH response to GHRH has been reported in severely head-injured patients, with a progressive increase in such response from day 2 to day 15 after injury in the patients with poor outcome [149]. The adequacy of GH reserve has also been investigated by dynamic testing both in acute and chronic phase of TBI.…”

Section: Gh-igf-i Axismentioning

confidence: 99%

Systemic illness

et al. 2008

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Systemic illnesses are associated with alterations in the hypothalamic-pituitary-peripheral hormone axes, which represent part of the adaptive response to stressful events and may be influenced by type and severity of illness and/or pharmacological therapy. The pituitary gland responds to an acute stressful event with two secretory patterns: adrenocorticotropin (ACTH), prolactin (PRL) and growth hormone (GH) levels increase, while luteinizing hormone (LH), follicle-stimulating hormone (FSH) and thyrotropin (TSH) levels may either decrease or remain unchanged, associated with a decreased activity of their target organ. In protracted critical illness, there is a uniformly reduced pulsatile secretion of ACTH, TSH, LH, PRL and GH, causing a reduction in serum levels of the respective target-hormones. These adaptations are initially protective; however, if inadequate or excessive they may be dangerous and may contribute to the high morbidity and mortality risk of these patients. There is no consensus regarding the type of approach, as well as the criteria to use to define pituitary axis function in critically ill patients. We here provide a critical approach to pituitary axis evaluation during systemic illness.

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Provocative hypothalamopituitary axis tests in severe head injury

Cited by 89 publications

References 32 publications

Neurosurgical Hyponatremia

Neurosurgical Hyponatremia

MANAGEMENT OF ENDOCRINE DISEASE: Neuroendocrine surveillance and management of neurosurgical patients

Systemic illness

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