The greatest challenge associated with endocrine complications in individuals with traumatic brain injury (TBI) is early recognition of these subtle problems. Endocrine complications can produce significant impact on the progress and outcome of TBI rehabilitation. Prompt diagnosis and treatment of endocrine complications following TBI facilitate the rehabilitation process of patients with TBI. Endocrine dysfunction as a result of TBI can significantly influence daily functioning, and yet it is frequently overlooked.

A  study published by the CDC demonstrated that 4% of patients with TBI sustained an associated neuroendocrine disorder of the hypothalamic-pituitary axis. This condition is underdiagnosed, as demonstrated by evidence that 40-63% of fatal cases of TBI reveal postmortem pathologic findings of the hypothalamus/anterior pituitary. 

What hormone problems can happen with TBI?

Someone with TBI can have one or more problems, depending on the injury. Problems that often occur soon after TBI include:

• Adrenal insufficiency: when the adrenal glands don’t make enough hormones; results in fatigue, weight loss, low blood pressure, vomiting, and dehydration. Adrenal insufficiency can be life-threatening if not treated.

  Primary adrenal insufficiency (PAI) is rare and presents with the superimposed psychiatric symptoms of depression, confusion, and apathy. PAI is associated with fatigue, weakness, anorexia, and weight loss. These problems may present insidiously over a prolonged period. The acute presentation of PAI includes nausea, vomiting, and hypertension.

• Diabetes insipidus: when the pituitary doesn’t make enough ADH; results in frequent urination and extreme thirst.

• Hyponatremia: when certain hormone problems upset the balance of salt and water in the body; can result in headache, fatigue, vomiting, confusion, and convulsions.

Problems that often occur as a result of TBI:

• Hypothyroidism (not enough thyroid hormone): fatigue, constipation, weight gain, irregular menstrual periods, cold intolerance

• Hypogonadism (not enough sex hormones): in women, a stop in menstruation and loss of body hair; in men, sexual dysfunction, breast enlargement, loss of body hair, and muscle loss

• Growth hormone deficiency (not enough growth hormone): in adults, increased fat, loss of muscle and bone, and decreased energy; in kids, growth problems

• Hyperprolactinemia (too much prolactin): irregular menstrual periods, nipple discharge, and erectile dysfunction

• Diabetes insipidus (DI) is an exception, as it does have a specific history. DI most commonly is associated with severe TBI and basilar skull fractures with cranial nerve involvement, craniofacial trauma, and postcardiopulmonary arrest. Delayed onset of DI is associated with a poor prognosis due to hypothalamic involvement causing permanent DI.

  Acute DI following a mild to moderate TBI indicates a posterior pituitary lesion with only a temporary antidiuretic hormone (ADH) deficiency.

• Hypopituitarism – Anterior hypopituitarism (AH) also has a specific history. AH usually is associated with moderate to severe TBI. With improvement of emergency and neurosurgical care for these patients, there are more survivors demonstrating AH. AH may present weeks to months after the TBI, typically in the acute or chronic rehabilitation phase. Any patient with unexplained malaise or a setback with regard to functional status should be examined and tested for AH or the other post-TBI endocrinopathies. In summary, risk factors for AH include relatively serious TBI (Glasgow Coma Scale score < 10), diffuse brain swelling, and hypotensive or hypoxic episodes.

  A literature review by the American Association of Clinical Endocrinologists and the American College of Endocrinology found that although TBI-induced hypopituitarism seems to occur most frequently in relation to severe TBI, hypopituitarism is also a risk for patients with mild TBI and for those who have suffered repeated TBIs or whose brain injury is sports or blast related.

  A study by Silva et al indicated that persons who sustain TBI in motor vehicle accidents, as well as those with posttraumatic seizures, focal cortical contusions, petechial brain hemorrhages, and/or intracranial hemorrhage, are more likely to suffer serious pituitary dysfunction, such as adrenal insufficiency and DI.

• Syndrome of inappropriate antidiuretic hormone is the most common TBI-associated neuroendocrinopathy causing hyponatremia. The incidence is reportedly as high as 33%.

• Cerebral salt wasting (CSW) is a less common cause of hyponatremia in the post-TBI population. These patients are dehydrated and lose weight.

Many patients who survive post–traumatic brain injury (post-TBI) demonstrate endocrine complications. 

• Hypothalamus: a part of the brain that controls the release of hormones made by the pituitary gland

• Pituitary gland: located at the base of the brain, it’s called the “master gland” because it makes hormones that tell other glands (such as the thyroid or adrenal glands) to make other kinds of hormones

• Thyroid gland:  found in the neck, it makes thyroid hormones, which control metabolism; helps the heart, muscles, and other organs work properly

• Adrenal glands: one located on top of each kidney, they make cortisol, which helps the body cope with stress, illness, and injury

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