Post Head Injury Endocrine Complications Treatment & Management

Updated: Jun 25, 2018
  • Author: Milton J Klein, DO, MBA; Chief Editor: Elizabeth A Moberg-Wolff, MD  more...
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Treatment

Surgical Intervention

Endocrine complications following traumatic brain injury (TBI) are treated by medical management and usually do not require surgical intervention.

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Consultations

Endocrinology subspecialty consultation may be needed following traumatic brain injury (TBI) in patients who demonstrate subtle findings of underlying endocrine abnormalities, as evidenced by a slowdown or complete halt in the progression of a TBI rehabilitation program. This group of patients includes those who have a growth delay (eg, pediatric patients) or unexplained constitutional symptoms of lethargy/poor appetite following TBI, and young female patients with amenorrhea following TBI.

From the endocrinologist's perspective, patients with vital endocrinopathies such as diabetes insipidus, secondary adrenal failure, and secondary hypothyroidism should be promptly treated with hormone replacement therapy (HRT). Secondary hypogonadism and severe growth hormone (GH) deficiency should be considered later, after replacement of other deficits and after retesting. Patients who are severely involved in a persistent vegetative state would not likely benefit from HRT for secondary hypogonadism or GH deficiency. GH replacement therapy outcomes include increased muscle mass/exercise tolerance and improved quality of life/sense of wellness.

Post-TBI patients functioning at a very low level who are institutionalized should receive HRT only for vital endocrine hormones, including hydrocortisone, vasopressin, and T4. All patients with moderate to severe TBI should receive a baseline pituitary hormone deficiency evaluation, especially if they were hospitalized for at least 1 day post-TBI.

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Other Treatment

Electrolyte therapy for patients with hyponatremia following traumatic brain injury (TBI)

See the list below:

  • Hyponatremia is a decrease in serum sodium concentration to less than 136 mmol/L. Dilutional hyponatremia (ie, SIADH) secondary to water retention is the most common form.

  • Hypotonic hyponatremia also results from water retention with essentially normal sodium stores. Most of the symptoms of hyponatremia are attributable to sequelae of central nervous system (CNS) dysfunction, such as headaches, nausea, muscle cramping, lethargy, restlessness, disorientation, and depressed deep tendon reflexes.

  • Slowly developing hyponatremia results in progressive cerebral edema and milder symptoms due to brain adaptation, with these patients experiencing minimal symptomatology. On the other hand, if the hyponatremia is characterized by a rapid onset, intracranial hypertension causes the more dangerous complications referred to above, especially in the more susceptible patient with brain injury. See the image below.

    Effects of hyponatremia on the brain and adaptive Effects of hyponatremia on the brain and adaptive responses. Within minutes after the development of hypotonicity, water gain causes swelling of the brain and a decrease in osmolality of the brain. Partial restoration of brain volume occurs within a few hours as a result of cellular loss of electrolytes (rapid adaptation). The normalization of brain volume is completed within several days through loss of organic osmolytes from brain cells (slow adaptation). Low osmolality in the brain persists despite the normalization of brain volume. Proper correction of hypotonicity reestablishes normal osmolality without risking damage to the brain. Overly aggressive correction of hyponatremia can lead to irreversible brain damage.
  • Aggressive treatment of hyponatremia, even by fluid restriction, can cause osmotic demyelination, a rare and serious complication. Brain shrinkage triggers pontine and extrapontine neuronal demyelination, causing disabling CNS dysfunction, including quadriplegia, pseudobulbar palsy, seizures, coma, and death. Hepatic failure, hypokalemia, and malnutrition are risk factors for osmotic demyelination.

  • Management of hyponatremia

    • Patients with less serious symptoms of hyponatremia and dilute urine concentrations of less than 200 mmol/L usually require fluid retention and close monitoring. More serious symptoms of hyponatremia include urine concentrations of greater than 200 mmol/L.

    • Insensate fluid loss contributes to hyponatremia, assisted by dermal and respiratory losses. Associated endocrinopathies (eg, hypothyroidism, adrenal failure) develop slowly. Hypothyroidism can masquerade as SIADH.

    • The correction of hyponatremia is no more than 8 mmol/L per day.

    • The initial correction is 1-2 mmol/L/h for several hours in patients with severe symptoms of hyponatremia (see table below). Indications to stop the rapid correction of hyponatremia include the need to control life-threatening complications, moderation of other symptoms, and serum sodium concentrations of 125-130 mmol/L.

    • The most common treatment for SIADH is fluid restriction to less than 800 mL/d to induce a negative water balance. If necessary, loop diuretics may be instituted by causing excretion of electrolyte-free water. If this treatment fails, use 600-1200 mg of demeclocycline to cause nephrogenic diabetes insipidus (DI). Assessment of renal function is necessary, because the condition is nephrotoxic, especially in patients with cirrhosis. Table. Formulas for Use in Managing Hyponatremia and Characteristics of Infusates

      Table. (Open Table in a new window)

      Formula*

       

      Clinical Use

      Change in serum Na+ =

      Infusate Na+ — serum Na+

      ——————————

      total body water +1

      Estimate the effect of 1 L on any infusate serum Na+

      Change in serum Na+ =

      (Infusate Na+ + infusate K+)—serum Na+

      ————————————————

      total body water +1

      Estimate the effect of 1 L of any infusate containing Na+ and K+ on serum Na+

       

       

       

      Infusate

      Infusate Na+

      Extracellular—Fluid

      Distribution

       

      mmol/L

      %

      5% sodium chloride in water

      855

      100†

      3% sodium chloride in water

      515

      100†

      0.9% sodium chloride in water

      154

      100

      Ringer lactate solution

      130

      97

      0.45% sodium chloride in water

      77

      73

      0.2% sodium chloride in 5% dextrose in water

      34

      55

      5% dextrose in water

      0

      40

      *The number in formula 1 is a simplification of the expression (infusate Na+ —serum Na+) X 1 liter, with the value yielded by the equation in mmol/L. The estimated total body water (in liters) is calculated as a fraction of body weight. The fraction is 0.6 in children; 0.6 and 0.5 in nonelderly men and women, respectively; and 0.5 and 0.45 in elderly men and women, respectively.†In addition to its complete distribution in the extracellular compartment, this infusate induces osmotic removal of water from the intracellular compartment.

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