Hypopituitarism following head trauma

678

Communications

Table

in brief

I. Lack of effect of HCG on serum

estrone

(El)

and

estradiol

(&)

levels

in ovariectomized

rhesus

monkeya

Da) 1 R542 El E2 686-V b E2 P-178 El EP C-l 42 El E2

15 24

21 <11

19 12

<15 12

415 23

16 37

24 16

17 15

<15
115 17

17 21




Measurements

are given

in picograms

Cl3
R. D.

LAWRENCE WILLIAM

WEISS,

M. J.

per milliliter

reported trauma

Cl5 21

24 16

20 29

19 25

16 15

23 15

Cl5 ‘19-


15 21

19 15

Cl5 16

Cl.5 Cl1


< 1.5
< I.5 13

115 12



14


I5

of serum

M.D M.D.

Departmezts of Mrdirine and Obstetk-Gynecology and the Endocrine Laboratory University of‘ Miami School of Medicine and the Medical Sewice, Veterans Administration Hospital, Miami, Florida ALTHOUGH

< 1 .:,
<15 25

M.D.*

FISHMAN,

IH 16

<15
M.D.

LEMAIRE,

-< I 5 I .i


following head trauma

JACOBI,

115 17

ilti

1. Poliak, A., Smith, J. J., Friedlander, D., and Romney, S. L.: Estrogen synthesis in castrated women: The action of human chorionic gonadotropin and corticotropin, AM. J. OBSTET. GYNECOL. 110:376. 1971. 2. van Hall, E. V., and Heintz, A. P. M.: Influence of HCG on the production of estrogens in the ovariectomized rhesus monkey. AM.J. OBSTET.GYNECOL. 108: 317, 1970.

STUART

Cl5 11

<15 13

REFERENCES

JORGE

18 12

115 <11

Unlike the findings of van Hall and Heintz,’ our results provide no evidence for HCG stimulation of estrogen production in ovariectomized monkeys and are in agreement with findings in clinical studies on castrated women. ’

Hypopituitarism

(15 11

HEAD TRAUMA is one of the rarest of causes of hypopituitarism,’ the frequency of and the greater likelihood of survival cJf such

Supported in part by National Institutes of Health Grant HD-05866, by Grant RR-261 from the General Clinical Research Centers Program of the Division of Research Resources (National Institutes of Health), and bv Ford Foundation Grant 0338. Reprint requests: Dr. Jorge D. Jacobi, Medical Service, Veterans Administration Hospital, 1201 N.W. 16th St., Miami, Florida 33125. *Dr. Weiss was supported by a Veterans Administration Training Grant in Endocrinology and Metabolism (TR-177).

patients suggest than an awareness of the possibility of posttraumatic hypopituitarism is appropriate. We report here the case of a young woman who manifested hypopituitarism two years after sustaining severe head trauma. A ZO-year-old woman was admitted to the hospital in May, 1972, following an automobile accident. The patient had multiple facial fractures. A left facial nerve palsy, cerebrospinal fluid otorrhea, blindness in the right eye, and facial lacerations were noted. A period of supportive care and observation &as followed by successful decompression of the left facial nerve. The patient was discharged home two months after the accident; she was much improved except for mental sluggishness. Cosmetic rhinoplasty was performed uneventfully 17 months later. Two years later, the patient reported a slight improvement in mental status. Although she previously had regular menses. following the accident the patient become amenorrheic. Two years after the injury, an injection of progesterone did not induce withdrawal bleeding. During this interval, the patient experienced cold intolerance, easy fatigability, somnolence, and increasingly dry skin. At no time did she manifest symptoms of diabetes insipidus. Two and a hall. years after the accident. she was readmitted for further evaluation. The patient was a thin woman. alert, but with a poor atten-

tion span and memory. The pulse rate was 68 beats per ruinute; blood pressure, 85175 mm. Hg supine and 75/60 mm. Hg standing. Vision was completely absent in the righr eye. The thyroid gland was not enlarged. The breasts were small and nonpigmented; there was no galactorrhea. Pelvic examination was normal except for evidence of estrogen defiricnr v. The skin was dry and had a sallow appearance. Deep tendon reflexes showed a delayed relaxation phase. The remainder of the physical examination was unremarkable. Laboratory values on admission included the following: hematocrit, 3 1 per cent; hemoglobin, 10.4 Gm. per 100 ml.; white blood cells, 4,100 per cubic millimeter with a normal differential; serum sodium, 142 mEq. per liter; potassium, 4.3 mEq. per liter; carbon dioxide. 23 mEq. per liter; chloride,

106 mEq. per liter; blood urea nitrogen. blood glucose, 85 mg. per 100 ml. per

Endocrine 100 ml.

evaluation included: (normal 5.5 to 12.5);

18 mg. per 100 ml.:

serum thyroxine, triiodothyronine

4.7 kg resin up-

Communications

Table I. Hormonal responses luteinizing hormone-releasing

following hormone

In.tulin-induced (0.05 Tivw (min.) -30 -15 0 10 15 20 30 60 90 120 *Standard

Glucose (mg.

administration (LRH)

h@oglycemia U./Kg.)

COl-tiSOl

$7)

(mcg.

80 72 50 42 52 68 78

(200 HGH (ng. lml.)

%)

-

was the Second

International

TSH

Reference

hor-

Transient posterior pituitary dysfunction is not uncommonly seen after head trauma,6 and permanent diabetes insipidus has been reported in several inlaboratory following

deficiencies

and

evidence head trauma

of anterior has rarely

3, ’ Pathologic studies of the anterior pituitary are at variance with clinical reports.‘, * Possible factors accounting for this disparity between clinical and pathologic findings include the apparent requirement that at least two thirds of the anterior lobe must be destroyed before clinically recognizable hormonal occur’

the

observation

sustaining this degree of trauma vive long enough for endocrine

that

patients

frequently do not surabnormalities to be-

come apparent. Partial or evolving anterior insufficiency may go clinically unrecognized years, as in patients with Sheehan’s7

pituitary for many

syndrome.

Preparation

(TRH).

and

LH* (ml. 1’. lml. 1

FSH* (ml. C. lml. )

6

8 10 5 10 12 9 10

7 6 13 12 10 13 of human

Hypothalamic producing

679

LRH (1011 mrg. subrutaneou$)

(ylilml.)

mone (TSH). 3.9 pU. per milliliter (normal 1.5 to 5.5); 8 A.M. plasma cortisol. 4.0 pg per 100 ml.; urinary 17-hydroxysteroids, 0.2 mg. per 24 hours, 17-ketosteroids, 1.0 mg. per 24 hours: after Metopirone, the levels remained within the same very low range. Further evaluation of pituitary reserve is summarized in Table I. Neither plasma cortisol nor growth hormone rose despite adequate hypoglycemia. Also, neither TSH, luteinizing hormone (LH), nor follicle-stimulating hormone (FSH) rose following administration of their respective hypothalamic releasing factors. Thus, the diagnosis of anterior pituitary insufficiency was made, and the patient was begun on replacement therapy with cortisone acetate, estrogen, and thyroid hormone. Subsequently, she has reported increasing physical endurance, a general feeling of well-being. and regular withdrawal menses.

or

hormone

ii 2.6 4.1 3.8 -

take, 22 per cent (normal 24 to 36); thyroid-stimulating

stances.“* 6 Clinical pituitary dysfunction been described.‘.

thyroid-releasing

TRH mcg. tntrarJenously)

1.2 1.2 1.2 1.2 1.2 1.2 1.2

3.8 3.8 5.0 4.8 5.9 3.6 5.1

employed

of insulin,

in brief

menopausal

gonadotropin.

dysfunction both

diabetes

following

head

insipidus

and

trauma, hypothy-

roidism, has recently been described.5a ‘Thus, anterior pituitary insufficiency consequent to head trauma may result from either hypothalamic or direct pituitary injury. These observations suggest that evaluation of the hypothalamic pituitary axis is indicated following severe head trauma, particularly if diabetes insipidus or amenorrhea occurs. The helpful acknowledged.

suggestions

of

Dr.

Robert

B. Daroff

are

REFERENCES

1. Altman, R., and Pruzanski, W.: Post-traumatic hypopituitarism. Ann. Intern. Med. 55: 149, 1961. 2. Ceballos, R.: Pituitary changes in head trauma, Ala. J. Med. Sci. 3: 185, 1966. 3. Goldman, K. P., and Jacobs, A.: Anterior and posterior pituitary failure after head injury, Br. Med. J. 2: 1924, 1960. 4. Kornblum, R., and Fisher, R.: Pituitary lesions in craniocerebral injuries, Arch. Pathol. 88: 242, 1969. 5. Pittman, J.* Haigler, E. C., et al.: Hypothalamic hypothyroidism, N. Engl. J. Med. 285: 844, 1971. 6. Porter, R. J.. and Miller, R. A.: Diabetes insipidus following closed head injury, J. Neural. Neurosurg. Psychiatry 11: 258, 1948. 7. Sheehan, H. C.: The incidence of postpartum hypopituitarism, AM. J. OBSTET. GYNECOL. 68: 202, 1954. 8. Witter, H., and Tascher, R.: Fortschr. Neurol. Psychiatr) 25: 523. 1957. 9. Woolf, P., and Schalch, D. S.: Hypopituitarism secondary to hypothalamic insufficiency, Ann. Intern. Med. 78: 88. 1973.