Journal ofNeurology, Neurosurgery, and Psychiatry, 1979, 42, 955-959

Bullet injury to the pituitary gland: a rare cause ofpanhypopituitarismIBRAHIM S. SALTI, FUAD S. HADDAD, ZAHER N. AMIRI,ALI A. KHALIL, AND AHMAD A. AKAR

From the Departments of Internal Medicine and Surgery, American University Hospital,Beirut, Lebanon

S UMMARY An unusual case of head injury with a direct bullet injury to the pituitary gland isdescribed. The hormonal profile one month after the injury showed severe panhypopituitarismwhich did not improve one month after surgical removal of the intrasellar bullet fragment.

Head trauma has rarely been implicated as a causeof hypopituitarism with only 17 patients reportedin the literature (Altman and Pruzanski, 1961;Klacho et al., 1968; Woolf and Schalch, 1973;Paxson and Brown, 1976). In one additional case,bullet injury to the pituitary region has been im-plicated, although the hypopituitary state was notwell documented (Frank, 1912). The recent avail-ability of hypothalamic releasing hormones per-mitted a full study of hypothalamic pituitaryfunction in only two patients (Woolf and Schalch,1973; Paxson and Brown, 1976). In this report wedescribe the hormonal profile of a patient whohad a bullet injury to the pituitary gland resultingin severe panhypopituitarism.

Case reports

A 32 year old single man was referred to thehospital because of a bullet injury to the head,one month before admission. He had been well,having had a normal puberty and normal second-ary sex characteristics. After the bullet injury, helost consciousness for two days, and regained itspontaneously and gradually without any residualsymptoms except for a mild left temporal head-ache, anosmia, sexual impotence, loss of libido,and lack of energy.Examination revealed a dry cold skin and the

scar at the site of entry of the bullet in the rightforehead (Fig. 1). His blood pressure was 115/80mmHg with no postural hypotension. Pulse ratewas regular at 88 per min. Movements and speechwere slow but the patient was well oriented in time

Address for correspondence and reprint requests: DrI. S. Salti, Depart-ment of Medicine, American University of Beirut, Beirut, Lebanon.Accepted 27 March 1979

95'

and place. Visual fields revealed a left homcny-mous hemianopsia. Both fundi were normal. Onneurological examination a mild left central facial

Fig. 1 Photograph of patient showing site of entryof bullet in the right forehead.

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paresis and bilateral anosmia were observed.External genitalia, including size and consistencyof both testes, were normal. He had a normalmale hair distribution.Haemoglobin, haematocrit, white blood cell

count, fasting serum glucose, creatinine, sodium,potassium, chloride, bicarbonate, calcium, phos-phorus, and cholesterol levels were all normal.Urine analysis was normal. An overnight urine

specific gravity was 1010, and the patient did nothave polyuria or polydipsia.

Skull radiographs revealed a hole in the rightfrontal bone with in-driven bone fragments in thebrain, and multiple fragments of the bullet. Thelargest, lodged in the sella turcica, measured9X10 mm (Fig. 2a and b). A brain scan showedan area of increased uptake of radioactivity in theregion of the in-driven bone fragments suggestive

Fig. 2 Pre-operative lateral (a) andanterior (b) skull radiographs showingin-driven bone fragments and multiplebullet fragments. A major fragmentnzeasuring 9X10 mm is seen within thesella turcica.

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Ibrahim S. Salti, Fuad S. Haddad, Zaher N. Amiri, Ali A. Khalil, and Ahmad A. Akar

of a reaction in that location. A right carotidarteriogram was normal.

Baseline serum thyroxine (T4), growth hormone(GH), prolactin (PRL), glucose, cortisol andfollicle stimulating hormone (FSH), and lutein-ising hormone (LH) levels are shown at the top ofTable 1. There was no response of serum TSHand PRL to administration of thyrotropin releasehormone (TRH) (Table 1), nor was there a re-

sponse of serum GH and cortisol to insulin-induced hypoglycaemia. On the other hand, therewas a sluggish, yet definite response of serum LHto administration of luteinising hormone releasehormone (LHRH), while serum FSH showed no

response. Baseline urinary 17-ketosteroid and 17-hydroxysteroid outputs were low and showed no

rise after metapyrone administration (Table 2).Baseline serum testosterone level was 0.027 nmol/l(normal range, 1.04-3.47 nmol/l) and rose to0.29 nmol/l on the fourth day of treatment withhuman chorionic gonadotropin (HCG), 5000 unitsintramuscularly per day.A right frontal craniotomy was performed with

excision of granulation tissue and in-driven bonefragments from the right frontal lobe. The rightsubfrontal area was explored through an extensionof the previous incision in the forehead. Thearachnoid mater was extremely thickened and hadto be cut with a sharp instrument. The opticnerves were normal, but a cavity filled with granu-lation tissue was found between the optic nerves.The bullet fragment was found within the granu-lation tissue, inferior and slightly medial to theright optic nerve. It was removed with no diffi-culty. The postoperative course was satisfactory.

Pituitary functions were re-evaluated fourweeks after the operation and were found un-

changed (Tables 1 and 2). The visual fields andanosmia were unchanged.The patient was discharged on replacement

therapy with prednisone 7.5 mg/day, levo-thyroxine sodium 0.2 mg/day and HCG, 5000

units intramuscularly every two days. One monthlater, he showed a definite improvement in hisenergy and potency. He continued to have no

polyuria or polydipsia and normal urinary specificgravity.Hormonal determinations were performed ac-

cording to methods previously reported (Arafahand Salti, 1978).

Discussion

The results of endocrine studies on this patientindicate that one month after the injury, he hadalmost total anterior pituitary insufficiency result-ing in hypogonadism, adrenocortical insufficiency,and absence of prolactin and growth hormonesecretions. The deficiencies improved on a secondevaluation a month after surgical removal of thebullet fragment. Although the patient did nothave overt evidence of diabetes insipidus, a partialdeficiency of antidiuretic hormone could havebeen masked by the coexistent adrenal and thyroiddeficiencies.The lack of response of serum PRL and TSH to

TRH stimulation indicate deficiencies of the thyro-tropic and lactotropic hormones in the pituitarygland. The absence of response of serum GH andcortisol to insulin-induced hypoglycaemia couldbe the result of either pituitary or hypothalamicinjury or both. The definite, albeit small responseof serum LH after LHRH administration suggeststhe presence in the pituitary of some residualluteotropic hormones. Thus the low baselineserum LH and testosterone could be, at least inpart, the result of a coexistent hypothalamic or

infundibular injury resulting in failure of releaseof LHRH.Endocrine evaluation of the previously des-

cribed patients revealed pituitary insufficiency ofvarying degrees. In one of the two patients whounderwent investigation with hypothalamic re-

leasing hormones, the pituitary failure was at-

Table 2 Results of metapyrone test

Day Treatment 17-Hydro.y-corticosteroids1 1 7-Ketosteroids2 Creatiniine Volumemg/24hr mg/24hr mmol/volunme ml/24hr

Pre* Postt Pre* Postt Pre* Postt Pre* Postt

I none 2.1 0 1.8 3.6 12.4 14.1 1109 11002 metapyrone+ 2.5 1.1 5.7 2.2 10.6 12.4 2800 10003 2.6 0.8 2.5 9.4 13.3 9.73 2200 850

Normal:1 Urinary 17-hydroxycorticosteroids: 2-10 mg/24hr maximal rise after m2tapyronc at least double baseline.2 Urinary 17-ketosteroids: 10-25 mg/24hr.* Preoperative.t Postoperative.I Dosage 750mg every 4 hours for 6 doses.

958

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Bullet injury to the pituitary gland: a rare cause of panhypopituitarism

tributed to a hypothalamic lesion (Woolf andSchalch, 1973). While hypopituitarism is appar-ently rare in patients who survive head trauma(Altman and Pruzanski, 1961), pituitary necrosiswas observed in as many as 22% of cases of fatalhead injury (Kornblum and Fisher, 1969). It hasbeen suggested that undetected, and hence un-treated hypopituitarism, may be a contributoryfactor to the fatal outcome of severe head trauma(Klacho et al., 1968).

It is possible that in some patients who survivehead injury, hypopituitarism may develop but maygo undetected indefinitely or may improve withtime. In the majority of the reported cases ofpost-traumatic hypopituitarism, the diagnosis wasmade several months or years after the trauma(Altman and Pruzanski, 1961; Klacho et al.,1968). The detection of the hypopituitary state inour patient as early as one month after the injurywas a reflection of the fact that there was directevidence of pituitary destruction which may ac-count for the failure to detect any improvementin pituitary function one month after surgicalremoval of the bullet. In head trauma, recoveryof pituitary function presumably involves regen-eration of pituitary portal vessels and anteriorpituitary cells (Daniel et al., 1959). It is possiblethat, in our patient, one month was too short a

period for this regenerative process to be of anyfunctional significance or that the hypopituitarismwas a permanent state.

References

Altman, R., and Pruzanski, W. (1961). Anteriorpituitary insufficiency following skull fracture.Annals of Internal Medicine, 55, 149-154.

Arafah, B. M., and Salti, I. S. (1978). Partial hypo-pituitarism following septic peritonitis with shock.Archives of Internal Medicine, 138, 1271-1273.

Daniel, P. M., Prichard, M. M. L., and Treip, C. S.(1959). Traumatic infarction of the anterior lobeof the pituitary gland. Lancet, 2, 927-930.

Frank, E. (1912). Ueber beziehungen der hypophysezum diabetes insipidus. Berliner Klinische Wochen-schrift, 49, 393-397.

Klacho, D. M., Winer, N., Burns, T. W., and White,J. E. (1968). Traumatic hypopituitarism occuringbefore puberty: survival 35 years untreated. Journalof Clinical Endocrinology and Metabolism, 28, 1768-1772.

Kornblum, R. N., and Fisher, R. S. (1969). Pituitarylesions in craniocerebral injuries. Archives ofPathology, 88, 242-248.

Paxson, C. L., and Brown, D. R. (1976). Post-traumaticanterior hypopituitarism. Pediatrics, 57, 893-896.

Woolf, P. D., and Schalch, D. S. (1973). Hypopituitar-ism secondary to hypothalamic insufficiency. Annalsof Internal Medicine, 78, 88-90.

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