Asia-Oceania J . Obstet. Gynaecol. VoI. 18, No. 2; 121-123 1992

Sheehan’s Syndrome Following Eclampsia : A Case Report

Joseph E. Uhiara, Raghwa Narayan, and S. Kumar Department of Obstetrics and Gynaecology, Lautoka Hospital, Fiji

Abstract A case of Sheehan’s syndrome following eclampsia is presented. The clinical features were not recognised early probably because the condition was not suspected, being a rare sequel of eclampsia. Non availability of specialist care may have been partly responsible and is highlighted. Increased awareness of all possible aetiological factors in this condition is necessary for clinicians.

Key words : Sheehan’s syndrome, eclampsia, hypopituitarism

Introduction Sheehan’s syndrome commonly results from severe obstetric haemorrhage and circulatory shock. However, factors other than blood loss are known to precipitate the disorder though rarely. The spectrum of the condition ranges from subclinical t o full-blown disease whose features are easy to recognise. We present a case of Sheehan’s syndrome associated with eclampsia and shock. Case Report

A 29-year-old unbooked Gravida 5, para 4 was referred from one of our peripheral hospitals after having several generalised fits at home. She had been briefly treated with intravenous 10 mg diazepam. On admission she was restless, oedematous and had a blood pressure of 160/100 mmHg. Her lung fields were normal the fundal height was 24 cm with the

fetus presenting by the vertex and the foetal heart rate was at 148 per’minute. There were no uterine contractions and the cervix was uneffaced and closed. The urine was concentrated and loaded with albumin. The diagnosis was antepartum eclampsia. The only abnormal laboratory results were a haemoglobin concentration of 9.4 g% and uric acid level of 550 umol/Z. Following adequate sedation (with a stat dose of intravenous 100 mg pethidine 50 mg promethazine) and control of the blood pressure, she had an emergency hysterotomy and bilateral tuba1 ligation-three hours after admission. The fetus was male and weighed 550g but succumbed shortly. The estimated gestational age was 24 weeks. The blood loss was 350mZ. She was transfused with one unit of blood. Her full recovery was slow with cerebral oedema and shock from which she slowly recovered by the 10th day and suffering from right lower lobe pneumonia. She was dis-

Received: Oct. 1,1991 Reprint request to: Dr. J. E. Uhiara, Department of Obstetrics and Gynaecology Fiji School of Medicine, Suva, Fiji

121

J. E. UHIARA ET AL.

charged to her district hospital on the 21st day for follow-up. She was referred again 10 months later with a history of amenorrhoea from the last delivery, fainting attacks and progressive weakness. She had in fact had two falls at home and lacerated her forehead. On examination she was moderately pale, dehydrated and aging. She was also amnesic, had slurred speech and a remarkable change in the voice. The blood pressure was 80/60 mmHg. Her previously luxuriant hair was now thin and short with complete loss of the axillary and pubic hair as well as marked loss of the outer half of her eyebrows. The breasts were atrophic in addition to marked muscle wasting and multiple septic spots. The genital tract was also atrophic. A diagnosis of Sheehan’s syndrome was made. The haemoglobin concentration was 7.9g% and the random blood sugar was 3.3 mmol/Z. The serum prolactin level was 2.5 ng/mZ (normal 0-25); T3, 1.1 nmol/Z (normal 1.23-2.46); free T4, 9 pmol/Z (normal 1125); FSH 2.7miulmZ (normal 3-12); LH, 4 miu/mZ (normal 0.5-18). Lateral view of the pituitary fossa was normal. She was transfused with two units of blood, placed on high protein and carbohydrate diet and treated with the following: 10 mg of cortisone acetate mane and 5 mg nocte, followed by daily doses of 50 pg of thyroxine tablets, 0.02 mg of ethinyl oestradiol and 5 mg norethisterone and a 5 day course of 6 hourly doses of 250 mg ampicillin orally. There was considerable improvement in her clinical state with a gradual return of physical strength, correction of anaemia, cessation of fainting attacks and healing of the septic spots. She was discharged to her district hospital on her drugs with instructions to return to us for review every 6 weeks. Her condition has remained stable.

Discussion Post partum pituitary necrosis due to severe blood loss was first described by Sheehan in 1937.1) Since then there have been many reports of the condition following massive obstetric haemorrhage. Most of these have been 122

postpartum but antenatal cases have also been described.2s8) A 2 to 3 fold increase in the size of the pituitary gland during pregnancy and a redistribution of the blood supply to the organ-both in favour of the anterior lobe make it more susceptible to damage. In the event of severe blood loss, hypovolaemia and vasospasm cause ischaemia of the gland resulting in cell damage. This may become irreversible after 6-8 hours.’) The ischaemia also causes oedema and, since the gland lies in an unyielding bony cavity (the sella turcica), increased tissue pressure will lead to failure of reestablishment of circulation. Our patient did not suffer severe blood loss but her hypopituitarism may have resulted from ischaemic damage due to vasospasm, tissue oedema and prolonged shock operating through the mechanism described above. I n fact arteriolar spasm is a pathologic feature of eclampsias) and so the eclamptic patient in prolonged shock could be particularly vulnerable to ischemic necrosis of the pituitary gland. Sheehan’s syndrome following eclampsia has been reported.6J) The clinical features of Sheehan’s syndrome vary widely depending on the degree of damage to the pituitary gland. Failure to lactate, weakness and secondary amenorrhoea are usually the earliest to manifest. In one series, these features (along with loss of pubic and axillary hair) occurred in over 80% of the cases.@ Failure to detect non-lactation in our patient may have been influenced by the loss of the baby and a consequent desire for nonlactation. It is difficult to say when the other features manifested. An earlier referral for specialist attention could have averted her further deterioration. The natural history of the condition is chronic and response to its management is variable. Successful treatment resulting in subsequent pregnancies have been reported.9) On the other hand failure to recognise it early and institute treatment can result in death. A previous impression of long intervals between the index pregnancy and onset of Sheehan’s syndrome has led to delay in investigations and prompt treatment even though the condition was suspected earlier on.’O)

SHEEHAN’S SYNDROME FOLLOWING ECLAMPSIA

Sheehan’s syndrome is now rare in developed countries because of better management of obstetric haemorrhage; eclampsia is also rare. The situation is different in developing countries. Thus there is need for greater awareness of this condition and its multiple etiology. Two major constraints will remain : confirmatory laboratory diagnosis may not always be available and given the socioeconomic background of many patients, close supervision of prolonged treatment will be difficult to achieve. This is likely to be the case with our patient who resides in a rural area far from her district hospital.

Acknowledgments We wish to thank the Resident Representative UNDP, Suva for consenting to this report by one of us (JU), and the Permanent Secretary for Health for permission to publish the article.

3.

4.

5.

6.

7.

8.

9.

References 1 . Sheehan HL. The recognition of chronic hypoptituitarism resulting from postpartum pituitary necrosis. Am J Obstet Gynecol 1971; 1 1 1 : 852-854 2. Agostinis G. Sheehan’s syndrome due to very grave haemorrhagic-shock caused by rupture

10.

of the splenic artery in pregnancy; pathogenesis and resucitational therapeutic consideration. Acta Anesth (Padoua) 1969; 20: 187-193 Taylor DS. Massive gastric haemorrhage in late pregnancy followed by hypopituitarism. J Obstet Gynaecol Br Comm 1972; 7 9 : 476-478 Sheehan HL, Stanfield JP. The pathogenesis of postpartum necrosis of the anterior lobe of the pituitary gland. Acta Endocrinoll961; 37: 479-510 Assnli NS, Holm LW, Parker HR. Systemic and regional hernodynamic alterations in toxaemia. Circulation 1964; 30: 53-57 Beemick FJ, Mckay DG. Pituitary insufficiency associated with pregnancy, panhypopituitarism, and diabetes insipidus. Am J Obstet Gynecoll962; 84: 318-338 Harlin RS, Givens JR. Sheehan’s syndrome associated with eclampsia and a small sella turcica. South Med J 1968; 61 :909-911 Ratarasarn C , Rajatanavin R, Himathongham T. Salient clinical features of Sheehan’s syndrome. J Med Assoc Thai (Bangkok)1989; 72: 4147 Grimes HG, Brookes MH. Pregnancy in Sheehan’s syndrome. Report of a case and review. Obstet Gytmecol Sum 1980; 35: 481-488 Lacdar AA, Mclaren EH, Davda NS, Makay EJ, Rubin PC. Pituitary failure from Sheehan syndrome in the puerperium: Two case reports. Br J Obstet Gynaecol 1987; 94: 998999

123

Sheehan's syndrome following eclampsia: a case report.

A case of Sheehan's syndrome following eclampsia is presented. The clinical features were not recognised early probably because the condition was not ...
201KB Sizes 0 Downloads 0 Views