Case Report ABSTRACTS

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An Unusual Presentation of Post-Partum Hypo-pituitarism Zoe Jones NHS Tripti Mahajan Aim We describe an unusual presentation of a young lady 2 weeks post-partum with acute panhypopituitarism. Case A 28 year old primipara presented with a 2 day history of wide based gait, diplopia, nausea and vomiting 2 weeks postpartum. Following an uneventful pregnancy her delivery was complicated by a third degree tear and significant blood loss resulting in an episode of hypotension. She had been unable to breast feed since the birth. A day prior to presentation she developed dysarthria and had a tonic/clonic seizure on arrival in ED, requiring high dependency unit care. Blood tests showed acute hyponatraemia, very low Random Cortisol, hypopituitary hypothyroidism and hypopituitary hypogonadism. A CT head and MRI pituitary done thereafter showed an enlarged postpartum pituitary. She was treated with steroid replacement resulting in complete resolution of her hyponatraemia. Following normalisation of her electrolytes she was commenced on Levothyroxine and made a rapid clinical recovery. Conclusion Differential diagnoses of Pituitary apoplexy and cavernous sinus thrombosis were considered due to visual and neurological symptoms. Although Sheehan’s syndrome (acute-type 1) was our primary differential classic symptoms of hypotension and tachycardia were absent at presentation. Her symptoms and seizure were secondary to acute hyponatraemia which is an uncommon manifestation of Sheehan’s syndrome 1 . This illustrates that cases of acute pan hypopituitarism can present atypically to the acute medical take causing potentially life threatening illness. We also demonstrate that a diagnosis of Sheehan’s syndrome cannot be made on acute imaging of the pituitary and sequential imaging might be necessary 2 References 1. Boulanger E, Pagniez D, Roueff S, et al. Sheehan syndrome presenting as early post-partum hyponatraemia. Nephrol Dial Transplant 1999;14:2714-5 2. Kapluna, C. Fratilac, A.Ferenczia et al. Sequential Pituitary MR Imaging in Sheehan Syndrome: Report of 2 Cases. American Journal of Neuroradiology, May 2008 29: 941-943
Atrioventricular block associated with benzodiazepine use. Ashutosh Sharma NHS Lothian James Dear Case Report I report a case of transient second degree atrioventricular block associated with administration of benzodiazepine for control of agitation in a young male. A 15 year old boy was brought to the emergency department(ED) after being found at home drowsy and difficult to rouse.A few tablets of diazepam were found on him.Initial vital signs were within normal parameters.He had GCS 14;E4V4M6.Pupils were dilated 6mm bilaterally,equally reactive.Physical examination was unremarkable.His admission ECG revealed normal sinus rhythm with PR interval of 192ms(Figure 1).He became agitated and aggressive in the ED requiring physical restraint.He received Haloperidol 5mg IM,Diazepam 10mg IV,and titrated doses of Midazolam upto total 60mg IV over 50 minutes.He was transferred to the medical admissions unit for further management. Over the course of the next fourteen hours he remained drowsy and developed second degree heart block(Mobitz Type 1),this was documented on serial ECGs performed at six hours(Figure 2),eight hours(Figure 3),twelve hours(Figure 4) and fourteen hours(Figure 5) post benzodiazepine administration.He was bradycardic with heart rate between 50 and 60 beats/min,requiring intermittent fluid boluses for hypotension.His serum calcium level was 2.14mmol/L,treated with 10mls 10% calcium gluconate IV.The atrioventricular block resolved spontaneously sixteen hours following the benzodiazepine administration,ECG performed at the time revealed normal sinus rhythm(Figure 6, 7).He admitted to ingesting diazepam but denied any other substance abuse.He was discharged from hospital the following day. Discussion Benzodiazepines(BZD) bind to specific receptors in the gamma aminobutyric acid(GABA) receptor complex,which enhances the binding of this inhibitory neurotransmitter.A second class of benzodiazepine binding sites,called the peripheral type benzodiazepine receptor(PBR),is found in peripheral tissues including the myocardium(1).BZD receptor agonists can reduce the current through transient and longacting calcium channels,hence BZD may behave like weak calcium channel blockers.There are also reports of the direct action of BZD on the suppression of atrioventricular node conductivity(2).This would account for the BZD associated atrioventricular block seen in our patient and explain the use of flumazenil in the reversal of benzodiazepine induced atrioventricular block(3).Flumazenil is a competitive antagonist of the BZD receptor. Given the frequent use of benzodiazepines in management of agitation in patients,this case would serve to remind clinicians of the potential complication associated with exposure to this agent. References 1.Zisterer DM,Williams DC.Peripheral-type benzodiazepine receptors.Gen Pharmacol 1997;29:305-14. 2.Nakajima T,Kaneshiro S,Yatabe Y,Azumi T,Iwasaki H.Negative dromotropic effect of diazepam on the AV node of dog heart in situ.Arch Int Pharmacodyn Ther 1979;241:153-64. 3.Mullins MEFirst-degree atrioventricular block in alprazolam overdose reversed by flumazenil.J Pharm Pharmacol 1999;51:367-70.
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