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SECONDARY ADRENAL INSUFFICIENCY SECONDARY ADRENAL INSUFFICIENCY

SECONDARY ADRENAL INSUFFICIENCY - PowerPoint Presentation

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SECONDARY ADRENAL INSUFFICIENCY - PPT Presentation

CAUSING VISUAL HALLUCINATIONS MON 453 KRISTAL RAGBIRTOOLSIE SABINA FINK MARCIA RASHELLE PALACE VIVIEN LEUNG BRONX LEBANON HOSPITAL CENTER BRONX NY 10457 USA Potential Conflict of Interest may exist Please refer to Meeting App ID: 577146

visual hallucinations adrenal normal hallucinations visual normal adrenal insufficiency case secondary history presenting diagnosis symptoms improvement treatment acute psychiatric

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Slide1

SECONDARY ADRENAL INSUFFICIENCY CAUSING VISUAL HALLUCINATIONS

MON

– 453

KRISTAL

RAGBIR-TOOLSIE, SABINA FINK, MARCIA RASHELLE PALACE*, VIVIEN LEUNG

BRONX LEBANON HOSPITAL CENTER, BRONX, NY 10457, USA

*Potential Conflict of Interest may exist. Please refer to Meeting App. Slide2

Introduction Secondary Adrenal Insufficiency

due to hypothalamic-pituitary failure

Prevalence

of 150-280 per million

[1]

Presents

with vague symptoms that make the diagnosis challenging

.

The psychiatric manifestations of the condition are often overlooked in the clinical setting, though well described in the literature

[2-6]

.Slide3

History of Presenting Illness69 year old blind female

Developed

progressive visual

hallucinations x 3 months

At

the onset of the

hallucinations, she was seen at the outpatient clinic of another hospital, and was

started on

quetiapine

.

The

hallucinations became increasingly complex, with animals walking in the apartment.

She was admitted to the other hospital, evaluation was unremarkable and the

quetiapine

was switched to haloperidol.

Later

she became very distressed that three men were entering her apartment through a window and one of the men attempted to set her house on fire, so she was brought to our

ED.Slide4

History of Presenting IllnessPast Medical / Surgical History

At age 38, underwent partial resection of a

suprasellar

meningioma

Complicated by

central

hypothyroidism on Levothyroxine

central diabetes

insipidus

on

Desmopressin

permanent optic

nerve

damage causing complete

blindness

Social history – lived alone, was functionally independent, but had adequate social support from her daughterSlide5

ExaminationPleasant lady, well nourished, in no cardiopulmonary distress

Alert and oriented to person, place, and time

GCS 15/15, normal muscular tone, full power and intact sensation throughout. Scars in the right

frontotemporal

region.

No light perception to both eyes, horizontal

nystagmus

and optic nerve pallor bilaterally on

funduscopy

Otherwise, no abnormalities

VITALS

Temp

36.5

0

C

Pulse

68 beats/min

Resp

18 breaths/min

BP

167/80 mmHg

SpO

2

100

% on Room Air

Weight

59 kg

Height

157.4cm

BMI

23.8 kg/m

2Slide6

Investigations

PARAMETER

INTERPRETATION

CBC

Mild

normochromic

normocytic

anemia

, no

leukocytosis

CMP

Within Normal Limits

PARAMETER

LABORATORY VALUE

NORMAL RANGE

ACTH

7.15 pg/ml

5.0 - 27.0 pg/ml

AM Cortisol

1.6 μg/dl

5.0 - 25.0 μg/dl

Post-Cosyntropin Cortisol

2.14 μg/dl

-

TSH

<0.07 mIU/L

0.40 - 4.50

mIU

/L

T3

168 ng/dL

60 - 181ng/dL

Free T4

1.44 ng/dL

0.80 - 2.00 ng/dL

Glucose

Range 62-100

70 - 120 mg/

dL

URINE

STUDIES

Urinalysis

Moderate leukocytes, bacteria and leukocyte esterase

Urine toxicology

NegativeSlide7

Investigations: CT HeadRemote

right frontal craniotomy and right

frontotemporal

craniectomy

Post-aneurysmal

clipping (two clips were seen in the

suprasellar

cistern);

Partially calcified multilobulated mass in the suprasellar cistern, measuring 3.1 x 1.7 x 3.5cm. Ex-vacuo

dilatation of the right frontal horn, associated with

encephalomalacia

of the inferior right frontal

lobe

No

acute hemorrhage or infarct. MRI for further evaluation was deferred due to the presence of aneurysm clips.Slide8

Investigations

At

another institution prior to this admission

:

EEG showed cerebral dysfunction

Video EEG reported as normalSlide9

TreatmentAfter confirmation of secondary adrenal insufficiency

- started oral

hydrocortisone

10

mg in

AM and

5 mg in

PM

UTI was treated - Ceftriaxone 1 g IV daily for 5 days. Low normal glucose levels were seen - levels below 70mg/dL

were corrected with oral glucose and

intravenous

dextrose administration. Slide10

Follow UpAt clinic follow up visits:

Reported improvement

of

hallucinations

Far

less intrusive

tone

Marked

improvement in

appetite Gained weight since dischargeSlide11

Diagnostic Considerations for Visual Hallucinations

Organic

causes –

Delirium unlikely due to the absence of metabolic derangements and the treatment of presumed urinary tract infection without improvement.

Other organic causes such as migraines, seizures, CVA and temporal masses were ruled out.

Charles

Bonnet Syndrome

[7]

Seen in blind patients with insight into their blindness.

Unlikely, given the duration of her blindness and the acuity of her symptoms.

Primary psychiatric diagnosis

Unlikely given the

lack of psychiatric or substance use history, late onset of psychosis, and acute onset of visual hallucinations.

Tried on several different anti-psychotics with no relief in symptomatologySlide12

Diagnostic Considerations for Visual Hallucinations

Chronic secondary adrenal

insufficiency

- Normal HPA function post op without overt AI x 3 decades post op

-

Re-exploration of HPA axis integrity warranted given acute

psycosis

Labs showed

- low baseline cortisol level - insufficient stimulation after corticotrophin injection - Inappropriately low-normal ACTH valueTreatment

- Glucocorticoid replacement therapy resulted in improvement of symptoms: visual hallucinations, appetite and weightSlide13

ConclusionsAs the presenting symptoms of chronic adrenal insufficiency are often nonspecific, a high index of suspicion for this condition is paramount, especially in patients with prior pituitary surgery.

In this patient, visual hallucinations were the only symptom of secondary adrenal insufficiency. Failure to recognize this condition led to mismanagement with ineffective anti-psychotic regimens before the correct diagnosis was made.

This case highlights the importance of periodically re-testing HPA axis function in patients with prior pituitary surgery, and re-examining organic causes of hallucinations when multiple anti-psychotic regimens fail.Slide14

References[1] Arlt W,

Allolio

B. Adrenal Insufficiency. Lancet. 2003;361:1881-1893

[2]

Anglin

RE, Rosebush PI,

Maxurek

MF. The Neuropsychiatric Profile of Addison's Disease: Revisiting a Forgotten Phenomenon. J Neuropsychiatry

Clin

Neurosci. 2006; 18(4):450-459[3] Nwokolo M, Fletcher J. Rare Case of hypopituitarism with psychosis. Endocrinology, Diabetes & Metabolism Case Reports. Published Online: 2013; doi: 10.1530/EDM-13-0007[4] Kate S, Dhanwal DK, Kumar S, et al. Acute psychosis as a presentation of hypopituitarism. BMJ Case Rep. Published Online: 2013;

doi

: 10.1136/bcr-2012-008516

[5] Abdel-

Motleb

M. The Neuropsychiatric Aspect of Addison's Disease: A Case Report.

Innov Clin Neurosci. 2012;9(10):34-35[6] Pavlovic

A,

Sivakumar

V.

Hypoadrenalism

presenting as a range of mental disorders. BMJ Case Reports. Published Online: 2011;

doi

10.1136/bcr.09.2010.3305

[7]

Teeple

RC, B.S.,

Caplan

, JP, et al. Visual Hallucinations: Differential Diagnosis and Treatment. Prim Care Companion J

Clin

Psychiatry. 2009; 11(1):26-32Slide15

Thank You