Sheehan’s Syndrome

Sheehan’s Syndrome: A case report

GOOD AFTERNOON!

DEPARTMENT OF FAMILY AND COMMUNITY MEDICINE

PGI Ramos, Jo Anne N.

General data R.C. 49 years of age Female Married Filipino Born Again Christian 6157 Feliciano St., Mapulang Lupa, Valenzuela

City Admitted for the 7th time on February 19, 2010

around 11:45AM

CHIEF COMPLAINT

BODY WEAKNESS

HISTORY OF PRESENT ILLNESS 3 days PTA muscle pain on both

upper and lower extremities described as cramping for

about minutes in duration every 1-2 hours, usually

occurring during the night and relieved by rest or

sleep Consult Meloxicam 15mg/tab once

a day which would afford temporary relief

Few ours PTA condition worsened now with

associated generalized body weakness

Admitted

PAST MEDICAL HISTORY (+) 2008, CKD @ MCUH- Folic Acid+Vit. B

complex, 1 tab once daily and EDA/DHA 1tab thrice daily

(+) AUG 2009, Metabolic encephalopathy, Hyponatremia probably secondary to salt wasting nephropathy @ MCUH

(+) HPN Olmesartan 10mg, 1 tab once daily (+) DM Sitagliptin 25mg, 1 tab once daily (+) Dyslipidemia Fenofibrate 160mg, 1 tab once

daily (-) Allergy (-) Asthma

FAMILY HISTORY (+) Hypertension- paternal (+) CVA- paternal (- ) Diabetes (- ) Cancer (- ) Kidney disease (- ) Asthma (- ) PTB in the household

PERSONAL AND SOCIAL HISTORY Housewife Daily chores serves as her exercise Diet: Low salt low fat diet Nonsmoker Alcohol beverage drinker (occasional), twice a

year, consuming 2-3 bottles of beer (San Mig Light)

Nuclear type of family, neolocal No prevalent disease in the community such

as dengue fever

OB-Gyne history G3P3 (3003) All pregnancies are delivered at home by a

midwife (+) surgical menopause, TAHBSO @ MCUH

(G3) 1981, secondary to postpartum hemorrhage secondary to uterine atony, home delivery assisted by a midwife

Physical examination General Survey- Patient is conscious,

coherent, not in cardiorespiratory distress

Vital Signs: BP 150/90 mmHg CAR 75 bpm RR 18 cpm T 36.5°C BMI 20 kg/m2

Wt 53kg Ht 150cm

Skin- hair distribution on the facial area is diminished, dry, pale with fair turgor

HEENT- No nasoaural discharge, no tonsillopharyngeal congestion, no

cervical lymphadenopathy Chest/Lungs-Symmetrical chest expansion, no

retractions, clear breath sounds Heart- Adynamic precordium, normal rate and

regular rhythm , no murmur

Abdomen- Flabby, normoactive bowel sounds, soft, non-tender

Extremities- Grossly normal, diminished axillary hair, full and equal peripheral pulses

Neurological Exam Cerebral- oriented 3 spheres Cerebellar- no ataxia, no dyskinesia Cranial Nerves

1 can smell II (+) pupillary light reflex III, IV, VI intact extraocular muscles V (+) bicorneal blink reflex VII no facial asymmetry VIII can hear IX, X (+) gag reflex XI able to shrug shoulders XII no tongue deviation

SENSORY MOTOR

100%

100%

100%

100%

3/5

3/5

3/5

2/5

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++

++

+++

+++

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++

Deep Tendon Reflex

GenogramRamos-Tadeo Family

6157 S. Feliciano St., Mapulang Lupa, Valenzuela City2-19-10, 9:30 AM

Jose, 79 Eliza, 73

Marcelina 62

Eduardo 61

Manuel 60

Federico 59

Renato 57

Celia 58

Leoplodo 48

Consolacion 49

Corazon 39

Romulo 38

Gabriel 45

Adoracion 76

Aurora 60

Crrisanto ?

Jun 44

Noel 40

Tomas 47

Crisanto 55

Cristina 57

Nestor 52

Nephtalie 32

Nerissa 31

Naneth 28

I.

II.

III.

FEMALEMALE

LIVING TOGETHER

INDEX PATIENT

DIABETES

HYPERTENSION

STROKEBREAST CANCER

DECEASED

Diagnostics (at the ER)

CBC RESULT Normal value

Hemoglobin 10.6 g/dL 13.5-18

Hematocrit 0.32 0.42-0.50

Leukocytes 3.5 4.5-11

Segmenters 0.61 0.56

Stabs 0.02 0.03

Eosinophils 0.07 0.027

Lymphocytes 0.25 0.34

Monocytes 0.05 0.04

Platelets 91 150-400

MCV 89.3 80-96

MCH 29.7 27-31

MCHC 0.33 0.32-0.36

Clinical Chemistry

Result Reference Value

Creatinine 112.7 umol/L 53-106

Sodium 114.0 mmol/L 135-148

Potassium 3.52 mmol/L 3.5-4.3

Admitting impression:

Hyponatremia HASCVD, NIF DM type 2

Differential Diagnosis:

Cerebrovascular Accident

Hypokalemic Periodic Paralysis/Electrolyte Imbalance

Cerebrovascular Accident HPP/Electrolyte Imbalance

• rapidly developing loss of brain function(s) due to disturbance in the blood supply to the brain, caused by a blocked or burst blood vessel.•leading to inability to move one or more limbs on one side of the body, inability to understand or formulate speech, or inability to see one side of the visual field.

•rare channelopathy characterized by muscle weakness or paralysis with a matching fall in potassium levels in the blood. 

Plan

To correct electrolyte imbalance

To determine the etiology of hyponatremia

To establish the diagnosis

Problem List

Body weakness Leg cramping Hyponatremia Anemia Dizziness

Admitting Orders Diet: LSLF diet, DM diet CHO- 200 kcal/day CHON- 67 kcal/day Fats- 29 kcal/day IVF: PNSS 1L FOR 8 HOURS Diagnostics: CBC w/ APC, Na, K, Creatinine, CBG tid premeals 12-lead ECG Therapeutics: Olmesartan 10mg/tab OD Sitagliptin 25mg/tab OD Fenofibrate 160mg/tab OD @ HS

C/O patient’s medications

Course in the Ward 1st day of hospitalization

S> (+) leg pain, (+) body weakness, occasional dizziness

O> BP 120-130/70-80 CAR 72 RR 20 T 36° A> Hyponatremia Anemia secondary Chronic Kidney Disease

secondary to DM Nephropathy Hypertensive Atherosclerotic Cardiovascular Disease DM type II P> Na Cl tablet , 1 tab, 2x daily for Urinalysis for Lipid profile, FBS, and SGPT

SGPT 105.9 U/L (4-24)

FBS 4.02 mmol/L (3.85-6.05)

Cholesterol 5.76 (3.9-6.5)

Triglycerides 1.81 (.11-2.09)

HDL 0.99 (1.15-1.68)

LDL 3.94 (3.37-4.12)

VLDL 0.82 (0-1.04)

urinalysis

Color Yellow

Specific Gravity 1.010

Character Clear

Reaction Alakali

Sugar Negative

RBC 0-1/hpf

PMN 0-1/hpf

Amorphous urates

Rare

Bacteria Rare

Epithelial cells Rare

12-lead ECG Sinus rhythm

1st degree AV block Non-specific ST-T wave changes

2nd day of hospitalization S> Decreased body weakness, (-) Dizziness, (+)

Headache, 6/10 squeezing bitemporal, (+) cramping leg pain, 7/10 (+) epigastric pain, (+) 1 episode of vomiting, previously ingested,

O> Comfortable BP 120/80 CAR 54-66 RR 18 (+) signs of hypothyroidism (+) epigastric tenderness, direct A> Patient is still manifesting signs of

hyponatremia as well as hypothyroidism. Fasting blood sugar is normal, which is assessed as DM controlled. Blood pressure is within normal limits.

Cont.. A> Hyponatremia Anemia secondary Chronic Kidney Disease

secondary to DM Nephropathy Hypertensive Atherosclerotic Cardiovascular

Disease P> Omeprazole 40mg/tab OD Folic Acid tab OD Paracetamol 500mg/tab 1 tab statP> For

repeat CBC w/ APC, Na, Creatinine For serum Calcium Discontinue Fenofibrate 160mg/tab OD

P> for thyroid function test (FT3, FT4, TSH) for UTZ of the whole abdomen for repeat serum Na, creatinine For GI referral to consider GI pathology Omeprazole 40mg/tab OD for epigastric pain D/C Fenofibrate 160mg/tab OD Paracetamol 500mg/tab stat for headache

3rd day of hospitalization S> (-) Calf pain, (-) headache, fair appetite, (+) epigastric

pain (+) vomiting, post-meal O> Stable vital signs (-) epigastric tenderness (+) still with signs of hypothyroidism

Na 109.2 mmol/L Ft3 1.21 pmol/l (3.1-6.8) Ft4 1.68 pmol/l (12-22) Tsh 1.37 uIU/ml (0.27-4.2)

A> Hyponatremia Hypothyroidism DM type 2 controlled HASCVD, not in failure

P> NaCl tab 1 tab BID Levothyroxine 100mg/tab OD, monitor heart

rate For repeat serum Na, K, Creatinine, Cl For HBA1C

Result: Whole abdomen UTZ Early signs of liver cirrhosis Mild vs acute cholecystitis Splenomegaly Chronic medical renal disease, bilateral Small lefty kidney Urinary retention Normal sonogram of the pancreas

4th day of hospitalization (AM) S> Still with calf pain, (+) epigastric pain, (+) difficulty

of sleeping, (+) vomiting, 1 episode post-meal O> Stable vital signs (+) signs of irritability Na- 117.2 mmol/L in comparison with previous

result HBA1C- 7.59 % (4.8-5.9) K- 3.24 mmol/L slightly decereased Cl- 87.80 mmol/L (96-106) A> Patient is still experiencing signs of electrolytes

imbalance as well as hypothyroidism. HBA1C revealed to be elevated which depicts an uncontrolled blood sugar for the past 3 weeks.

P>Diphenhydramine tab OD KCl tab, BID Na tab 2 tab bid repeat Na, K Regular diet

4th day of hospitalization (PM) S> (+) mental disturbance, combative O> awake, incoherent A> Metabolic encephalopathy is highly considered P> 4 point restraint was contemplated

5th day of hospitalization S> (+) shouting spells, (+) blank stares, not

conversant O> Awake, incoherent, delirium Still in 4 point restraint Na- 122.8 mmol/L A> Hyponatremia, still correcting salt loss Metabolic encephalopathy secondary to

hyponatremia P> Hydration is continued Diazepam 25mg/IV PRN Repeat Na, K

6th day of hospitalization (AM) S> Still unable to sleep, combative, with episodes

of shouting spells O> BP 170/100 Awake, delirium Na- 125 mmol/L K- 3.37 mmol/L A> Correcting salt loss, elevated BP may be

secondary to inability to sleep P> Diphenhydramine 50mg/IV Clonidine 75 mcg/tab SL

6th day of hospitalization (PM) S> Patient is able to sleep O> BP 140/80 Asleep, comfortable A> Metabolic encephalopathy Patient was able to sleep and calm down after

administration of Diphenhydramine P> still correcting electrolyte imbalance for serum cortisol, repeat Na, K remove patient from restraint

7th day of hospitalization S> (-) BM for 3 days, difficulty to move bowel, no

headache, no leg cramps, no epigastric pain, able to sleep

O> Stable VS Coherent, comfortable, not in distress Na- 129 mmol/L K- 4.33 mmol/L A> Patient had manifested hypotituitarism as

showed previously by hypothyroidism and possibly hypocortisolism Sheehan’s syndrome is highly entertained.

P> Bisacodyl 5mg/tab, 1 tab before bedtime Methylpredinisolone 4mg/tab BID KCl tab discontinue

8th day of hospitalization S> No subjective complaints O> Stable vital signs Patient is conscious, conversant, coherent Cortisol- 46.84 nmol/L (171-536 nmol/L) A> Hypopituitarism secondary to Sheehan’s

Syndrome P> C/C Methylpredinisolone 4mg/tab, 2 tab BID Cont. Omeprazole 20mg/tab OD for 9 more

days

9th day of hospitalization S> No subjective complaints O> BP 120/80 CAR 86 RR 19 Patient is conscious, conversant, not in distress A> Hypopituitarism secondary to Sheehan’s Syndrome Hypertensive Atherosclerotic Cardiovascular Disease, not

in failure Diabetes mellitus, type II Chronic Kidney Disease secondary to DM nephropathy P> C/C NaCl tab, 1 tab BID MGH:

1. Levothyroxine 100mg/tab, 1 tab OD 2. Methylprednisolone 4mg/tab, 1 tab OD 3. Cont Amlodipine 5mg/tab, 1 tab OD 4. Folic Acid + Vit. B complex tab, 1 tab OD 5. Cont. EDA/DHA tab, 1 tab TID

Pregnancy Physiologic hyperplasia of the pituitary gland due to increase demand of lactotrophs (2nd tri up to 1st week

pospartum)

Physiologic hyperplasia of the pituitary gland due to increase demand of lactotrophs (2nd tri up to 1st week

pospartum)

Peurperium: Increased blood loss due to uterine atony

Peurperium: Increased blood loss due to uterine atony

Hypotension and vasospasm of hypophyseal arteries

Hypotension and vasospasm of hypophyseal arteries

Compromised blood supply of the pituitary gland

Compromised blood supply of the pituitary gland

Estrogen

Ischemia of the glandIschemia of the gland

Partial/Complete loss of the gland endocrine function

Partial/Complete loss of the gland endocrine function

Thyroid

Stimulating Hormones

(TSH)

Thyroid

Stimulating Hormones

(TSH)

Leutinizing Hormone (LH)

and Follicle Stimulating

Hormone (FSH)

Leutinizing Hormone (LH)

and Follicle Stimulating

Hormone (FSH)

Growth

Hormone

Growth

Hormone

Prolactin (PRL)

Prolactin (PRL)

Adrenocortico- tropic Hormone

(ACTH)

Adrenocortico- tropic Hormone

(ACTH)

T3, T4 decrease

Low sex hormone

concentrations

Dec protein synthesisInc water,

Na, K excretionDec IGF

Failure to lactate

Dec serum cortisol

Dec serum aldosterno

neLow sex hormone

concentration

TirednessWeaknessDry skinCold intoleranceHair lossBradycardiaPuffy face, hands, and feet

AmenorrheaInfertilityDec vaginal secretionDec libidoBreast atrophyReduced body hair growth

-Dec energy and drive-Dec lean body mass-Abnormal lipid profile - IGF leads to inc blood glucose

FatigabilityWeaknessHyponatremiaHyperkalemiaHypertension

Partial/Complete loss of the gland endocrine function

Partial/Complete loss of the gland endocrine function

OxytocinOxytocin Antidiuretic Hormone (ADH)Antidiuretic Hormone (ADH)

Patient lacks the signs and symptoms of an anterior

pituitary gland loss of function

Sheehan’s Syndrome

Discussion

Pituitary Gland

An endocrine gland about the size of a pea and weighing 0.5 g (0.02 oz.)

Major endocrine gland. “Master gland”

Pituitary Gland

The blood supply of the pituitary arises from 2 sets of vessels: The superior

hypophyseal arteries, from the internal carotid arteries and circle of Willis.

The inferior hypophyseal arteries, from the internal carotid arteries alone.

Most of the anterior lobe of the pituitary has no direct arterial supply.

Sheehan’s syndrome, first described by Sheehan in 1937, is a well-known cause of panhypopituitarism secondary to pituitary apoplexy.

This syndrome generally occurs after an intra- or postpartum bleeding episode characterized by severe hypotension or hemorrhagic shock.

During pregnancy, the pituitary gland enlarges and is vulnerable to ischemic insults.

The mechanism of ischemia is not clear.

Hypotension, along with vasospasm of the hypophyseal arteries is currently believed to compromise arterial perfusion of the anterior pituitary.

Damage to the anterior pituitary causes partial or complete loss of thyroid, adrenocortical or gonadal function.

The extent of pituitary damage determines the rapidity of onset as well as the magnitude of pituitary hypofunction.

The prevalence of Sheehan’s syndrome in 1965 was estimated to be 100 to 200 per 1,000,000 women.

With advances in obstetric care, this disease is becoming rare in the developed countries.

There are currently no available literature on the prevalence of Sheehan’s syndrome in the Philippines.

Phil. J. Internal Medicine, 46: 295-298, Nov.-Dec., 2008. SHEEHAN’S SYNDROME IN A 44-YEAR OLD FILIPINO FEMALE

The gland has a great secretory reserve, and more than 75% must be destroyed before clinical manifestations become evident.

Most patients, however, have mild disease and remain undiagnosed and untreated for years.

The reported percentage for hormone deficiencies following ischemic infarction of pituitary include: growth hormone (88%) gonadotropin (58 -76%) corticotrophin (66%) secondary hypothyroidism (4-5. 3%) prolactin deficiency (67-100%).

Veldhuis J, Hammond J: Endocrine Function After Spontaneous Infarction of the Human Pituitary: Report, Review, and Reappraisal. Endocr Rev. 1: 100, Winter 1980.

In 1995, Justiniano (unpublished) reviewed the medical records of the Philippine General Hospital from January 1, 1987 to October 31, 1995 for patients diagnosed with this disease entitity.

There were 21 cases of Sheehan’s syndrome recorded for the said census period.

Eight women (38 %) had hyponatremia, with serum sodium levels ranging from 120-128 mmol/L.

This data is comparable to a cohort of patients in Turkey reviewed by Sert, et. al.1where nine (32%) out of 28 women had disturbances in sensorium associated with hyponatremia.

1 Sert, M, Sert M, Tetiker T, Kirim S, Kocak M: Clinical Report of 28 patients with SheehanÊs Syndrome. Endocr J. 50(3): 297, 2003.

The mechanisms responsible for the development of hyponatremia in patients with hypopituitarism have been shown to be multifactorial: (1) increased secretion of vasopressin because of

glucocorticoid deficiency or other factors, such as decreased volume or cardiac output;

(2) urinary loss of sodium caused by aldosterone deficiency;

(3) impaired water excretion because of thyroid hormone deficiency

(4) impaired water excretion caused by vasopressin independent factors, such as decreased tubular fluid delivery to the diluting site.

CONCLUSION The most important clues for diagnosis of

Sheehan’s syndrome are lack of lactation and failure of menstrual resumption after delivery that was complicated with severe hemorrhage.

The aim of treatment is to replace deficient hormones.

A high index of suspicion and a meticulous history and physical examination are important in recognizing Sheehan’s syndrome.

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