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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
++
++
++
+++
+++
++
++
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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