INTRODUCTION

Adrenal insufficiency (AI) or Addison's crisis is a life-threatening

condition caused by an imbalance in the secretion of adrenal glucocorticoid and
mineralocorticoid hormones. Addison’s Disease (AD) is a manifestation of low
glucocorticoid production or activity, with or without mineralocorticoid
deficiency.1,2 Clinical manifestations of adrenal insufficiency include weakness,
anorexia, abdominal pain, weight loss, orthostatic hypotension and skin
hyperpigmentation.1,2 Based on the underlying mechanism, adrenal insufficiency
is classified into primary, secondary and tertiary. Primary Adrenal Insufficiency
(PAI) is caused by intrinsic disease of the adrenal cortex. Central adrenal
insufficiency (secondary and tertiary) is caused by impaired corticotropin
production or activity. Tuberculosis is the leading cause of PAI in developing
countries.1,2
The incidence of adrenal insufficiency is rare, with an incidence of
<0.01% in the general population. However, in certain groups the risk for
developing adrenal insufficiency in critically ill patients varies from 0 – 77%. The
prevalence of primary insufficiency in Europe has increased from forty to seventy
percent of cases per one million population.2,3 About 70-80% of reported cases of
AD are caused by autoimmune disorders, 20% by tuberculosis and rest are
4
idiopathic.
Tuberculosis (TB) is still an important health problem in the world.
Indonesia is the 5th country with the highest number of TB cases in the world. TB
in children is an important component in TB control program because the number
of children aged less than 15 years is 40-50% of the total population and there are
about 50,000 children in the world suffer from TB every year.5
Spinal TB is reported in infants as latent TB. The incidence of spinal TB
in children varies. Reported as 58% of all spinal tuberculosis in Korea, 1/3 of all
patients as reported from Chennai (India) and 26% in Hong Kong. Spinal TB
causes severe bone loss and delays growth; so that serious sequelae can occur.
Vertebral in children is cartilage. The younger the child, the greater the volume of
cartilage in each vertebral body. Therefore, whenever tuberculosis infection
affects the vertebral bodies, cartilage loss occurs rapidly and severe deformity
occurs sequentially in a short time span compared to adults. 6
Associated with AD, tuberculosis can affect the kidneys and adrenals
either as a primary infection or secondary spread from other organs or as a by-
product of antituberculous therapy.4,7 Isolated adrenal tuberculosis accounts for
less than 2% of adrenal incidentalomas. Tuberculosis of the adrenals can always
manifest in the acute phase, accounting for about 7-20% percent of cases of PAI
in developed countries, which are generally catastrophic leading to death. 4 The
possibility of adrenal tuberculosis should be considered when patients with a
history of tuberculosis, either active disease or a positive tuberculin skin test,
present with the classic manifestations of adrenal insufficiency.7
CASE REPORT
A 15 year old girl came to the Pediatric Endocrinology Polyclinic, Dr. M.
Djamil Padang was consulted from the Dermatology Clinic with a diagnosis of
hypermelanosis ec Susp. AD. The patient came with the chief complaint that the
skin began to appear blackish since 7 months ago. Initially 7 months ago, the skin
appears blackened starting from the fingers and toes to the mouth and back. The
tongue does not appear black. Patients often feel tired since 1 month ago and
decreased appetite. The patient also complained of joint pain in the hip and thigh
area. In addition, since 2 months the patient's hair began to fall out. Patients prefer
to eat foods with a salty taste. In the past 2 weeks, the patient suddenly fainted and
was then admitted to the hospital. The patient was already menstruating and the
age of menarche was 13 years. The patient had no previous history of the same
disease. Family history of illness with similar complaints was denied.
On physical examination, the general condition of the patient appeared to
be moderately ill, co-operative compos mentis consciousness, blood pressure
104/70 mmHg, pulse 80 times/minute, respiratory rate 20 times/minute, body
temperature 37oC, weight 43 kg, height 153 cm. On examination the skin appears
black on the fingers, toes and back. Hair is black and falls out easily. The head is
normocephal and symmetrical. Lips look black. Conjunctiva not anemic, sclera
not icteric, pupil isocor with diameter 2mm/2mm, normal positive light reflex.
Ears and nose within normal limits. Tonsils T1-T1, not hyperemic. On cardiac
examination, ictus cordis was not visible, ictus cordis was palpable in the left
midclavicular line, RIC V, auscultation of the heart, regular heart rhythm and no
murmur. On lung examination, there were normochest, no retractions, vesicular
breath sounds, no rales and no wheezing. There is no abdominal distension, the
liver and spleen are not palpable, bowel sounds are normal. No abnormalities in
genitalia, pubertal status A1M5P2. Extremities palpable warm with good
perfusion CRT <2 seconds and normal positive physiological reflexes and
negative pathological reflexes.
Laboratory examination showed sodium levels 135 mmol/L, potassium
levels 4.2 mmol/L, chloride levels 106 mmol/L, calcium levels 9.5 mg/dL, blood
sugar levels 83 mg/dL and morning serum cortisol levels 3, 1 ug/dL and afternoon
serum cortisol level of 2.7 ug/dL (normal level 3.7-19.4 ug/dL). On chest X-ray
examination, the PA projection shows the trachea in the middle, the superior
mediastinum is not dilated. Good aorta. The heart is in a normal position, the size
is not enlarged (VRT <50%). Both hilus are not thickened/widened. The
bronchovascular pattern of both lungs was good. Right and left diaphragm
smooth. The right and left costophrenic sinuses are acute. There were no
infiltrates or nodules in both lung fields. Radiological impression of the thorax
showed no radiological abnormalities. Radiological examination of the lumbar
spine showed deformities in the 2nd and 3rd lumbar which caused narrowing of
the intervertebral discs lumbar 1-2, lumbar 2-3 and lumbar 3-4. The end plates of
the other lumbar vertebral bodies are sclerotic. Osteophytes were seen in the
bodies of the other lumbar vertebrae. The impression from the lumbar radiological
examination is spondylosis of the lumbar spine. On MRI examination, the lumbar
spine showed deformities in the bodies of the 2nd, 3rd and 4th lumbar vertebrae
causing narrowing of the intervertebral discs of lumbar 1 2, lumbar 2-3 and
lumbar 3-4 and causing a 'protruded disc' to appear in the lumbar intervertebral 1-
2, lumbar 2 -3 and lumbar 3-4 accompanied by herniation of the nucleus pulposus
towards the posterior diffuse and causing bilateral spinal canal and spinal root
compression accompanied by changes in the intensity of lumbar signals 2,3 and 4
which gave inhomogeneous hypointense signals on T1W1 and increased on
T2W1 and inhomogeneous hyperintense on TIRM accompanied by soft tissue
thickening at the level of the lumbar paravertebral 2-5 suggestive of spondylitis
with paravertebral abscess. On the Mantoux test, the result was 20 mm. The
patient was diagnosed with AD with hypovitaminosis D with suspected TB
spondylitis. The patient was given genison therapy 18 mg orally in the morning
and 9 mg orally in the afternoon. In addition, the patient is scheduled for a Gene
Xpert examination.
Based on complaints of low back pain and other complaints as well as the
results of investigations from the pediatric clinic, the patient was then referred to
the orthopedic surgery clinic to further review the patient's suspicion of TB
spondylitis and related management. After consultation to the orthopedic clinic,
the patient was confirmed to have TB spondylitis and was planned for
decompression stabilization and laminectomy. Preparations made before the
patient underwent surgery were the patient was given OAT umbrella therapy for 2
weeks after being consulted to the pediatric respirology section.
The pediatric endocrinology section provides pre-operative therapy in the
form of hydrocortisone, the following is the hydrocortisone premediation protocol
given to the patient:
1. Preoperative
(Not recommended for fasting more than 6 hours, keep getting regular
hydrocortisone doses until the time of surgery or given intravenously)
 (07.00) - Check RBG (regular blood glucose) Morning
 (07.30) - Hydrocortisone intravenously 1x18 mg IV (10 minutes bolus) 30
minutes before surgery
2. Intraoperative
 (08.00) Infusion of 0.9% NaCl 800 cc/8 hours equivalent to 100 cc/hour
while the child is fasting.
 (08.00) Immediately before anesthesia, Hydrocortisone 86 mg IV was
given as a bolus within 10 minutes to avoid vascular injury, then continued
Hydrocortisone drip 150 mg in 0.9% NaCl solution up to 24 cc for 24
hours IV, syringe pump speed of 1 cc /o'clock.
3. Post operation
 hourly RBG.
  If the condition is stable and can be taken orally, take 2x the dose of
hydrocortisone for 48 hours and then gradually reduce it to the normal
dose.
 24 hours post op, if condition is stable give Genison 2 times maintenance
dose: Genison 1x36 mg po Morning; 1x18 mg po Night
 Day 2 Post op tappering off: Genison 1x24 mg PO Morning; 1x13 mg po
Night
 Day 4 Post op : Genison 1x18 mg po Morning; 1x9 mg po Night
 RBG then every morning and evening.
Furthermore, in intraoperative patients, a pedicle screw was installed at L1-L4
and laminectomy at L2 & L3. The patient is planned to undergo an adrenal
ultrasound examination, adrenal CT, TB AFB and sputum. Post surgery was
treated in the orthopedic surgery department and planned for medical
rehabilitation.
DISCUSSION
Adrenal insufficiency is a life-threatening condition. Adrenal insufficiency
was first described by Thomas Addison2 in the second half of the 19th century,
who characterized this syndrome by weakness, fatigue, anorexia, salt craving, and
orthostatic hypotension.1 PAI (PAI or AD) is characterized by low cortisol. and
high ACTH from destruction of the adrenal glands.8 The most common causes at
that time were tuberculosis and autoimmune adrenalitis. Because the signs and
symptoms of AD are non-specific, as in our patient who was consulted by a
dermatologist. Doctors must have a high index of suspicion. One of the primary
adrenal insufficiency is AD.1
AD is also known as PAI which cause by three categories of adrenal gland
defects that result in the inability to produce adequate amounts of glucocorticoid,
mineralocorticoid, and adrenal androgens, despite an increased concentration of
adrenocorticotropic hormone (ACTH). The first category is adrenal dysgenesis,
which refers to congenital adrenal structural developmental defects (X-linked
form of congenital adrenal hypoplasia/ CAH which typically presents in males
with life-threatening adrenal crisis in the new born periode and hypogonadotropic
hypogonadism later in adolescence). The second category of adrenal gland defect
is impaired steroidogenesis. The most common subtype results from complete
enzyme deficiency, with defective production of both glucocorticoids and
mineralocorticoids, and presents with severe salt wasting and adrenal crisis in the
first 2 to 3 weeks after birth. Consequently, this conditions leading to
overproduction of adrenal androgens. The excess androgens cause virilization in
the female fetus. The last category is adrenal destruction, refers to pathologic
processes that damage the adrenal gland such as autoimmune, infections (TB is
the most common cause in the developing countries, meningococcal, fungi, etc),
metabolic and infiltrative or metastatic diseases and drugs effect. 9

Figure 1 Pathophysiology of Adrenal Tuberculosis10

As mentioned above, that one of the causes of adrenal insufficiency is

tuerculosis, which is the most common cause of the infectious agent group.
Adrenal TB develops from hematogenous or lymphatic spread, hence is often
associated with extra-adrenal infection. The rich vascularity of the adrenal gland
and high levels of local corticosteroids that suppress cell mediated immunity
create an ideal microenvironment for the growth of Mycobacterium tuberculosis.
The patterns of adrenal gland involvement in TB are both primary adrenal failure
and secondary adrenal insufficiency are possible. The presentation of primary
adrenal failure can be both acute and chronic. In patients with acute presentation
usually within 2 years of tuberculous infection, the pathological presentations
could be one of the three noted. Chronic primary adrenal failure is pathologically
defined by atrophic and fibrosed glands.10
 In response to environmental stressors, the hypothalamus releases
corticotropin-releasing hormone (CRH). CRH stimulates the anterior pituitary to
release adrenocorticotropin hormone (ACTH), which travels through the
bloodstream to the adrenal cortex and increases cortisol production. Cortisol is the
main hormone involved in the human stress response and has many effects
throughout the body such as causing vasoconstriction, inhibiting pro-
inflammatory cytokines, as well as regulating the supply of glucose in the body by
triggering gluconeogenesis or stimulating glycogen synthesis in the liver and the
production and release of amino acids from free fatty acids.8
Most children who have Addison disease experience ill-defined fatigue,
generalized muscular weakness, loss of appetite, and poor weight gain. Some
patients crave salt. Teenagers may notice loss of pubic and axillary hair. Signs and
symptoms generally are nonspecific and can mimic a gastrointestinal disorder,
with nausea, vomiting, and abdominal pain, or a psychiatric disorder, especially
depression. “Muddy” hyperpigmentation is an important physical sign. 9 Skin and
mucosal hyperpigmentation, which was also manifest in our patient, raises the
index of suspicion because hyperpigmentation is a classic finding and occurs in
more than 90% of patients with adrenal insufficiency. Hyperpigmentation appears
as a brownish discoloration of the oral mucosa (eg, gums, lips, and inner cheeks),
skin folds (eg, hands), scars, areolas, and genitals. Hyperpigmentation results
from increased secretion of melanocyte-stimulating hormone that results from
increased pro-opiomelanocortin production along with increased ACTH. 1
The other signs that appeared in our patient were fatigue, decreased
appetite, hair loss, and the child likes to eat salty foods. The classic clinical signs
of adrenal insufficiency include decreased vascular tone (manifested by
orthostatic hypotension or shock). Classic biochemical signs including
hyponatremia, hyperkalemia, hypoglycemia, and ketonemia or ketonuria may
occur as a result of aldosterone deficiency. Aldosterone deficiency is usually seen
in more severe cases as a major cause of electrolyte regulation impairment in
more severe cases of adrenal gland dysfunction. 1,8 Surprisingly, hyperkalemia is
not a prominent feature.1 On electrolyte examination we did not find any
electrolyte abnormalities in this case. Acute renal failure (ARF) may be the
presenting feature of Addison disease. When hyponatremia and hyperkalaemia are
present in association with ARF, they may erroneously be considered a
manifestation of renal insufficiency, increasing the likelihood of a delay in
diagnosis. That means, normal electrolyte results do not rule out the possibility of
AD. It is possible that the normal value is due to the condition of the kidneys that
can still compensate.11
Our patients were tested for cortisol in the morning and evening, which
resulted in low cortisol (3.1 mg/dL). Initial screening for suspicion should include
a morning cortisol measurement. A proportionally low serum cortisol
concentration (<10 mg/dL [<275.9 nmol/L]) greatly raises the suspicion of
glucocorticoid deficiency. The biochemical diagnosis of adrenal insufficiency is
made by an adrenal stimulation test with exogenous synthetic ACTH. This test is
required most often in inpatients, making it difficult to perform on an outpatient
basis as in our case.1 A morning cortisol of < 3 ug/dL is indicative of adrenal
insufficiency, while cortisol level >18 mcg/dL rules out adrenal insufficiency. A
diagnosis of primary AI is confirmed if the serum cortisol level is < 18 mcg/dL, in
the presence of markedly elevated ACTH and plasma renin activity.12
Most medical centers give high doses of ACTH (250 mg) as an
intravenous injection testing. Serum cortisol was measured immediately before
injection and then 30 and 60 minutes after injection. The normal physiologic
response is an increase in serum cortisol levels to a peak of at least 18 mg/dL (500
nmol/L) or higher after 60 minutes. Adrenal insufficiency is confirmed if the
cortisol response is below normal, especially in the setting of stress. For the
diagnosis of primary vs. secondary adrenal insufficiency, measurement of plasma
ACTH is useful because it is elevated in AD and normal or low in secondary
adrenal failure.1 In addition, positive adrenal antibodies establish autoimmune
adrenal insufficiency or AD.12
Treatment of acquired adrenal insufficiency is no different from treatment
for PAI. This patient was given genisone which contain of hydrocortisone 18 mg
in the morning and 9 mg in the afternoon. In PAI, maintenance therapy requires
glucocorticoids and mineralocorticoid replacement. The daily basal cortisol
production rate in children is about 6-8 mg/m2/day. When given orally, the
recommended physiological replacement dose of hydrocortisone in pediatric
patients is approximately 10-12.5 mg/m2/day divided into two or three doses,
which compensates for incomplete intestinal absorption and hepatic metabolism.
Hydrocortisone is preferred in children over other glucocorticoids because it is
easily titrated and has a short half-life with fewer side effects, compared to the
more potent long-acting glucocorticoids. It is recommended that glucocorticoids
should be given with food to prolong the half-life of hydrocortisone and to
facilitate the production of a more physiological cortisol profile. 12
This patient was also diagnosed with tuberculous spondylitis based on his
history and radiological findings. Spondilitis TB one of extrapulmonary TB
(EPTB) region. The incidence of EPTB is low at 3%, but there has been no
significant reduction in incidence of EPTB when compared to pulmonary TB
(PTB). Skeletal TB (STB) contributes to around 10% of EPTB, and spinal TB has
been the most common site of STB, amounting to around half of skeletal EPTB.
Thoracolumbar junction remains to be the most affected region of the spinal
column.13
Spinal TB usually is insidious in onset and the disease progresses at a slow
pace. Based on this theory, which is also seen in patients with symptoms of
spondylitis appeared about 8 months ago. The diagnostic period, since onset of
symptoms, may vary from 2 weeks to several years. The manifestation of spinal
TB depends on the severity and duration of the disease, site of the disease, and the
presence of complications such as abscess, sinuses, deformity, and neurological
deficit.13
Based on TB treatment guidelines, the implementation given is by giving
the standard anti-tuberculosis regimen consisting of isoniazid, rifampin,
pyrazinamide, and ethambutol.4 These drugs accelerate hepatic glucocorticoid
metabolism including rifampin, mitotane, anticonvulsants such as phenytoin,
carbamazepine, oxcarbazepine, phenobarbital , and topiramate so the dose of
hydrocortisone needs to be increased to ensure adequate cortisol replacement
when taken with drugs that induce hepatic cortisol by inducing cytochrome P450
3A4 enzymes. In contrast, patients treated with drugs that inhibit CYP3A4 such as
antiretroviral drugs may require a reduced dose of hydrocortisone.1
 Spondylitis TB in the pediatric in some scenarios is likely to develop
significant instability and a "buckling effect." The combined approach is often
used in children. The conservative treatment with anti-TB drugs, the role of
planned surgical intervention in our patient, remains unclear. There is no clear
indication for surgery. However, in a review of randomized controlled trials of
surgical intervention in spinal TB, the presence of neurologic impairment,
deformity, and instability were the main criteria for surgical intervention,
regardless of the anatomical area of the spine affected. Resistance to treatment,
large abscesses, and sequestrum formation were also found to be reasons for
surgical intervention.14
Preparation of surgical intervention for spondylitis in patients with AD,
may require special attention. The general consensus is to supplement with a
physiologic suppressive dose of corticosteroid according to the level of surgical
stress intensity. Moderate stress (orthopedic surgery), Corticosteroid dose
equivalent to 50 mg hydrocortisone succinate intravenously at induction of
anesthesia and then 25 mg every 8 hours for a total of 24 hours. 1

Figure 2 Recommended doses for intra- and postoperative steroid cover in children with
adrenal insufficiency15

The use of stressful doses of corticosteroids in high-stress situations after

HPA axis suppression is paramount; however, data are lacking on how long
patients should receive stress doses (a common recommendation is to administer
stress corticosteroid doses for the first 6-12 months after discontinuation of
corticosteroid therapy during periods of stress).1 Addison's Clinical Advisory
Panel (ACAP) recommends 100mg of hydrocortisone IM or IV intermittently.
before anesthesia. Immediately followed by 100 mg IM or IV every 6 hours or a
continuous infusion of 200mg/24 hours (8.33mg per hour). After surgery, the dose
of hydrocortisone given is 100 mg IM or IV every 6 hours or a continuous IV
infusion of 200 mg/24 hours or until you can eat & drink normally (discharged
from ICU). If good, then double oral dose for 48+ hours. Then tappering back to
normal dose.16 In addition to corticosteroids given before surgery, anti-
tuberculosis drugs is also given to the patient for a maximum of 2 weeks with
better outcome then if the drug is given for 2-4 weeks. The cause of such findings
may lie in the time to receive nerve decompression of spinal cord, in the first
group, they had received earlier management: therefore, their outcome was better
compared to the second group, because of chance to get the regeneration and
healing of compressed nerves.17
Neurological impairment and deformity are the most feared complications
of spondylodiscitis. Neurological deficits can occur in 20% to 40% of cases in
endemic areas and developing countries. The average vertebral column collapse
with conservative treatment alone is 15ᵒ and in 3% to 5% of cases it can be severe
in up to 60ᵒ cases. Measurement of deformity correction was the most frequently
described outcome followed by neurologic deficit and identification of fusion.
Functional outcomes and patient-related quality of life are rarely reported in the
major surgical literature reviewed.14
CT scan findings that may appear in adrenal TB patients are
bilateral/unilateral/normal adrenal enlargement. Low attenuation in the center with
peripheral rim enhancement of the lesions on contrast-enhanced CT. While non-
enhanced CT scan revealed calcification.18 Ultrasound scan of the abdomen found
to have bilaterally enlarged adrenal glands.19 But, in this patient neither
examination was performed.
Acute complications in cases of adrenal insufficiency are life-threatening.
Addisonian crisis occurs most often in patients with known adrenal insufficiency,
either primary or secondary because of long-term suppression of the
hypothalamic-pituitary axis. Each year about 8% of those with known adrenal
insufficiency experience an adrenal crisis, and the mortality rate is about 6%. If
the Addisonian crisis is identified quickly and given prompt treatment with IVF
and steroids, the patient has a good prognosis and recovery. Those who are
critically ill with significantly altered mental status or advanced endocrinopathy
(severe diabetes, uncontrolled thyroid disease) or multiple comorbidities have
increased mortality and residual disability. Patients may require physical or
occupational therapy and rehabilitation to regain independent function.6
Patients and their families need to be educated about strategies to prevent
acute decompensation and how each triggering event requires an adjustment of
their steroid dose. A team-based approach between healthcare provider and patient
is essential in maintaining control of this condition. 6
The patient will be planned to undergo medical rehabilitation. Soon after
the surgical operation, the patients were mobilized. Extensor strengthening
exercises were applied on the spinal extensors and isotonic and tractional
exercises were performed to the abdomen, pelvis and lower extremities in flexor
and extensor muscles. In the long period, these exercises should decreasethe
potential for kyphosis in patients who do not have stabilization, and will decrease
the weight upon the metals in those who had stabilization.20
CONCLUSION
AD is a condition of PAI that is very life-threatening in the acute setting.
The diagnosis is quite difficult to make because the signs and symptoms are not
specific. Early morning screening for serum cortisol is mandatory if AD is
suspected. Treatment with hydrocortisone is preferable to other types of
glucocorticoids, especially in pediatric patients. Patients with comorbid TB
spondylitis may require higher doses of hydrocortisone due to the interaction of
one of the anti-TB drugs, rifampicin, which accelerates hepatic metabolism.
Combination of conservative treatment (OAT) and surgical intervention may be
required in these cases, especially in the presence of an abscess which is an
indication for surgery in cases of tuberculous spondylitis. Specific hydrocortisone
dosage adjustments are required in preparation for surgery in patients with AD. It
is very important to explain the acute complications and their management to the
patient and family.
From this case report, it is hoped that a study of the effect of corticosteroid
therapy on TB treatment can be carried out, the key to correct diagnosis and
clinical outcome of adrenal TB therapy for a better prognosis.
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ATTACHMENT

Figure 3 Photo comparison before and when the patient is sick

Figure 4 Hyperpigmentation manifestation in patient

Figure 5 Lung X-ray Figure 6 Lumbosacral X-ray

Figure 7 Intraoperation Procedure

Figure 8 Postoperative X-ray