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American Journal of  Medical 
Science and Innovation (AJMSI) 

Miliary Tuberculosis Causing Presumed Primary Adrenal Insufficiency and Addisonian 
Crisis: A Case Report from Rural Kenya

Vonwicks C. Onyango1*, Boniface Mutiso2, Nicholas M. Mutuma2, Collins P. Malalu2, Nicholas Auma3, William C. Fryda MD.1

Volume 3 Issue 1, Year 2024
ISSN: 2836-8509 (Online)

DOI: https://doi.org/10.54536/ajmsi.v3i1.2773
https://journals.e-palli.com/home/index.php/ajmsi

Article Information ABSTRACT

Received: April 05, 2024
Accepted: May 10, 2024
Published: May 14, 2024

Primary adrenal insufficiency (Addison’s disease) is characterized by inadequate production 
of  cortisol from the adrenal glands due to diseases of  the adrenal gland. Due to the insidious 
onset and non-specific nature of  the symptoms of  adrenal insufficiency, diagnosis is often 
delayed until patients present with an adrenal crisis. The three most common causes are 
autoimmune adrenalitis, infections, e.g., disseminated tuberculosis, HIV, systemic mycoses, 
and adrenal hemorrhage or infarction. Miliary tuberculosis of  the adrenal gland occurs in 
high-TB burden populations by hematogenous spread of  tuberculous bacilli to the gland, 
causing caseous necrosis, or by extra-adrenal infection and rifampicin-induced adrenal 
insufficiency. In this study, we report on the case of  a middle-aged woman in rural Kenya 
who initially presented with missed features of  adrenal insufficiency and subsequently went 
into an adrenal (Addisonian) crisis, which was successfully managed with glucocorticoids, 
fluids, and supportive therapy.

Keywords
Primary Adrenal Insufficiency, 
Addison’s Disease, Adrenal 
Crisis, Addisonian Crisis, Miliary 
Tuberculosis, Tuberculous Adrenal 
Insufficiency, Glucocorticoid, Kenya

1 Department of  Medicine, St. Joseph Rift Valley Hospital, Gilgil, Nakuru County, Kenya
2 Department of  Outpatient, St. Joseph Rift Valley Hospital, Gilgil, Nakuru County, Kenya
3 Department of  Endoscopy, St. Joseph Rift Valley Hospital, Gilgil, Nakuru County, Kenya
* Corresponding author’s e-mail: drvonczelo@gmail.com

INTRODUCTION
Adrenal insufficiency is characterized by an absolute or 
relative deficiency in the production of  glucocorticoid 
(cortisol) from the adrenal cortex due to destruction 
of  the adrenal cortex or a lack of  stimulation of  
adrenocorticotrophic hormone (ACTH) (Hahner et 
al., 2021). This can be primary (caused by diseases 
of  the adrenal gland), secondary (caused by impaired 
secretion of  ACTH by the pituitary gland, e.g., in 
panhypopituitarism from any cause, brain injury, high 
dose progestins, etc.), or tertiary (caused by interference 
with the secretion of  corticotropin-releasing hormone 
(CRH) by the hypothalamus, typically by exogenous 
administration of  high dose glucocorticoid therapy) 
(Grossman, 2010; Hahner et al., 2021; Joseph et al., 
2016). Primary adrenal insufficiency (Addison’s disease) 
is caused by the destruction or dysfunction of  the 
adrenal cortex and manifests with features of  cortisol 
and aldosterone deficiency. The most common causes 
of  Addison’s disease are autoimmune adrenalitis, 
infections (e.g., disseminated tuberculosis, HIV, and 
disseminated fungal infections like histoplasmosis), 
adrenal hemorrhage and infarction, metastatic cancers 
(e.g., primary colon, breast, lung, gastric, and lymphoma), 
and drugs, e.g., ketoconazole, fluconazole, rifampicin, 
etc. (Barthel et al., 2019). Tuberculosis causing Addison’s 
disease is due primarily to the hematogenous spread of  
tubercle bacilli into the adrenal cortex, leading to caseous 
necrosis of  the glands, or by extra-adrenal infection, 
and as a by-product of  anti-tuberculous therapy with 
rifampicin (Vinnard & Blumberg, 2017). Typically, >90% 

of  the gland has to be destroyed before symptoms of  
adrenal insufficiency ensue. Although the incidence of  
tuberculous Addison’s disease has been declining globally 
due to more effective TB management (Nomura et al., 
1994), TB is still a major cause of  adrenal insufficiency 
in high TB burden populations, e.g., Kenya (Enos et al., 
2018). In a 2024 systematic review, the pooled prevalence 
of  adrenal insufficiency in tuberculosis was 33% (Kibirige 
et al., 2024). Clinical features of  adrenal insufficiency are 
often insidious and nonspecific and may include features 
of  adrenal crisis or chronic adrenal insufficiency. Adrenal 
crisis is predominantly characterized by shock as well 
as multisystemic features (Burke, 1985). (See Table 1). 
Patients with chronic primary adrenal insufficiency have 
an insidious onset and gradual development of  features 
of  both cortisol and aldosterone deficiency. A diagnosis 
of  adrenal insufficiency is often delayed due to the non-
specificity of  the clinical features, e.g., gastrointestinal 
symptoms (like nausea, vomiting, anorexia, vomiting, 
abdominal pain, etc.), fatigue, weight loss, musculoskeletal 
pains, and neuropsychiatric symptoms like altered mental 
status, psychosis, hallucinations, etc. Nonetheless, the 
occurrence of  hyperpigmentation, salt craving, and 
postural hypotension strongly suggests primary adrenal 
insufficiency. The diagnosis of  adrenal insufficiency is 
primarily by the adrenocorticotropic hormone stimulation 
test (Synacthen or Cosyntropin tests) (Ospina et al., 2016). 
The management of  adrenal insufficiency primarily 
involves the use of  corticosteroids (hydrocortisone), 
mineralocorticoids, supportive therapy, and the treatment 
of  underlying diseases, e.g., the use of  anti-TB drugs as 



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per local guidelines (Lewis et al., 2023).  Comprehensive 
guidance for the diagnosis and management of  adrenal 
insufficiency can be found in ‘The Clinical Guidelines 
Subcommittee of  the Endocrine Society’ (Bornstein et al., 
2016).

HIV rapid test, and stool studies showed no ova or 
parasites and no blood or mucus. She also had normal 
liver function tests. Her creatinine was elevated at 1.9 mg/
dL, but she had profound hyponatremia with serum Na+ 
of  109 mmol/L (135-145), K+ of  4.1 mmol/L (3.5-5.5), 
and Cl- of  75 mmol/L (95-108). Her lumbar puncture 
with cerebrospinal fluid analysis was normal. Her chest 
x-ray showed a miliary pattern bilaterally consistent with 
miliary tuberculosis (see Figure 1). An abdomino-pelvic 
ultrasound and a gastroscopy were both unremarkable. 
A diagnosis of  miliary tuberculosis with acute 
gastroenteritis complicated with pre-renal acute kidney 
injury and severe symptomatic hyponatremia was made. 
Following a successful resuscitation, she was started on 
anti-TB therapy as per local guidelines, with Rifampicin, 
Isoniazid, Ethambutol, Pyrazinamide, and pyridoxine 
(the latter to mitigate isoniazid-induced peripheral 
neuropathy), and supportive care. The hyponatremia was 
successfully managed with a hypertonic saline infusion. 
She was discharged five days later while lucid and in 
normal clinical status.

Table 1: Clinical and Laboratory Findings Suggesting 
Adrenal Crisis
Dehydration, hypotension, or shock out of  proportion 
to the severity of  the current illness
Nausea and vomiting with a history of  weight loss and 
anorexia
Abdominal pain, so-called "acute abdomen"
Unexplained hypoglycemia
Unexplained fever
Hyponatremia, hyperkalemia, azotemia, hypercalcemia, 
or eosinophilia
Hyperpigmentation, or vitiligo
Other autoimmune endocrine deficiencies, such as 
hypothyroidism or gonadal failure

Adapted from: Burke CW. Adrenocortical insufficiency. Clin 
Endocrinol Metab 1985; 14:947. (Burke, 1985)

Case Presentation
Presenting Illness and Physical Examination
A 52-year-old woman, mother of  four, and businesswoman 
from Kabatini, Nakuru County, Kenya, presented to us 
in September 2023 with altered mental status. She had 
a preceding 2-week history of  recurrent post-prandial 
and unprovoked non-bilious vomiting, watery, non-
bloody diarrhea (2-3 episodes every 2-3 days), generalized 
abdominal pains, progressive lethargy, and a day-long 
history of  visual hallucinations. These occurred on a 
background history of  recurrent dry cough, drenching 
night sweats, a 4kg weight loss, and anorexia in the 6 weeks 
prior. There was no clear history of  food poisoning. She 
neither smoked nor took ethanol. On initial examination, 
she was severely dehydrated with a tachycardia of  113 
bpm, a blood pressure of  117/77 mmHg, afebrile, 
normal oxygen saturation in room air, and a random 
blood sugar of  74 mg/dL. Her abdomen was diffusely 
tender but soft, with no organomegaly and no features 
of  peritonism. Her Glasgow coma scale was 12/15; she 
had no meningism and no focal neurology, though she 
was actively hallucinating during the exam. Her skin had 
no rashes or peripheral hyperpigmentation. She was 
cool to touch in the peripheries with low-volume pulses, 
but she had normal heart sounds. She had orthostatic 
hypotension, with her BP dropping from 117/77 mmHg 
to 90/58 mmHg from recumbent to upright positions. 
The rest of  the exam was unremarkable. 

Diagnostic Workup and Management
Her baseline laboratory tests showed a normal complete 
blood count (CBC), an elevated ESR of  50 mm/hr., no 
malaria parasites on a blood smear microscopy, a negative 

Figure 1: Initial CXR showing bilateral diffuse miliary 
infiltrates, consistent with miliary tuberculosis

Re-admission in an Addisonian Crisis
However, she was re-admitted 1 month later in a comatose 
state (GCS of  8/15) with hypothermia (a temperature of  
34oC), a tachycardia of  104 bpm, and hypotension (BP 
of  85/63 mmHg, which dropped to a nadir of  60/42 
mmHg). She had a reported 3-week history of  recurrent 
post-prandial vomiting but no diarrhea, vague abdominal 
pains, dysuria, anorexia but craving salt and licking it several 
times, lethargy, and confusion. Her urinalysis showed 
leukocytosis and positive nitrites consistent with cystitis. 
She had neutrophilic leukocytosis with a total leucocyte 
count of  13x103u/L, severe hyponatremia with Na+ of  
100 mmol/L, K+ of  5.7 mmol/L, Cl- of  79 mmol/L, and 
a normal creatinine of  0.6 mg/dL. A thyroid profile and 
an uncontrasted CT scan of  the brain were normal. She 
initially had a persistently low random glucose of  70 to 
90 mg/dL, hypotension needing inotropic support, and 
hyponatremia with borderline hyperkalemia. In light 
of  these, we made a presumptive clinical diagnosis of  
adrenal crisis precipitated by cystitis on the background 



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of  adrenal insufficiency caused by miliary tuberculosis. 
Due to a lack of  finances, we could not do further 
confirmatory tests. The patient was put on intravenous 
hydrocortisone, normal saline, and supportive therapy. 
Six days later, she had a full resolution of  the adrenal 
crisis and was discharged home stable. See Table 2 for 
a summary of  her blood pressure readings, significant 
laboratory results, and the specific interventions given.
During outpatient follow-up, we kept her on tapered 
doses of  oral prednisone (the cheapest available option), 
with omeprazole and vitamin D/calcium combo tablets 
for gastroprotection and osteoprotection, respectively. 
We continued the TB treatment for 6 months as per 
local protocols and monitored her for any complications 
related to the steroid therapy. By the end of  the 4th 
month of  TB treatment, we stopped the steroids, and 
her subsequent serum electrolytes, blood pressure, and 
random blood glucose remained normal until the end of  
TB treatment and on follow-up so far. Her CXR has since 
normalized. (See Figure 2).

Figure 2: Repeat CXR done 4 months after initiating TB 
treatment showing a complete resolution of the miliary infiltrates

Table 2: Summary of  Significant Blood Pressure, Laboratory Results, and Specific Interventions
Date Blood Pressure

(mmHg)
Creatinine
(mg/dL)
(0.5-1.0)

Sodium 
(mmol/L)
(135-145)

Potassium
(mmol/L)
(3.5-5.5)

Glucose
(mg/
dL)
(72-200)

Specific
Interventions

30/9/2023 117/77, 90/58 1.9 109 4.1 7 3% NaCl, RHZE, B6, IVFs
3/10/2023 112/76 126 3.4 RHZE, B6, ORS
18/10/2023 116/76 133 4.8 RHZE, B6
6/11/2023 85/63, 60/42 0.6 100 5.7 131, 80 RHZE, B6, 3% NaCl 

Inotropes, IVFs, Abx
7/11/2023 92-138/55-72 114 5.9 70, 224, 

86
RHZE, B6, 3% NaCl 
Inotropes, IVFs, Abx, 
Steroids

9/11/2023 124-148/64-84 0.7 126 5.8 145, 96, 
78

RHZE, B6, 3% NaCl 
Inotropes, IVFs, Abx, 
Steroids

10/11/2023 96-122/62-70 136 4.4 264, 186, 
144

RHZE, B6, IVFs, Abx, 
Steroids

23/11/2023 121/85 126 4.5 155 RHZE, B6, Steroids, ORS, 
Slow Na tabs

6/12/2023 126/85 0.7 126 4.0 146 RH, B6, Steroids, ORS, 
Slow Na tabs

5/1/2024 118/84 0.9 133 4.1 115 RH, B6, Steroids, Slow Na 
tabs

4/3/2024 119/64 0.9 147 4.8 130 RH, B6
3/4/2024 124/83 1.0 150 5.2 150
8/4/2024 126/78 142 4.9 174

KEY: 3% NaCl= 3% sodium chloride (hypertonic saline infusion), RHZE= rifampicin, isoniazid, pyrazinamide, ethambutol, 
B6=vitamin B6 (pyridoxine), IVFs=intravenous fluids (including dextrose and saline infusions), Abx=antibiotics, Inotropes=adrenaline 
infusion, Steroids=intravenous hydrocortisone or oral prednisone, ORS=oral rehydration salt, Slow Na tabs=slow sodium tablets.

DISCUSSION
The symptoms and signs of  adrenal insufficiency are 
often non-specific and insidious in onset, and may go 

undetected until some physiological stress precipitates 
an adrenal crisis. Disseminated TB (e.g., miliary TB) 
remains an important cause of  adrenal insufficiency in 



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high-TB burden populations (Anaforoğlu et al., 2012; 
Enos et al., 2018; Vinnard & Blumberg, 2017; Yokoyama 
et al., 2009). In retrospect, during her first admission, 
our patient already had some clinical features of  adrenal 
insufficiency. Her recurrent diarrhea and vomiting, 
abdominal pains, persistent hyponatremia despite 
replacement, and postural hypotension were all in keeping 
with adrenal insufficiency (Hahner et al., 2021), even 
though acute gastroenteritis complicated with severe fluid 
and electrolyte anomalies could also explain them. She 
later presented with a classical adrenal (or Addisonian) 
crisis (Rathbun & Singhal, 2024) in her second admission, 
most likely precipitated by acute cystitis. The diagnosis 
this time was easily made on the basis of  gastrointestinal 
symptoms, salt craving, persistent shock, hyponatremia, 
hyperkalemia, and hypoglycemia. (See Table 1). 
Adrenal crisis, principally presenting as shock, is a life-
threatening emergency that requires urgent treatment 
with intravenous glucocorticoids, fluids, and supportive 
care (Rathbun & Singhal, 2024). Treatment must not be 
delayed for all suspected patients in order to perform any 
diagnostic tests, as it carries a high mortality rate of  up to 
10% (Ngaosuwan et al., 2021). Biochemical tests for the 
diagnosis of  adrenal insufficiency include measurement 
of  cortisol levels, ACTH-stimulation assays, etc., as well as 
diagnostic tests to determine the underlying causes as per 
endocrinological society guidelines (Bornstein et al., 2016). 
The glucocorticoid of  choice is hydrocortisone (it has 
both glucocorticoid and mineralocorticoid properties), 
given as a bolus dose of  100mg, followed by 50mg every 
6 hours for 24 hours (or 200 mg/24 hours as a continuous 
infusion), and thereafter tapered to clinical response. One 
may alternatively use intravenous methylprednisolone or 
dexamethasone (Bornstein et al., 2016).  In her case, we 
gave a bolus dose of  intravenous hydrocortisone 200mg, 
followed by a maintenance dose of  100mg every 8 hours 
a day for 3 days, before de-escalating to oral prednisone 
(which is cheaper and more readily available). Whereas 
hyponatremia and hypokalemia are expected to resolve 
with hydrocortisone and normal saline infusions, in our 
patient, we administered a 3-day course of  hypertonic 
saline to correct the profound hyponatremia causing 
altered mental status. This is in line with conventional 
practice (Adrogué et al., 2022). We elected to keep her 
on oral slow sodium tablets until the complete resolution 
of  the hyponatremia. The hypoglycemia resolved with 
the steroid and dextrose infusions. Hypotension caused 
by an adrenal crisis responds rapidly (usually within 
a few hours) to intravenous glucocorticoid and fluid 
administration. Our patient had persistent hypotension, 
most likely superimposed by urosepsis, and needed 
inotropic support with an adrenaline infusion and 
intravenous ciprofloxacin before a full resolution. 
Various society guidelines have protocols for tapering 
off  the glucocorticoids following the resolution of  an 
adrenal crisis, depending on whether the patient has 
known or unknown underlying adrenal insufficiency 
(Bornstein et al., 2016). The principal determination is 

the clinical status of  the patient and adequate monitoring. 
In our patient, we made a clinical decision to taper her 
prednisone from 20, 10, and 5 mg over a 4-month’s 
duration as we took mitigating measures against the 
complications of  the steroids. Rifampicin, which is the 
main drug in TB treatment, has been reported to induce 
adrenal insufficiency and adrenal crises (Campbell et al., 
2023; Kyriazopoulou et al., 1984). Most of  these cases 
occurred in patients with underlying adrenal insufficiency, 
and following adequate glucocorticoid replacement, the 
drug was continued safely with close patient monitoring. 
Our patient has successfully finished her TB therapy 
containing rifampicin for the past six months without 
recurrent adrenal insufficiency or crisis. We believe that 
with the cure of  the TB, the adrenal glands have fully 
recovered their functions.

CONCLUSION
Primary adrenal insufficiency (Addison’s disease) should 
be considered in patients on treatment for disseminated 
tuberculosis, who present with recurrent gastrointestinal 
symptoms, hyponatremia, hyperkalemia, salt craving, 
and postural hypotension. Adrenal crisis occurs when 
persistent hypotension and shock ensue in the setting 
of  adrenal insufficiency and recent physiological stress. 
This carries a high mortality rate of  up to 10%. When an 
adrenal crisis is suspected, it needs emergency treatment 
without any delays, with intravenous glucocorticoids 
(preferably hydrocortisone), fluids, and supportive therapy. 
Subsequent glucocorticoid therapy should be tapered 
off  based on clinical response. Primary care physicians 
in resource-limited clinical settings should successfully 
recognize and manage tuberculous Addison’s disease.

Learning Points
1. Consider adrenal insufficiency in patients with miliary 

tuberculosis who present with non-specific abdominal 
pains, nausea, vomiting, anorexia, lethargy, hyponatremia, 
salt craving, dehydration, altered mental status, etc.

2. An adrenal crisis must be considered in any patient 
who presents in shock. The clues include persistent 
hypotension, hyponatremia, hyperkalemia, hypoglycemia, 
azotemia, and hyperpigmentation in the setting of  non-
specific abdominal pains, nausea, vomiting, weight loss, 
and lethargy.

3. An adrenal crisis is a medical emergency with a 
high mortality rate. When suspected, treatment must be 
initiated immediately with intravenous hydrocortisone, 
fluids, and supportive therapy. Treatment must not be 
delayed by the need to perform diagnostic tests.

ACKNOWLEDGEMENT
The authors acknowledge the nursing staff  in the female 
wards and TB clinic of  St. Joseph Rift Valley Hospital, 
Gilgil, for their help in managing this patient.

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