ADDISONIAN CRISIS- A CASE PRESENTATION

Dr.Ritaja Sathe, 2nd Yr M.D.Scholar, Dept. of Kayachikitsa, COA, BVDU

Dr.D.L.Shinde, Prof. & Hod, Dept. of Kayachikitsa, COA, BVDU
 CASE:
A 52 years old male patient, with past H/o Pulmonary Tuberculosis, presented to K.C.OPD, Bharati Ayurved Hospital
with the C/O-
• Anorexia
• Extreme fatigue since 2-3 months
• Somnolence
• Dyspnea on exertion
• Giddiness on standing up since 3-4 days.
Past Medical H/o-
 H/o Pulmonary Tuberculosis- 10 years back- has completed 9 months of AKT.
 K/C/O Renal Parenchymal Disease, diagnosed in April, 2022 – on medical management.
 Recent creatinine-
Past Surgical H/o- Nil
ON EXAMINATION:

 General examination: Cachexic+, Emaciated

 P- 104/min, regular, radial not palpable, brachial feeble, palpable
 BP- severe hypotension+ ~ systolic BP= 60 mmHg
 Temp- 97 deg F
 RS- few right basal wheeze+
 CVS- S1S2+, no murmurs
 CNS- patient is conscious but prefers to sleep. Easily arousable, obeys commands. Moving all 4 limbs.
 Per Abdomen- soft, non-tender
 Extremities: cool
 Stools- passed, urine- passed
WHAT’S THE DIAGNOSIS?
DIFFERENTIAL DIAGNOSIS:

 Septic shock – No H/o fever, no cough, no urinary complaints.

 Hypovolemic shock- no h/o GI losses (vomiting//diarrohea), no use of diuretics.
 Haemorrhagic shock- no h/o GI bleed/trauma.
 ACTH deficiency  Normal mineralocorticoid production, no hyperkalemia.
 Patient’s with secondary adrenal insufficiency  lack ACTH and lack normal skin pigmentation.
 Acute abdomen  neutrophilia must be present, whereas in adrenal insufficiency  lymphocytosis with
eosinophilia is present.
 Hyperkalemia  rhabdomyolysis, GI bleeding, drugs like ACE inhibitors, spironolactone etc
 Hyponatremia  vomiting, diarrhoea, diuretic use,
 LAB FINDINGS (01/07/22) :

 Haemogram: Hb-11.4gm%, TLC- 5,900/cumm, Platelet count- 4,48,000/cumm

 LFTs: Sr.Bil(T)- 0.2mg/dl, (D)- 0.1mg/dl, (I)- 0.1mg/dl, S.G.O.T.- 16 IU/L, S.G.P.T.- 10 IU/L, Sr.Alk.Phos.- 88IU/L,
Sr.Proteins(T)- 5.0mg/dl, Sr.Albumin- 1.0mg/dl
 Blood urea- 79mg/dl, Sr.Creatinine- 3.1mg/dl
 Sr.Electrolytes- Sr.Na+ 137.2 mEq/L, Sr.K+ 3.5 mEq/L, Cl- 103.9mEq/L
 Urine R- proteins 3+, sugar 2+, pc- 4-5/hpf, ec- 2-3/hpf
 ECG- sinus rhythm
 CXR-PA: Fibrotic changes in b/l UL
 2D echo- No RWMA, EF-60%
 HIV, HbsAg, HCV- Negative
 PT- 13.7 sec, INR- 1.09
 TREATMENT GIVEN:

 IV FLUIDS: NS 500cc bolus

 Inj.Dexamethasone 8mg iv stat
 Cap.Uprise D3 60k once/week
 Tab.Calamol 1 OD
 Tab.Nephrosave 1 BD
 Tab.Sobosis forte 1BD
 Foley’s catheterization done

 Patient shifted to ICU for further management.

 Central line insertion done i/v/o monitoring volume status to guide fluid resuscitation.
 Vasopressor support: Inj.Norad 8mg 2ml/hr, titrated as per BP.
LABS CONTD…

 Serum cortisol levels - <0.2

ANATOMY & PHYSIOLOGY OF ADRENAL GLAND:

 Each gland measures 6-11 gm.

 Arterial blood flow is from outer cortex to
inner medulla.
 Adrenal cortex produces three classes of
corticosteroid hormones:
1. Glucocorticoids (E.g.: cortisol)
2. Mineralocorticoids (E.g.: Aldosterone)
3. Adrenal androgen precursors (E.g.:
Dehydroepiandrosterone DHEA)
CONTD. …

• Production of glucocorticoids and adrenal androgens is

under control of H-P-A axis  inhibitory feedback control
by hypothalamus and pituitary.
• CRH released in response to endogenous/ exogenous stress
 ACTH released. P
• Mineralocorticoids are regulated by RAAS
ADRENAL INSUFFICIENCY/ ADDISON’S DISEASE

 Deficiency of cortisol and mineralocorticoid from destruction of the adrenal cortex.

 Addison disease refers to chronic deficiency of cortisol caused by adrenocortical insufficiency.

ADRENAL
INSUFFICIENCY

PRIMARY
SECONDARY

• Caused d/t dysfunction or absence of

• Caused by deficient ACTH secretion
adrenal cortices
• Only Glucocorticoid deficiency
• Loss of Glucocorticoid &
• Consequence of dysfunction of
mineralocorticoid secretion
Hypothalamic pituitary component
• Mostly caused by autoimmune adrenalitis
of HPA axis
 ACUTE ADRENAL INSUFFICIENCY:

 It is an emergency, often observed in patients with primary adrenal insufficiency d/t loss of both glucocorticoid and
mineralocorticoid secretion.
 Hypotension  hypovolemic shock
 May mimic  f/o acute abdomen  abdominal tenderness, N, V, fever
 Decreased responsiveness  coma/stupor
 Triggers–

- Severe stress (infection/trauma/surgery)

- Hyperthyroidism/ prescribing thyroid hormone to patients with untreated adrenal insufficiency
- B/l adrenal damage (trauma/infection/haemorrhage/thrombosis etc)
- Sudden destruction of pituitary gland(d/t necrosis)
- Non adherence to glucocorticoid replacement or sudden withdrawal of adrenocortical hormone.
SIGNS AND SYMPTOMS:

 ACUTE ADDISONIAN CRISIS:

 Postural hypotension  hypovolemic shock
 May mimic f/o acute abdomen  nausea, vomiting, fever, abdominal tenderness
 Decreased responsiveness  stupor/coma

GLUCOCORTICOID DEFICIENCY MINERALOCORTICOID DEFICIENCY

Fatigue, lack of energy Abdo. pain, nausea, vomiting

Wt.loss, anorexia Dizziness, postural hypotension
Myalgia, joint pain Salt craving
Fever Low B.P., postural hypotension
Hypoglycemia Increased Sr.creatinine d/t volume depletion
Hyponatremia Hyponatremia, hyperkalemia
Normochromic anaemia
 TREATMENT:
 Immediately initiate rehydration  Saline infusion @ 1 lit/hr OR 2–3 L is given quickly with continuous cardiac
monitoring.
 Vasoconstricting agents like noradrenaline, dopamine can be used.
 When I/V saline is stopped, mineralocorticoid replacement is commenced with fludrocortisone, starting with 0.1 mg orally
daily and adjusted according to serum electrolytes.
 Glucocorticoid replacement  Inj.Hydrocortisone 100mg iv bolus f/b 100-200mg divided doses (50mg 6 hrly or 100mg 8
hrly) over 24 hrs by continuous infusion or bolus IV/IM injections
 Mineralocorticoid  Fludrocortisone acetate has a potent sodium-retaining effect. Dose- 0.05–0.3 mg orally daily or every
other day
 Maintenance therapy  15–30 mg of Hydrocortisone orally daily in 2-3 divided doses (eg, 10 mg at 7 am, 10 mg at 1 pm,
and 5 mg at 7 pm) OR
Prednisone or Methylprednisolone ~ 3–6 mg daily in divided doses.
 Consider broad spectrum antibiotics if bacterial infection are the precipitating cause of acute adrenal crisis.
 Treat electrolyte abnormalities, hypoglycemia, dehydration, as indicated.
TREATMENT CONTD…

 Patients who take excessive doses of corticosteroid replacement can develop Cushing syndrome.
 Rapid treatment is usually life saving in adrenal crisis, but if it is unrecognized or untreated, may result in
refractory shock that is unresponsive to fluid replacement or vasopressors.
CLASSIFICATION OF STEROIDS:

1. Short acting (1/2 life < 12 hrs)  Cortisol (hydrocortisone), Cortisone

2. Intermediate acting (1/2 life = 12-36 hrs)  Prednisone, Prednisolone, Methyl prednisolone
3. Long acting (1/2 life > 48 hrs)  Betamethasone, Dexamethasone

If potency of cortisol=1, then that of prednisolone will be 4 and dexamethasone will be 8-10 times more potent than
prednisolone.

Ref- Bedside clinics in medicine, Arup Kumar Kundu

 ADVERSE EFFECTS OF STEROIDS:

 MINERALOCORTICOIDS-
- Sodium and water retention
- Edema
- Hypokalemic alkalosis
- Progressive rise in BP

 GLUCOCORTICOIDS-
- Cushingoid features  moon facies, buffalo hump, obesity
- Hyperglycemia, muscular weakness
- Susceptibility to infections, peptic ulceration, delayed wound healing, osteoporosis
THANK YOU!