Carcinoid Crisis

Carcinoid Crisis

Definition:

-Carcinoid crisis is the most serious and life-threatening complication of carcinoid syndrome and is generally found in people who already have carcinoid syndrome.

-Carcinoid crisis occurs when all of the symptoms of carcinoid syndrome come at the same time. 

Causes:

➧ Spontaneous 

➧ Precipitating factors: 

-Stress, Sympathetic stimulation 

-Hypotension 

-Histamine-releasing drugs 

-Tumour manipulation 

-Regional anesthesia due to hypotension 

-Infection 

-Chemotherapy 

Clinical picture:

-Tachycardia, Arrhythmia 

-Hypotension, Shock 

-Flushing, Hyperthermia 

-Bronchospasm 

-Abdominal pain, Diarrhea 

Management:

Inhibit growth h. & vasoactive peptides release:

-Somatostatin analogs (Octreotide, Lanreotide) 

Anti-serotonin:

-Methesergide, Ketanserin, Cyproheptadine, Ondansetron, Alpha-methyl dopa 

Anti-kallikrein:

-Corticosteroids, Aprotinin

Anti-histamine:

-H1 blockers (Diphenhydramine) & H2 blockers (Ranitidine) 

R of Bronchospasm:

-Salbutamol, Aminophylline 

R of Diarrhea:

-Loperamide 

R of Hypotension:

-Vasopressin, Phenylephrine 

R of Hypertension:

-Alpha-blockers, Beta-blockers 

R of Rt. Heart failure:

-Digitalis, Diuretics

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Diabetic Ketoacidosis (DKA)

Physiology:

Hyperglycemia:

➧ Increased hepatic production of glucose.

➧ Diminished glucose uptake by peripheral tissues.

➧ Insulinopenia / Hyperglucagonemia.

Ketoacidemia:

➧ The ketoacid is acetoacetic acid. The byproduct is acetone. The non-keto-acid is beta-hydroxybutyric acid.

➧ Increased lipolysis and hepatic ketogenesis

➧ Reduced ketolysis by insulin-deficient peripheral tissues.

Fluid and Electrolyte Depletion:

➧ Osmotic diuresis and dehydration due to hyperglycemia.

➧ On average, water deficit is about 5L, sodium 500 mmol, potassium 400 mmol, and chloride 400 mmol.

General Considerations:

➤ Initial presentation of Type I DM (Can also occur in Type II DM).

➤ Increased insulin requirements in Type I DM (Infection, Trauma, Myocardial infarction, Surgery).

➤ Mortality is 5% in patients under 40 y. Up to 20% of the elderly.

➤ Estimates of 5-8 episodes per 1000 at-risk diabetics annually.

➤ One of the more common serious complications of insulin pump users – occurs 1 per 80 months of treatment. Typically due to unrecognized pump failure.

➤ Essentials of Diagnosis:

➧ Acidosis with pH < 7.3.

➧ Serum bicarbonate < 15 .mEq/L.

➧ The serum is positive for ketones.

➧ Elevated anion gap (variable, may occur without gap).

➧ Hyperglycemia > 250 mg/dL (no correlation between the severity of hyperglycemia and severity of ketoacidosis).

Clinical picture:

Symptoms:

➧ Early: Polyuria, Polydipsia, Fatigue, N/V.

➧ Late: Stupor – Coma.

Signs:

➧ Rapid, Deep Breathing.

➧ Fruity breath odor of acetone.

➧ Tachycardia, Hypotension, mild Hypothermia.

➧ Abdominal Pain and Tenderness.

Laboratory Findings:

➧ Glycosuria 4+, Ketonuria.

➧ Hyperglycemia, Ketonemia, Low arterial blood pH, and Low plasma bicarbonate.

➧ Elevated serum potassium (despite total body potassium depletion).

➧ Elevated serum amylase (not specific for pancreatitis in this setting, use lipase).

➧ Leukocytosis.

➧ If hyperthermic, likely due to infection since pts with DKA are hypothermic if uninfected.

Management of DKA:

Insulin Replacement:

➧ Regular Insulin IV bolus 0.1-0.2 units/kg to ‘prime’ insulin receptors.

➧ Regular Insulin infusion at 0.1 units/kg/h.

➧ Then replaced with SC regular insulin when hyperglycemia and ketoacidosis are controlled.

➧ Then oral intake + SC intermediate-acting insulin.

Fluid Replacement:

➧ The typical deficit is 4-5 L.

➧ Initially, NS 1 L/h. x 2 h., then 0.5 L/h. x 1-2 h., then 200-300 mL/h. till correction.

➧ Switch to ½ NS if serum Na > 150 mEq/L. 

➧ Add D5W if the glucose falls below 250 mg/dL, to maintain serum glucose 250-300 mg/dL to prevent hypoglycemia and cerebral edema.

Sodium Bicarbonate:

➧ 50 mmol

➧ Clinical benefit has not been demonstrated.

➧ Use to correct pH < 7, target pH of 7-7.2.

Potassium:

➧ 10-30 mEq/h. replacement to be started during the second or third hour of treatment.

Phosphate:

➧ Replete hypophosphatemia of < 1 mg/dL.

➧ 15 mmol K or Na phosphate in 100 mL saline.

➧ Replete slowly (3-4 mmol/h.) to avoid hypocalcemic tetany.

Treatment of Associated Infection:

➧ Antibiotics: as indicated.

➧ Cholecystitis and pyelonephritis may be particularly severe in these patients.

Read more ☛ Hypoglycemic Coma

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Hypoglycemic Coma

Hypoglycemia in Type I DM:

➧ Common in patients intensively controlled with insulin.

➧ Asymptomatic blood glucose levels of < 50 mg/dL occur daily in up to 56% of patients.

➧ Symptomatic hypoglycemia occurs 2X/week on average.

Severe Hypoglycemia:

➧ An episode requires intervention by another person for the patient to recover function.

Causes of Hypoglycemia in Diabetes:

➧ Delayed, reduced, or missed CHO intake.

➧ Increased glucose utilization (exercise).

➧ Decreased insulin clearance (renal failure).

➧ Alcohol -inhibits hepatic gluconeogenesis.

➧ Adrenal insufficiency or glucocorticoid dosage reduction.

Clinical picture:

Adrenergic:

➧ Tremor, anxiety, palpitations, hunger.

Neuroglycopenic:

➧ Dizziness, decreased concentration, blurred vision, tingling, lethargy.

Severe Hypoglycemia in Intensively Controlled Type I DM:

➧ Up to 25% yearly incidence.

➧ Disabling cognitive effects may take hours to fully resolve.

➧ May lead to seizures, and rarely, permanent neurological deficits.

➧ Estimated to be a causative factor in 4% of deaths.

Hypoglycemia Unawareness:

➧ Loss of autonomic warning symptoms of hypoglycemia.

➧ Occurs in 25-50% of patients with type I DM.

➧ Patients are no longer prompted to eat.

➧ Results in a 7X increased frequency of severe hypoglycemia.

Defective Glucose Counter-regulation in Type I DM:

➧ Reduced or absent glucagon response is common after 2-4 years.

➧ Deficient epinephrine response is common after 5-10 years.

➧ Results in a 25X increased frequency of severe hypoglycemia.

Hypoglycemia Unawareness and Defective Glucose Counter-regulation:

➧ Reversible by short-term avoidance of hypoglycemia.

Reduction of Hypoglycemia in Type I DM:

➧ Identify patients at increased risk:

- History of severe hypoglycemia.

- History of hypoglycemia unawareness.

- Normal or near-normal glycohemoglobin levels.

➧ Raise glycemic targets in the short term to regain symptom recognition.

➧ Education of patients and family members to recognize and treat hypoglycemia.

➧ Have unaware patients test blood glucose before performing a critical task (driving).

➧ Patients should have rapid-acting carbohydrates available at all times.

➧ Apply principles of intensive insulin therapy:

- Frequent home glucose monitoring.

- Flexible insulin regimens with dosage adjustments based on meal size, monitored blood glucose levels, and anticipated exercise.

➧ Replace insulin more physiologically:

- Multiple insulin injections.

- New ultra-short-acting insulin analogs: lispro, aspart, glulisine.

- Long-acting insulin analogs: glargine, detemir.

- Insulin pumps.

Subcutaneous, Continuous Glucose Monitors:

➧ Now available with alarms for high and low glucose readings.

➧ Useful for catching periods of hypoglycemia (especially overnight) of which patients are unaware.

➧ Shown to reduce the incidence of hypoglycemia in type I DM patients with prior severe hypoglycemia.

Management of Hypoglycemic Coma:

-If delayed, can cause permanent neurologic damage.

➧ 50% Dextrose in water: 50 ml IV over 3-5 min. followed by 5% dextrose in a water infusion.

➧ Glucagon: 0.5-1 mg IM/SC.

- Mobilizes hepatic glycogen stores.

➧ Hydrocortisone: for adrenal insufficiency.

➧ Hospitalize: those on sulfonylureas for 24 h.

Read more ☛ Diabetic Ketoacidosis (DKA)

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Acute Hypocalcemia

Causes:

1-Hypoparathyroidism

➧ Destruction of parathyroids (most commonly surgical – parathyroid resection or accidental).

➧ Acute hypomagnesemia

2-Reduced 1,25 (OH) vit D

3-Chronic renal insufficiency

➧ Acute systemic illness

➧ Drugs: ketoconazole, doxorubicin, cytarabine

➧ Increased uptake of Ca in bone

➧ Osteoblastic metastases

➧ Hungry bone syndrome

4-Complexing of Ca from the circulation

➧ ↑ albumin binding in alkalosis

➧ Acute pancreatitis with the formation of Ca soaps

➧ Transfusion-related citrate complexing

Clinical Picture:

Symptoms:

➧ Perioral numbness

➧ Tingling paresthesias

➧ Muscle cramps

➧ Carpopedal spasm

➧ Seizures

Signs:

➧ Hyperreflexia

➧ Chvostek's sign: (Figure 1, Figure 2)

(Tap on facial n. anterior to the earlobe or between the zygomatic arch and angle of the mouth → Unilateral spasm of facial muscles)

Figure 1: Chvostek's sign

Figure 2: Chvostek's sign

➧ Trousseau's sign: (Figure 3) 

(Inflate BP cuff 20 mmHg > SBP → Carpopedal spasm)

Figure 3: Trousseau's sign

➧ Hypotension

➧ Bradycardia

➧ Arrhythmias

➧ Prolonged QT interval (Figure 4)

Figure 4: Prolonged QT interval

ECG Changes: (Figure 5)

Figure 5: ECG changes in Acute Hypocalcemia

Biochemical Workup:

➧ S total Ca⁺², Albumin and Ionized Ca⁺² 

➧ S PO4⁺² 

➧ S Mg⁺² 

➧ Plasma PTH

- Low in hypoparathyroidism

- High in hungry bones syndrome

➧ 25 (OH)D3 and 1,25 (OH)D3 

➧ S. Amylase and Lipase

Management of Hypocalcemia:

1- First correct low Mg⁺²

2- Control of Tetany:

➧ Calcium gluconate: 10 ml of 10% solution IV over 5-10 min. and repeat as necessary in cases with frank generalized tetany.

➧ Slower continuous infusion of Calcium in less acute cases:

- 10% calcium chloride, 8 ml or 10% calcium gluconate, 22 ml in 100 ml isotonic saline over 10 min.-then continuous infusions of 1-2 mg/kg/h elemental calcium, lasting 6-12 h.; Oral daily maintenance 2-4 g.

- Vitamin D: 1-3 mg/d. oral.

3- Correction of alkalosis:

➧ Isotonic saline.

➧ Ammonium chloride: 2 g/4 h. oral to stop tetany.

Read more ☛ Acute Hypercalcemia

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Acute Hypercalcemia

Most Common Causes:

1-Endocrine:

➧ Hyperparathyroidism

➧ MEN

➧ PTH-related peptide (PTHrP) by solid tumors

2-Neoplastic:

➧ Ca with bone metastases

➧ Myeloma

3-Granulomatous:

➧ Sarcoidosis 

➧ Tuberculosis

Clinical picture:

➧ History of polyuria and polydipsia 

➧ Dehydration

➧ Bone pain

➧ Confusion

➧ Anorexia 

➧ Constipation

ECG Changes: (Figure 1)

Figure 1: ECG changes in Acute Hypercalcemia

Workup:

S – Ca (High) ➔ PTH (High) ➜ Primary Hyperparathyroidism

➔ PTH (Low) ➜ Malignancy or other cause

S – Ca > 3.0 is 90% of the time of malignant origin

Management of Hypercalcemia:

Volume repletion and diuresis:

➧ NaCl 0.9%: 4 L in first 24 h.

➧ Loop diuretics: Furosemide: 40-80 mg/2 h. IV

-Natriuresis promotes calcium excretion.

Bisphosphonates IV: (Pamidronate /Zoledronate)

-Potent inhibitors of bone resorption.

Corticosteroids:

➧ Prednisone: 30-60 mg/d.

➧ Hydrocortisone: 200mg/d. IV

-Impeding growth of lymphoid neoplastic tissue & enhancing vit. D actions.

Calcitonin:

-4 units/kg/12 h. IM/SC

-Inhibits bone resorption.

Plicamycin-antineoplastic:

-Inhibits resorption.

Dialysis:

-Patients with renal failure.

Urgent Parathyroidectomy

Read more ☛ Acute Hypocalcemia

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Thyroid Storm

Definition:

➧ Acute life-threatening exacerbation of thyrotoxicosis

Precipitating factors:

➧ Withdrawal of antithyroid drugs

➧ Severe infection

➧ Diabetic ketoacidosis (DKA)

➧ Cerebro-vascular accident (CVA)

➧ Cardiac failure

➧ Surgery

➧ Trauma 

➧ Radioiodine

➧ Drug reaction

➧ Iodinated contrast medium

Clinical picture:

➧ Patient with Graves disease who has discontinued antithyroid medication OR is previously undiagnosed

➧ Hyperpyrexia (40ºC)

➧ Sweating

➧ Tachycardia with or without AF

➧ Nausea, vomiting, and diarrhea

➧ Tremulousness and delirium, occasionally apathetic

Diagnosis:

➧ Free T4, free T3 elevated

➧ TSH suppressed

➧ Note that findings are not different than those of hyperthyroidism, but the difference is in the setting

Management of Thyroid Storm:

1-Inhibition of hormone production:

➤ Antithyroid agents:

➧ Thionamides (1st line therapy):

➧ Carbimazole/Methimazole 20-25 mg/6 h. orally or rectally (although once stable, the frequency of dosing can be decreased to once or twice daily).

-Carbimazole is metabolized to methimazole after ingestion.

-Halt synthesis of thyroid hormone by interfering with thyroid peroxidase.

➧ Propylthiouracil (PTU): 200 mg or 300 mg/6 h.

-Blocks peripheral conversion of T4 to T3 through inhibition of type 1 deiodinase.

2-Inhibition of thyroid hormone release:

➤ Iodine: (high concentration) 0.2-2 g/ d.

-Blocks release a stored hormone (Wolff-Chaikoff effect).

-Decreases iodide transport.

-Prevents oxidation in follicular cells.

-Iodine is given 1 hr after PTU to prevent incorporation into a new hormone.

-Above effects are only transient (48 h.).

-Lower concentration accelerates thyroid metabolism.

➧ Lugol’s solution: (assuming 20 drops/mL, 8 mg iodine/drop) 4-8 drops/6-8 h. oral.

➧ Potassium iodide: (with 20 drops/mL, 38 mg iodide/ drop) 5 drops/6 h.

➧ Oral iodinated contrast agents: 

-Competitively inhibit Types 1 and 2 50-mono-deiodinase in the liver, brain, and thyroid, blocking the conversion of T4 to T3, resulting in a rapid decrease in T3 and an increase in reverse T3. 

-Inhibit binding of T3 and T4 to cellular receptors. 

➧ Sodium ipodate: (308 mg iodine/500mg capsule) 1-3 g/ d.

➧ Iopanoic acid: 1g/8 h. for the first 24 hours, followed by 500 mg/12 h.

3-Controlling of cardiovascular manifestations:

➤ β-blockers:

-Control cardiovascular and hyperadrenergic manifestations.

-Decrease T4-T3 conversion.

➧ Propranolol: 60 to 80 mg/4 h., or 80 to 120 mg/4 h.

-The onset of action after oral dosing takes place within 1 hour. 

➧ For a more rapid effect, propranolol can also be administered parenterally, with a bolus of 0.5-1 mg over 10 min. followed by 1-3 mg over 10 min., every few hours, depending on the clinical context.

-Relatively large doses of propranolol are required in the setting of thyrotoxicosis because of the faster metabolism of the drug, and possibly because of a greater quantity of cardiac beta-adrenergic receptors.

➧ Esmolol: 50-100 µg/kg/min. IV.

➧ Longer-acting cardioselective β-adrenergic receptor antagonists: such as ➧ Atenolol and Metoprolol may be used also.

➤ Anticoagulation of AF:

➧ One of the significant cardiovascular complications of thyrotoxicosis is atrial fibrillation, occurring in 10% to 35% of cases. In the largest retrospective study, it appears that thyrotoxic patients who have atrial fibrillation are not at greater risk for embolic events, compared with age-matched patients who have atrial fibrillation due to other causes.

➧ Standard therapy with warfarin or aspirin is indicated, according to standard guidelines for atrial fibrillation.

➧ Thyrotoxic patients may require a lower maintenance dose of warfarin than euthyroid patients because of increased clearance of vitamin K-dependent clotting factors.

4-Steroids:

➤ Hydrocortisone: 100mg /8 h. IV with tapering as the signs of thyroid storm improve.

- Decreases T4-T3 conversion.

5-Alternative therapies:

-Several therapeutic agents used in the treatment of thyrotoxicosis are only considered when the first-line therapies of thionamides, iodide, beta-blockers, and glucocorticoids fail or cannot be used owing to toxicity.

➤ Potassium perchlorate: 1g qid oral

-Amiodarone induced thyrotoxicosis

-Inhibits iodide uptake by the gland.

➤ Lithium: 300 mg/8 h. 

-When thionamide is contraindicated.

-Inhibits new hormone synthesis.

-Decreases hormone secretion.

-To avoid lithium toxicity, lithium levels should be monitored regularly (perhaps even daily) to maintain a concentration of about 0.6-1.0 mEq/L.

➤ Guanethidine: 30-40 mg/6 h. orally

➤ Reserpine: 2.5-5 mg/4 h. IM

- Before β-adrenergic receptor antagonists were used to counteract the peripheral effects of thyroid hormone, the antiadrenergic agents, reserpine and guanethidine, were often used.

-Reserpine is an alkaloid agent that depletes catecholamine stores in sympathetic nerve terminals and the central nervous system.

- Guanethidine also inhibits the release of catecholamines.

-Side effects of these medications include hypotension and diarrhea. Reserpine can also have central nervous system depressant effects.

-These agents are indicated only in rare situations where β-adrenergic receptor antagonists are contraindicated, and when there is no hypotension or evidence of central nervous system-associated mental status changes

➤ Cholestyramine: 4 g four times a day oral.

-Decreases enterohepatic reabsorption of thyroid hormone.

➤ Plasmapheresis:

-When clinical deterioration occurs in thyroid storm, despite the use of all of these medications, removal of thyroid hormone from circulation would be a therapeutic consideration. Plasmapheresis, charcoal hemoperfusion, resin hemoperfusion, and plasma exchange are effective in rapidly reducing thyroid hormone levels in thyroid storms.

6-Supportive care:

➤ Supportive care is an important part of the multisystem therapeutic approach to thyroid storm.

➤ Antipyretics should be used; paracetamol is the preferable choice. Salicylates should be avoided in thyrotoxicosis because salicylates can decrease thyroid protein binding, causing an increase in free thyroid hormone levels. External cooling measures can also be used.

➤ Fluid loss and dehydration are also common in severe thyrotoxicosis. The fluid loss could result from the combination of fever, diaphoresis, vomiting, and diarrhea.

➤ Intravenous fluids with dextrose: (isotonic saline with 5% or 10% dextrose) should be given to replenish glycogen stores.

➤ Multivitamins, particularly thiamine, to prevent Wernicke's encephalopathy, which could result from the administration of intravenous fluids with dextrose in the presence of thiamine deficiency.

➤ If indicated digoxin for congestive heart failure.

➤ Treating the precipitating cause of thyrotoxicosis is particularly important, considering that the most common precipitant is thought to be an infection.

Prognosis:

➧ Mortality dropped since the 1920s from 100% to 20 – 30%

➧ Mortality is most frequently associated with serious underlying medical conditions 

Read more ☛ Myxedema Coma

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Myxedema Coma

Definition:

➧ The end-stage of untreated or insufficiently treated hypothyroidism.

Pathogenesis of Myxedema: (Figure 1)

Figure 1: Pathogenesis of Myxedema Coma

Precipitating factors:

➧ CVA

➧ Myocardial infarction

➧ Infection (UTI, Pneumonia)

➧ Gastrointestinal hemorrhage

➧ Acute trauma

➧ Administration of sedative, narcotic, or potent diuretics

Typical clinical picture:

➧ Elderly obese female

➧ Becoming increasingly withdrawn, lethargic, sleepy, and confused

➧ Slips into a coma

History:

➧ Previous thyroid surgery

➧ Radioiodine

➧ Default thyroid hormone therapy

Physical findings:

➧ Comatose or semi comatose

➧ Dry coarse skin

➧ Hoarse voice

➧ Thin dry hair

➧ Delayed reflex relaxation time

➧ Hypothermia

➧ Pericardial, pleural effusions, ascites

Laboratory tests:

➧ Free T4 low and TSH high

➧ If the T4 is low and TSH low normal consider pituitary hypothyroidism

➧ Blood gases

➧ Electrolytes and creatinine 

➧ Distinguish from the euthyroid sick syndrome

➧ Low T3, Normal or low TSH, normal free T4

ECG in a patient with Myxedema Coma: (Figure 2)

Figure 2: ECG in Myxedema Coma

Management of Myxedema:

➧ ICU admission: may be required for ventilatory support and IV medications.

➧ Parenteral thyroxine: Loading dose of 300-500 μg IV, then 50-100 μg/d. IV or 100-200 μg/d. oral

➧ Glucocorticoids: Hydrocortisone: 100 mg/8 h. for 1 week, then taper.

-Controversial but necessary in hypopituitarism or multiple endocrine failures.

➧ Electrolytes:

-Water restriction for hyponatremia 

-Avoid fluid overload

➧ Avoid sedation

Prognosis:

➧ Mortality is 20% and is mostly due to underlying and precipitating diseases.

Read more ☛ Thyroid Storm

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Acute Adrenal Insufficiency

Causes:

➧ Usually presents as an acute process in a patient with underlying chronic adrenal insufficiency

➧ Causes of Primary adrenal insufficiency:

   - Auto-immune

   - TB of adrenals

   - Metastatic malignancy to adrenals

➧ Causes of Secondary or Tertiary adrenal insufficiency

   - Pituitary or hypothalamic disease

➧ Acute destruction of the adrenals can occur with bleeding in the adrenals:

   - Sepsis

   - Disseminated intravascular coagulopathy (DIC)

   - Complication of anticoagulant therapy

Precipitating factors:

➧ Omission of medication

➧ Precipitating illness:

   - Severe infection

   - Myocardial infarction

   - Cerebro-vascular accident (CVA)

   - Surgery without adrenal support

   - Severe trauma

➧ Withdrawal of steroid therapy in a patient on long-term steroid therapy (Adrenal atrophy)

➧ Administration of drugs impairing adrenal hormone synthesis e.g. Ketoconazole

➧ Using drugs that increase steroid metabolism e.g. Phenytoin and Rifampicin

Clinical picture:

➧ Nausea and vomiting

➧ Hyperpyrexia

➧ Abdominal pain

➧ Dehydration

➧ Hypotension and shock

Clues to underlying Chronic Adrenal Insufficiency:

➧ Pigmentation in unexposed areas of the skin:

   - Creases of hands

   - Buccal mucosa

   - Scars

➧ Consider adrenal insufficiency if hypotension does not respond to pressors

Laboratory diagnosis:

➧ Hyponatremia and hyperkalemia (Hyponatremia might be obscured by dehydration).

➧ Random cortisol is not helpful unless it is very low (less than 5 mg/L) during a period of great stress.

➧ ACTH (Cosyntropin) stimulation test:

- Failure of cortisol to rise above 552 nmol/L 30 min after administration of 0.25 mg of synthetic ACTH IV

➧ Basal ACTH will be raised in primary adrenal insufficiency but not in secondary.

➧ CT of the abdomen will reveal enlargement of adrenals in patients with adrenal hemorrhage, active TB, or metastatic malignancy.

Management of Acute Adrenal Insufficiency:

➧ Hydrocortisone: 200 mg IV stat then 100 mg/8 h. for 24 h

-Taper slowly over the next 72 h.

-When oral feeds are tolerated change to oral replacement therapy.

-Overlap the first oral and last IV doses.

➧ Dexamethasone: 10 mg/6 h. IV

➧ Fludrocortisone: 0.05-0.3 mg/d. (if hydrocortisone less than 100 mg/d).

-Patients with primary adrenal insufficiency may require mineralocorticoid therapy (fludrocortisone) when shifted to oral therapy.

➧ 5% dextrose: IV for hypoglycemia

➧ Normal saline: IV for volume expansion

➧ Treat precipitating diseases

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