Endocrinopathies in critical illness are not uncommon and require special attention due to their systemic and sometimes nonspecific presentation. Thyroid StormThyroid storm, or thyrotoxic crisis, is an acute, potentially life-threatening state that can occur with undertreated or partially treated hyperthyroidism. Diagnosis is made on clinical grounds in the setting of an elevated T4 (thyroxine) and decreased thyrotropin (thyroid-stimulating hormone, or TSH). Due to its rarity, no prospective randomized clinical trials comparing treatment strategies are available. Electrolyte abnormalities, especially hyponatremia, are common and should be treated and monitored aggressively. Nonthyroidal Illness SyndromeNonthyroidal illness syndrome (NTIS), formerly known as sick euthyroid syndrome, remains a clinical entity in need of further study. Vasopressin DeficiencyVasopressin, a hormone secreted by the posterior pituitary in response to increased osmolarity and hypotension, plays a key role in critical illness. Vasopressin is also emerging as an important hormone for maintaining vasomotor tone during hemorrhagic shock. Adrenal InsufficiencyDepletion of adrenocortical reserve has been linked to the pathogenesis of shock in critically ill patients. Because surgery and anesthesia can elicit major physiologic stress, patients chronically treated with steroids may not be able to respond accordingly. ConclusionEndocrinopathies may often be underappreciated in the setting of critical illness. Iron deficiency also causes decreases in work and intellectual performances, neurological functions and immune defences. Low level of iron in infants and children causes retardation of physical, mental and motor development.
Iron deficiency is one of the main causes of anaemia as the mineral is essential in normal red blood cells production.
Other effects of iron deficiency include skin problem such as itching around the arms, legs, genitals and pica.
Studies suggest that ten per cent of all women suffer from iron deficiency and one out of three women has low iron stores.
The elderly are also prone to iron deficiencies because they produce less hydrochloric acid in their later years, which is necessary for successful iron absorption. Iron is needed to form haemoglobin (found in red blood cells) and myoglobin (found in muscle cells). Iron is also a part of erythropoietin hormone that is important in red blood cells production regulation. Iron is a co-factor in nucleic acid synthesis and conversion of beta-carotene to vitamin A.


Iron is a part of several intracellular enzymes such as cytochrome that is needed for cells respiration, catalase that inhibits oxidising agent such as hydrogen peroxide and myeloperoxidase that is essential in white blood cells production.
Nonhaem iron is found in eggs, dark green leafy vegetables, nuts, legumes, brocolli, carrots, peaches, potatoes, grapes, brewer’s yeast and whole grain and herbs such as alfalfa, dong guai, dandelion and milk thistle.
Another loss occurs when food is peeled and discarded since iron is concentrated near the surface of these foods. Losses can be minimised by cooking the food at low temperatures, in less water (steaming is preferred) and in large pieces.
Iron reduces the effects of antacids and ulcer-healing drugs, antibiotics (such as doxycycline, ketoconazole, tetracycline) and anti-cholesterol drugs (atorvastatin, celestipol, cholesytramine, simvastatin, probucol).
Allupurinol (gout treatment drug), dexatrim, amaphen, clofibrate, para-aminosalicyclic acid, vitamin E, cooper and zinc reduce iron absorption. Diseases associated to iron overdose include haemosiderosis, thalasemia, polycythemia and haemochromatosis.
Iron supplement is used to prevent hypothermia (drop of body temperature below normal level, 370 C).
Before taking any course of treatment, you are advised to check with your doctor, pharmacist or other health-care professionals.
Importantly, they may mimic signs and symptoms of the primary cause of the patient’s critical illness. Although an elevated serum TSH and low free T4 value support the diagnosis, treatment should be initiated on clinical suspicion and not when laboratory data become available. Administration of intravenous T3, T4, or a combination of these, have been employed (see Table 1). Diagnosis is based on clinical suspicion of thyroid dysfunction, with critically ill patients routinely demonstrating low serum T3 concentrations. With prolonged hemorrhage and aggressive resuscitation, vasopressin levels decline and vasopressors are frequently required. Adrenal insufficiency can be caused by derangements at any level of the hypothalamic-pituitary-adrenal axis. Critically ill patients may develop a state of “relative adrenal insufficiency” or acquired glucocorticoid resistance.
The iron intake for adolescent girls cannot match their needs due to menstrual losses and the increased demands of adolescent growth. The choice of contraception methods may also affect the extent of blood loss in some women. Even bleeding haemorrhoids increase the risk of an iron deficiency.
It is also needed by neutrophiles and lymphocytes to produce antibodies that are improtant in immune system and body defence system against microorganisms’ infections. High level of iron also causes infections because iron is also needed for microorganisms’ growth and development too.


Adrenal insufficiency may exist concurrently and treating hypothyroidism may precipitate an adrenal crisis. Cardiac monitoring is essential during initial treatment as tachyarrhythmias have been described.(9) Supportive care is critical in the reversal of this process, including passive rewarming, hemodynamic support with isotonic fluids and vasopressors, mechanical ventilation, and empiric antibiotics. These findings were confirmed in the Vasopressin in Septic Shock Trial (VASST) where the addition of vasopressin to norepinephrine also resulted in a reduction in the need for norepinephrine. Although primary adrenal insufficiency in the critically ill is rare, secondary insufficiency can be caused by any disease process or medication that interferes with adrenocorticotropic hormone secretion.(21) Not surprisingly, therapeutic glucocorticoid use is the most common cause of drug-induced secondary adrenal insufficiency, becoming clinically apparent when the physiologic stress exceeds the anticipated glucocorticoid requirement. Thyroid storm, myxedema coma, NTIS, vasopressin deficiency, and adrenal crisis can all have nonspecific signs and symptoms that can be misleading.
Non-thyroidal illness syndrome is a manifestation of hypothalamic-pituitary dysfunction, and in view of current evidence, should be treated with appropriate replacement therapies. Low-dose vasopressin infusion in patients with severe vasodilatory hypotension after prolonged hemorrhage during general anesthesia. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock.
Meta-analysis: the effect of steroids on survival and shock during sepsis depends on the dose. Aldosterone control in critically ill patients: ACTH metoclopramide, and atrial natriuretic peptide. These two components are then reused to form new red blood cells and will be excreted through the faeces. TSH levels are typically normal to low.(10) Medications frequently used in the critically ill – such as dopamine, glucocorticoids, amiodarone, and propranolol – may also contribute to depressed thyroid levels.
These patients may present with lifethreatening hypotension, but more commonly with nonspecific symptoms such as diffuse abdominal pain, nausea, vomiting, fever, lethargy, and mental status changes.
It is important to maintain a high index of suspicion in the critically ill when disease is recalcitrant to the prescribed therapy.
Due to its rapid progression to shock and death, treatment of acute adrenal crisis should be based on clinical suspicion. Current recommendations include administration of 100 mg of intravenous hydrocortisone followed by a daily schedule of 200 mg in divided doses. After the underlying illness has been treated and the patient is hemodynamically stable, glucocorticoids may be tapered to baseline dosing regimens.



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