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NTIS refers to a syndrome found in seriously ill or starving patients with low fT3, usually elevated RT3, normal or low TSH, and if prolonged, low fT4. It is found in a high proportion of patients in the ICU setting, and correlates with a poor prognosis if TT4 is <4ug/dl. The patho-physiology includes suppression of TRH release, reducedT3 and T4 turnover, reduction in liver generation of T3, increased formation of RT3, and tissue specific down-regulation of deiodinases, transporters, and TH receptors. Although long debated, tissue TH levels are definitely reduced, and tissue hypothyroidism is presumably present. This is often not clinically evident because of the brief duration, and reduced but not absent tissue levels of TH. Although recognized for nearly 4 decades, interpretation of the syndrome is contested, because of lack of data. Some observes, totally without data, argue that it is a protective response and should not be treated. Other observers (as in this review) present available data suggesting, but not proving, that thyroid hormone replacement is appropriate, not harmful, and may be beneficial. The best form of treatment (TRH,TSH,or T3+T4) and possible accompanying treatments (GHRH, Cortisol, nutrition, insulin) lack consensus. In this review current data are laid out for reader’s review and judgment.
The vast majority of glucocorticoid activity in most mammals is from cortisol, also known as hydrocortisone. Corticosterone, the major glucocorticoid in rodents, is another glucocorticoid. Cortisol binds to the glucocorticoid receptor in the cytoplasm and the hormone-receptor complex is then translocated into the nucleus, where it binds to its DNA response element and modulates transcription from a battery of genes, leading to changes in the cell's phenotype. Only about 10% of circulating cortisol is free. The remaining majority circulates bound to plasma proteins, particularly corticosteroid-binding globulin (transcortin). This protein binding likely decreases the metabolic clearance rate of glucocorticoids and, because the bound steroid is not biologically active, tends to act as a buffer and blunt wild fluctuations in cortisol concentration.
For patients in extremis from respiratory failure or shock, securing vascular access is crucial, along with establishing an airway and ensuring adequacy of breathing and ventilation. Peripheral intravenous catheter insertion is often difficult, if not impossible, in infants and young children with circulatory collapse. Intraosseous (IO) needle placement, shown in the images below, provides a route for administering fluid, blood, and medication. An IO line is as efficient as an intravenous route and can be inserted quickly, even in the most poorly perfused patients.
Learn the SIRS Criteria and how to calculate it. Greater than or equal to 2 or more of the following: Temperature Fever of greater than 38°C (100.4°F) or Less than 36°C (96.8°F) Heart Rate Greater than 90 beats per minute Respiratory Rate Greater than 20 breaths per minute or PaCO2 of less than 32mm Hg White Blood Cell Count Greater than 12,000cells/mm³ or Less than 4,000cells/mm³ or Greater than 10% Bands
The dural venous sinuses are spaces between the endosteal and meningeal layers of the dura. They contain venous blood that originates for the most part from the brain or cranial cavity. The sinuses contain an endothelial lining that is continuous into the veins that are connected to them.
This is a diabetic foot ulcer. The patient reportedly went on vacation and noticed this ulcer upon their return. Debridement (removal of damaged tissue) to the level of healthy bleeding tissue is medically necessary as damaged tissue acts an impediment to wound healing. Due to their diabetic neuropathy, they did not feel any pain or indication that a wound was forming. This ulcer appeared to have penetrated to the level of subcutaneous tissue or even fascia, but turned out to be much deeper than that. These are serious wounds and are the beginnings of what lead to foot and leg amputations if they are not treated promptly by your healthcare provider, AKA Podiatrist.
Delayed puberty is defined as the absence of any signs suggestive of puberty by 14 years of age. In this case, the patient's pubertal delay appears to be constitutional because of his positive family history, absence of syndromic features or systemic illness, and bone age of 12 years. Puberty correlates more closely with bone age than chronological age. On follow-up, the patient will most likely demonstrate a similar onset of puberty as his father.
There is a strong association with obesity. In children younger than 10 years, it is associated with metabolic endocrine disorders {hypothyroidism, panhypopituitarism, hypogonadism, renal osteodystrophy, growth hormone abnormalities). SCFE is considered chronic if it has been present more than 3 weeks and acute if it has been present for 3 weeks or less. It is called "stable" if the patient can bear weight and "unstable" if the patient cannot ambulate. Unstable SCFE is associated with more complications, including avascular necrosis of the femoral head (AVN). SCFE is diagnosed by x-ray of the pelvis and bilateral hips. The underlying cause is a widened epiphyseal growth plate, due to abnormal cartilage maturation and endochondral ossification. The treatment is surgical, requiring immediate internal fixation with a single screw. Delay in treatment {> 24 hours) leads to increased AVN, SCFE progression from stable to unstable, and high risk of future degenerative arthritis. Prophylactic contralateral fixation of the unaffected hip is not routinely done in the U.S., except in patients with endocrine abnormalities.