Hypothermia development

In neonatal manifestation of OTC deficiency, lethargy, vomiting, refusal to take food, hyperventilation and hypothermia develop quickly. Death ensues in coma within a few days. Manifestation in infants or adolescents is based upon the residual activity of the defective enzyme. This course is also characterized by vomiting and lethargy. The clinical picture is aggravated by a protein-rich diet, whereas protein reduction improves the clinical situation. Without treatment, death occurs in a hepatic coma. 

Hypothermia is the condition of reduced temperatures. Most cases of hypothermia develop when air temperatures are between 2° and 10°C (30° to 50°F). Uncontrollable shivering and the sensation of cold lead to decreased and/or irregular heartbeats, cool skin, impaired judgment and mental functioning, low blood pressure, and fatigue. Severe hypothermia can result in death. 

Septic patients may have an elevated, low, or normal temperature. The absence of fever is common in neonates and elderly patients. Hypothermia is associated with a poor prognosis. Hyperventilation may occur before fever and chills and may lead to respiratory alkalosis. Disorientation and confusion may develop early in septic patients, particularly in the elderly and patients with preexisting neurologic impairment. Disorientation and confusion may be related to the infection or due to sepsis signs and symptoms (e.g., hypoxia). 

Carbamyl phosphate synthetase deficiency. Carbamyl phosphate synthetase deficiency is rare. Neonates quickly develop lethargy, hypothermia, vomiting and irritability. The hyperammonemia typically is severe, even exceeding 1 mmol/1. Occasional patients with a partial enzyme deficiency have had a relapsing syndrome of lethargy and irritability upon exposure to protein. Brain damage can occur in both neonatal and late-onset groups. 

Everyone is sensitive to extreme weather conditions. But with age, the body may become less able to respond to long exposure to very hot or very cold temperatures. Some older people might develop hypothermia when exposed to cold weather. Hypothermia is a drop in internal body temperature, which can be fatal if not detected and treated. 

Cyclo(His-D-Leu) acts as a hydrolytic catalyst. Cyclo(Leu-Gly) blocks the development of (1) physical dependence on morphine, (2) tolerance to the pharmacological effects of /3-endorphin, (3) tolerance to haloperidol-induced catalepsy and hypothermia, and (4) dopaminergic supersensitivity after chronic morphine administration. Cyclo(Tyr-Arg), a synthetic analogue of kyortorphin (an endogenous analgesic peptide), and its A-methyl tyrosine derivatives are more potent than kyotorphin in the mouse tail pressure test. ... 

IWo days after a full-term normal delivery, a neonate begins to hyperventilate, develops hypothermia and cerebral edema, and becomes comatose. Urinalysis reveals high levels of glutamine and orotic acid. The BUN is below normal. Which enzyme is most likely to be deficient in this child ... 

Gray baby s5mdrome Premature babies develop vomiting, hypothermia, abdominal distension, shallow irregular respiration and further leading to gray cyanosis, vascular collapse, shock and death. 

A 23-year-old pregnant woman developed antepartum bleeding at 35 weeks and a tonic-clonic convulsion and hypothermia at 39 weeks, having used heroin 4 hours before. She had further tonic-clonic seizures, became obtunded, and required intubation. She had occasional runs of ventricular bigeminy. A cesarean section was performed. The neonate had poor respiratory effort and required ventilation. Blood chemistry suggested inappropriate secretion of antidiuretic hormone, acute renal insufficiency, and acute pancreatitis. She and the baby recovered after 2 weeks. 

The next phase involves the development of acidosis, in which the body s pH level begins to fall. In an acid environment, the body s many vital systems go awry and start trying to compensate for the imbalance. Breathing may speed up and then slow down. The kidneys may attempt to excrete more acids. Blood pressure rises. All of these conditions—hypoglycemia, hypothermia, and acidosis—begin in most people when BAL reaches 0.15 to 0.20 percent and higher. 

The need to cool patients quickly while at the same time reducing complication rates has led to the development of simpler methods of rapidly inducing and maintaining hypothermia. More modest hypothermia can now be achieved in awake patients with acute stroke by surface cooling with the forced air method in combination with pethidine to treat shivering (75), and several intravenous vascular cooling techniques look encouraging (48-50). 

Dempsey R. J., Combs D. J., MaleyM.E.,CowenD.E., Roy M.W., and Donaldson D. L. (1987) Moderate hypothermia reduces postischemic edema development and leukotriene production. Neurosurgery 21,177-181. 

The concept of neuroprotection relies on the fact that delayed neuronal injury occurs after ischemia, and each step along the ischemic cascade provides a target for therapeutic intervention. Thus, understanding the cellular and molecular mechanisms that underlie the development of neuronal and vascular injury is critical to optimize treatment. This chapter reviews experimental evidence from studies on focal cerebral ischemia and mild hypothermia, as well as the mechanisms involved in mild hypothermic neuroprotection. 

Taking these data into account, it is difficult to believe that the neuroprotective effects of hypothermia are due mainly to alterations in metabolic rate or CBF. On the other hand, it seems reasonable to think that hypothermia reduces membrane functions that are critical for the development of ischemic neuronal damage. 

A large effort examining the potential efficacy of mild hypothermia to protect neurons from ischemic injury has shown promise in experimental stroke models and is now being translated into clinical trials. To develop the use of mild hypothermia as an efficacious and safe... 

Mild hypothermia has been easily incorporated into the overall care of patients in various clinical settings. However, there is a potential for multisystem complications when it is used. Although mild hypothermia (32-34°C) is not usually responsible for cardiac dysrhythmias, it has been associated with electrical conduction disturbances secondary to its potentiation of other drugs, particularly neuromuscular blocking agents (4,45,46). There is a tendency to develop atrial fibrillation at temperatures below 32°C (47). During periods of mild hypothermia,... 

Shimizu T., Naritomi H., OeH., et al. (1996) Mild hypothermia prevents the development of cerebral edema and hemorrhagic transformation in acute embolic stroke. Cerebrovasc. Dis. (Suppl 2), 32-178. 

Extravasation of polymorphonuclear leukocytes (PMNs) in the area of injury occurs very early after injury in several different models of experimental TBI, and has been shown to correlate with the development of cerebral edema (101,102). Early canine studies conducted by Rosomoff (16,57) demonstrated that treatment with hypothermia decreased the posttraumatic cellular inflammatory response incited by experimental head injury compared to normothermic controls. This effect of hypothermia is likely mediated by several mechanisms including preservation of the BBB, thereby limiting extravasation of inflammatory cells and mediators into the area of injury (103), suppressing release of cytokines (22), and reducing CBF. 

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