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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The resuscitation of the massively bleeding patient may seem superficially to be successful once the patient's vital signs have stabilized. The restoration of stable vital signs, however, does not confirm two critical elements of a thorough physiologic resuscitation: that there is truly adequate delivery of oxygen to all tissue beds and that physiologic disturbances that may have occurred because of massive transfusion during the resuscitation process have resolved. With respect to the adequacy of oxygen delivery, the current clinical endpoints, including mixed venous oxygen saturation, cardiac output, and serum lactate, reflect global perfusion and not regional oxygenation. Of these global measures, serum lactate is currently the best indicator as to whether some circulatory beds remain inadequately perfused. Serum lactate should be followed, and, in the event that elevated levels persist, measures to augment oxygen delivery (e.g., increasing cardiac output, hemoglobin concentration, oxygen saturation) should be undertaken. Gastric tonometry provides a method for specific examination of the splanchnic circulation. The current measurement techniques, however, require steady-state conditions and make it impractical in many physiologically dynamic situations. The physiologic disturbances associated with massive resuscitation (e.g., hyperkalemia, hypocalcemia, hypomagnesemia, hypothermia) should be anticipated. Coagulation disturbances occur, especially when massive transfusion is accompanied by hypotension, hypothermia, or acidosis. Coagulation parameters should be measured with the loss of each one half of blood volume or after each 30-minute interval, whichever occurs first. Evaluation at blood volume intervals is relevant to the development of a strictly dilutional coagulopathy. The development of DIC, occurring because of tissue factor exposure or acidosis, however, is related more to the time lapsed than to the absolute volume lost or replaced.
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PMID:The massively bleeding patient. 1177 75

A 2-year-old female spayed domestic shorthair cat was examined because of lethargy, inappetance, vocalization, and abnormal aggressive behavior of 1 day's duration. The cat had been groomed the previous day with a d-limonene-based insecticidal shampoo. Skin lesions consisted of coalescing erythematous patches. Despite supportive care, the cat's condition deteriorated. Dermatohistopathologic changes included multifocal areas of acute coagulative epidermal necrosis. The dermis was infiltrated by a dense population of bacilli. d-Limonene toxicosis has been rarely described in dogs and cats. Toxic effects such as hypersalivation, ataxia, shivering, hypothermia, scrotal irritation, hypotension, and erythema multiforme major have been reported. Treatment for septicemia and disseminated intravascular coagulation, along with intensive supportive care, may be necessary.
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PMID:Acute necrotizing dermatitis and septicemia after application of a d-limonene-based insecticidal shampoo in a cat. 1236 86

Massive haemorrhage in elective surgery can be either anticipated (e.g. organ transplantation) or unexpected. Management requires early recognition, securing haemostasis and maintenance of normovolaemia. Transfusion management involves the transfusion of packed red cells, platelet concentrates and plasma (fresh frozen plasma and cryoprecipitate). Blood product support should be based on clinical judgment and be guided by repeated laboratory tests of coagulation. Although coagulation tests may not provide a true representation of in vivo haemostasis, they do assist in management of haemostatic factors. Below critical levels (prothrombin time or activated partial thromboplastin time >1.8; fibrinogen <1.0 g/l; platelet count < 80 x 10(9) 1(-1)) it is difficult to achieve haemostasis. Despite seemingly adequate blood component therapy there remain situations where haemorrhage is uncontrollable. In this setting, alternative approaches must be considered. These include the use of other blood products (e.g. prothrombin complex concentrates; fresh whole blood; fibrin glue) and pharmacological agents (e.g. aprotinin). Complications of massive transfusion result in significant morbidity and mortality. These may be secondary to the storage lesion of the transfused blood products, disseminated intravascular coagulation, hypothermia or hypovolaemic shock. The use of fresh blood products and leucocyte-reduced packed red cells and platelets, may minimise some of the adverse clinical sequelae.
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PMID:Massive blood transfusion in the elective surgical setting. 1220 74

The initial aim in massive transfusion (MT) is to supply crystalloids, colloids, and plasma-poor red cell concentrates (RCCs) to maintain normovolemia and oxygen supply. This frequently leads to dilution coagulopathy, which is frequently aggravated and accelerated by hypothermia, acidosis, shock-induced impairment of liver function and disseminated intravascular coagulation (DIC), and increased consumption of clotting factors and platelets at extensive wound sites. Disorders of hemostasis deteriorate the prognosis of massively transfused patients dramatically. Therefore, the second therapeutic objective is the timely administration of plasma and platelet concentrates as required to halt the microvascular bleeding (MVB) induced by impaired hemostasis. Close laboratory monitoring, to include as a minimum platelet count, prothrombin time (PT), activated partial thromboplastin time (APTT), and fibrinogen, is essential to identify hemostatic disorders requiring therapeutic intervention. Coagulopathy promoting microvascular bleeding can be assumed when PT or APTT values exceed 1.5 times mean controls and/or when fibrinogen levels fall below 1.0 g/l. Repeated rapid infusion of 10-15 ml plasma per kg of body weight will be required to raise clotting factor levels significantly and to achieve adequate hemostasis. The turnaround time for obtaining laboratory results and for readying plasma for transfusion must be taken into particular consideration in cases of rapid blood loss.
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PMID:Indications for plasma in massive transfusion. 1237 88

Urea Cycle Disorders (UCD) is an inborn error of urea synthesis in which ammonium and other nitrogenous precursors of urea accumulate leading to episodic coma and a high mortality rate. Therapy with peritoneal dialysis, essential amino acids or their nitrogen-free analogues has increased survival. The authors report 5 cases of urea cycle disorders, all of whom developed and were rescued from hyperammonemic coma. However, the eventual outcome was quite variable. Argininosuccinate lyase deficiency (ALD) Case 1. A 2 month old male infant, a product of a consanguineous marriage (Suphanburi province); developed poor feeding on day 7, lethargy, convulsion, hepatomegaly and respiratory alkalosis leading to respiratory failure and coma. Hyperammonemia, elevation of glutamic acid and argininosuccinic acid and its anhydrides confirmed the diagnosis of ALD. He is now 9 years old and severely retarded. Case 2. A male infant with history of lethargy, poor feeding on day 3, treated as sepsis and required respiratory support for 6 days; subsequently readmitted at age 2 weeks with vomitting, lethargy, seizure activity and hyperammonemia, and was treated by a local pediatrician in Songkhla province. There was a history of parental consanguinity and he was referred to Siriraj Hospital on day 64 with severe essential amino acid deficiency and acrodermatitis enteropathica with markedly elevated plasma citrulline level. In spite of aggressive treatment; the patient developed sepsis and he expired on day 78. Ornithine transcarbamylase deficiency (OTC) Case 3. An eleven-month-old male infant, the product of a non-consanguineous marriage, developed neonatal onset of hyperammonemia on day 5 after poor feeding, lethargy, hypothermia, seizure, apnea and coma. He was rescued from neonatal hyperammonemic coma on day 9 after aggressive treatment, but expired at eleven months of age after overwhelming sepsis. Case 4. A male infant, sibling of case 3 was referred to Siriraj Hospital on day 8 with hyperammonemia and coma. In spite of intensive genetic counseling given after the birth of their first child with OTC, the couple chose to have another baby without informing any physician. The baby developed vomiting and lethargy on day 2; subsequently hyperammonemia was noted. In spite of aggressive treatment given; hepatic dysfunction, renal failure and disseminated intravascular coagulation defects occurred on day 15. He expired on day 18 after parental permission for discontinuation of all treatment. Argininosuccinate synthetase deficiency (ASS) or Citrullinemia. Case 5. A seven week old female infant, the product of a consanguineous marriage and of Pakistani ethnic origin; developed intermittent vomiting from day 6. Initial diagnoses included ruminations, sepsis and pyloric stenosis for which she was operated on (day 30); however, vomiting continued; subsequently seizures, hyperammonemic coma developed and she was rescued from hyperammonemic coma within 30 hours. Significant elevations of citrulline and L-glutamine were demonstrated. She was discharged in excellent condition to her home in Dubai, the United Arab Emirates.
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PMID:Urea cycle disorders in Thai infants: a report of 5 cases. 1240 52

A 62-year-old man was transported to the emergency room. He was in the state of shock and hypothermia of 34.2 degrees C. Fluid therapy was started using a HOTLINE to raise the body temperature, with vasopressors, vitamin B1 and sodium bicarbonate after checking arterial blood gas. Diagnosis of panperitonitis was made and operation was started immediately. We used HOTLINE before and during the operation. Body temperature returned to normal ranges, and hemodynamic state was stabilized at the end of the operation. After the operation, he received controlled artificial ventilation and nutrition support with intravenous hyperalimentation. Though he was complicated with disseminated intravascular coagulation, he went to general ward 17 days, and was discharged at 47 days after the operation. Sepsis accompanied with hypothermia leads to poor prognosis. We used fluid therapy with rapid-heating, and obtained good outcome. HOTLINE is effective for hypothermia in an emergency patient, because its effect is sure and does not obstruct the examination and management.
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PMID:[Efficacy of active core rewarming using fluid heating system HOTLINE before and during the operation in a patient with for panperitonitis in state of shock and hypothermia]. 1242 25

In order to test the practicability and safety of whole-body cooling in term neonates with moderate-to-severe hypoxic-ischaemic encephalopathy (HIE) and to report outcomes, a prospective pilot study was carried out in 25 term infants (median postmenstrual age 38 weeks, range 36 to 41 weeks; 20 males, five females). Whole-body cooling, to a target core temperature of 33 to 34 degrees C, started within 6 hours of birth and was maintained for 72 hours. Of the 25 newborn infants (19 Sarnat II and six Sarnat III, 18 outborn), 18 survived, including 13 (72%) with normal cerebral signal by MRI. Temperature instability occurred during cooling in 15 infants, but neither severe haemodynamic instability nor renal failure was seen. Thrombocytopenia developed in 12 infants, including seven with biological disseminated intravascular coagulation. One patient had hypoxaemia with right-to-left shunting through the ductus arteriosus, and seven had limited meningeal or subdural bleeding. Whole-body cooling is feasible in term neonates, with no life-threatening adverse events. Improvements are needed to obtain stable hypothermia for 72 hours.
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PMID:Whole-body cooling after perinatal asphyxia: a pilot study in term neonates. 1255 98

Five cases of severe hemorrhagic shock of abdominal origin treated with abbreviated laparotomy due to the onset of hypothermia, acidosis and consumption coagulopathy are described. The abdomen was temporarily closed and the patients were transferred to these Intensive Therapy Unit for the treatment correction of these disorders. Patients were then re-operated on 30 hours after the reestablishment of vital functions. Clinical complications of hemorrhagic shock, in which the "Abbreviated Laparotomy" technique is applicable, are presented.
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PMID:[Abbreviated laparotomy in patients with hemorrhagic shock]. 1269 7

The dramatic advances that have taken place in recent years in the care of sick and premature infants also have been matched by a similar increase in the use of blood transfusion therapy. Haematological features indicate that a newborn has a blood volume of 85-125 ml/kg the foetal haemoglobin is 60-85% and average Hb in full term infant is 18 gm/dl. By 2-3 months it falls to 11-12 g/dl the main cause of anemia are iron poor diet, weaning diets recurrent or chronic infections and hemolytic episodes in malarious areas. The red cells transfusions are usually top up transfusions, exchange transfusions, partial exchange transfusions. Top up- are for investigational losses and correction of mild degrees of anemias, upto to 5-15 ml/kg. They comprise 90% of all neonatal transfusions and are used in low birth babies in special care units for a maximum of 9-10 episodes. The walk in donor programs once popular are not much in vogue. The threshold for transfusion is 8-10 g/dl Hb for upto 5 weeks. Exchange transfusions are done for correction of anemia, removal of bilirubin, removal of antibodies and replacement of red cells. Ideally plasma reduced red cells that are not older than 5 days are used. It is prepared by removal of 120 ml of standard whole blood donation. The advantage of fresh cells is that hyperkalemia is avoided and good post transfusion survival acceptable red cell oxygen affinity. However it has to be screened for sickle cell disease and G6PD deficiency. Indications for exchange transfusion are kernicterus, neonatal hemolysis, G6PD deficiency, ARDS, neonatal sepsis, DIC and neonatal isoimmune thrombocytopaenia. Complications include over transfusion, perforation of major vessels, hypocalcaemia, citrate toxicity, hypothermia, hypoglycaemia, thrombocytopenia, necrotizing enterocolitis, GVHD, bacterial, viral infections. Partial exchange transfusions are done for symptomatic anemia, where Hb<10 g/dl, it is indicated in polycythemia and hyperviscosity syndromes. Exchange volume = Blood volume x (observed Hct-Desired HCt) divided observed Hct. Points to consider-there is weak expression of ABO antigens so particular care while grouping. Transfusing volumes should be 2-5 ml/kg/hour in paediatric bags of 50-100 ml with infusion devices. Platelet transfusion are indicated in neonatal throbocytopaenia, thrombocytopaenia due to sepsis, DIC, bacterial pathogens, CMV, TORCHS, Obstetric conditions such as pre eclampsia, intrauterine death abruption placenta birth injury hypoxia schock neonatal iso immune thrombocytopaenia and maternal ITP. Administration 1 RDE/pack per 2.5 kg single dose of fresh platelets less than 24hrs which contains 55 x 10(9) cells. This also contributes fresh plasma so is useful for coagulation defects also, though there is a risk of CMV and GVHD due to leucocyte contamination. Granulocyte concentrate; Gravity leucopheresis-1:8 ratio of 60 ml of 6% HES made to stand for 1hr.
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PMID:Component therapy. 1451 88

A 69-year-old woman caught a cold resulting in nausea, vomiting, diarrhea and severe anorexia. Then she suffered progressively from dyspnea and leg edema, and finally became delirious. On admission severe hypoglycemia, hypothermia, marked tachycardia, generalized edema, mild jaundice and cachexy were noted. EKG showed atrial fibrillation. A chest X-ray, chest CT and echocardiography showed congestive heart failure. Therapeutic use of diuretics induced shock leading to serious liver dysfunction and disseminated intravascular coagulation. However, combined therapy by intravenous glucose, digitalis, diuretics, anti-fibrinolytic drug and hydrocortisone were effective. Addition of antithyroid therapy brought a further favorable outcome.
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PMID:Severe starvation hypoglycemia and congestive heart failure induced by thyroid crisis, with accidentally induced severe liver dysfunction and disseminated intravascular coagulation. 1580 13


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