PubMed Health⌕ Search

PubMed · 8974199

Massive transfusion.

Abstract

The management of patients receiving large amounts of blood is often difficult. The complications associated with massive transfusion are reviewed. Methods for preventing or treating these complications are presented. Excessive involvement of the transfusion medicine specialist provides the optimum way of managing patients undergoing massive transfusion.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J T Crosson. 1996. Massive transfusion.. https://pubmed.ncbi.nlm.nih.gov/8974199/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

[Serum lactate level as a indicator of tissue hypoxia in severely ill patients].

Adequate oxygen supply to the tissues is of vital importance to survive critical illness and trauma. Shock can be defined as an imbalance between oxygen demand and oxygen supply. Clinical features of shock, like hypotension, tachycardia, cold clammy skin et cetera, are poorly correlated with presence of tissue hypoxia. A high lactate level is an early sign of tissue hypoxia. In severely ill patients tissue hypoxia is the most important cause of increased lactate levels. Increased blood lactate levels are related to increased mortality. Optimizing oxygen supply by fluid resuscitation is the intervention of first choice.

Acid-Base Imbalance↗

Inhibition of the human intermediate-conductance, Ca2+-activated K+ channel by intracellular acidification.

The effect of changes in pH on the gating properties of the cloned human intermediate-conductance, Ca2+-activated K+ channel (hIK) was studied using the patch-clamp technique. Multi-channel inside-out recordings of patches from HEK-293 cells stably expressing hIK channels revealed that the channel activity is modulated by changes in intracellular pH (pHi). Changes in extracellular pH (pHo) in the range from pH 6.0 to 8.2 did not affect the hIK whole-cell current. Intracellular acidification gradually decreased the activity of the hIK channel, approaching zero activity at pHi 6.0. Decreasing pHi altered neither the conductance nor the inward rectification of hIK channels. The proton-induced inhibition of the multi-channel hIK patch current could not be counteracted by increasing the cytosolic Ca2+ concentration to 30 microM. The molecular sensory mechanism underlying the proton-induced modulation of hIK gating is at present unknown.

Acid-Base Imbalance↗

Kidney stones as a manifestation of hypercalcemic disorders. Hyperparathyroidism and sarcoidosis.

When hypercalcemia is detected in a kidney stone formation, an intact parathyroid hormone measurement should be made. Detection of hyperparathyroidism (HPT) is important to prevent further stone episodes and to avoid the complications of high serum calcium in other organ systems. Stones in patients with HPT often contain apatite salts in addition to calcium oxalate because parathyroid excess may create a renal tubular acidosis. The calculi seen in patients with sarcoidosis, another hypercalcemic state that may cause stone formation, however, are usually pure calcium oxalate. Excess generation of 1,25-dihydroxyvitamin D results in intestinal hyperabsorption of calcium and secondary hyperoxaluria.

Acid-Base Imbalance↗