Haematological emergencies

Author(s):  
Drew Provan ◽  
Trevor Baglin ◽  
Inderjeet Dokal ◽  
Johannes de Vos ◽  
Hassan Al-Sader

Septic shock/neutropenic fever - Acute transfusion reactions - Delayed transfusion reaction - Post-transfusion purpura - Hypercalcaemia - Hyperviscosity - Disseminated intravascular coagulation - Overdosage of thrombolytic therapy - Heparin overdosage - Heparin-induced thrombocytopenia - Warfarin overdosage - Massive blood transfusion - Paraparesis/spinal collapse - Leucostasis - Thrombotic thrombocytopenic purpura - Sickle crisis

Author(s):  
Drew Provan ◽  
Trevor Baglin ◽  
Inderjeet Dokal ◽  
Johannes de Vos

Septic shock/neutropenic fever - Acute transfusion reactions - Delayed transfusion reaction - Post-transfusion purpura - Hypercalcaemia - Hyperviscosity - Disseminated intravascular coagulation - Overdosage of thrombolytic therapy - Heparin overdosage - Heparin-induced thrombocytopenia - Warfarin overdosage - Massive blood transfusion - Paraparesis/spinal collapse - Leucostasis - Thrombotic thrombocytopenic purpura - Sickle crisis


Author(s):  
Anne Craig ◽  
Anthea Hatfield

Part one of this chapter tells you about the physiology of blood and oxygen supply, about anaemia and tissue hypoxia, and the physiology of coagulation. Drugs that interfere with clotting are discussed. Bleeding, coagulation, and platelet disorders are covered as well as disseminated intravascular coagulation. Part two is concerned with bleeding in the recovery room: how to cope with rapid blood loss, managing ongoing blood loss, and how to use clotting profiles to guide treatment. There is also a section covering blood transfusion, blood groups and typing. Massive blood transfusion is clearly described, there are guidelines about when to use fresh frozen plasma, when to use platelets, and when to use cryoprecipitate. The final section of the chapter is about problems with blood transfusions.


1980 ◽  
Vol 8 (2) ◽  
pp. 125-131 ◽  
Author(s):  
Bryan Rush ◽  
Newton L. Y. Lee

Due to the sophistication of red cell compatibility testing, the majority of transfusion reactions are non-haemolytic in origin. This paper reviews the clinical presentation of these reactions, emphasising that blood transfusion reaction must always be considered in the differential diagnosis when a patient develops unexpected complications during his hospital stay. Fever, allergic reactions, respiratory distress, hypotension and jaundice may all be manifestations of a transfusion reaction.


Blood ◽  
1973 ◽  
Vol 42 (5) ◽  
pp. 805-814 ◽  
Author(s):  
P. B. Neame ◽  
J. Lechago ◽  
E. T. Ling ◽  
A. Koval

Abstract The nature and etiology of the vascular occlusions encountered in thrombotic thrombocytopenic purpura (TTP) have been subject to controversy for a number of years. Disseminated platelet thrombosis has been suggested in the earlier literature, although later views have favored fibrin thrombi resulting from vascular damage or disseminated intravascular coagulation (DIC). The serial coagulation study and the lightand electron-microscopic findings in a case of TTP are described here. The multiple vascular occlusions were due to the presence of densely packed platelet aggregates in which a variable quantity of fibrin was present. Less commonly, loose platelet aggregates were noted. Fibrin under the endothelial lining was occasionally observed in relationship to the vascular occlusion and was thought to be secondary to the release of various substances from aggregating platelets. The serial coagulation study and the histologic examination of tissues showed no evidence of disseminated intravascular coagulation. This case shows that the occlusions observed in TTP can be due to disseminated intravascular platelet aggregation in the absence of DIC. Although TIP might be of variable etiology, it is felt that cases showing disseminated intravascular platelet aggregation should be distinguished from DIC in order to plan therapy on a rational basis.


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