Laboratory investigations
The cardinal features of purpura investigations are the same as those of disseminated intravascular coagulation: prolonged plasma clotting times, thrombocytopenia, reduced plasma fibrinogen concentration, increased plasma fibrin-degradation products and occasionally microangiopathic haemolysis. Prevention
For people who have severe congenital protein C deficiency, protein C replacement therapies are available, which is indicated and approved for use in the United States and Europe for the prevention of purpura fulminans. Protein C replacement is often in combination with anticoagulation therapy of injectable low molecular weight heparin or oral warfarin. Before initiating warfarin therapy, a few days of therapeutic heparin may be administered to prevent warfarin necrosis and other progressive or recurrent thrombotic complications. Complications of prevention
The amount of fresh frozen plasma required to reverse disseminated intravascular coagulation associated with purpura fulminans may lead to complications of fluid overload and death, especially in neonates, such as transfusion-related acute lung injury. Exposure to multiple plasma donors over time increases the cumulative risk for transfusion-associated viral infection and allergic reaction to donor proteins found in fresh frozen plasma.Allergic reactions and alloantibody formation are also potential complications, as with any protein replacement therapy.Concomitant warfarin therapy in subjects with congenital protein C deficiency is associated with an increased risk of warfarin skin necrosis. Treatment
Early stage sepsis-associated purpura fulminans may be reversible with quick therapeutic intervention. Treatment is mainly removing the underlying cause and degree of clotting abnormalities and with supportive treatment (antibiotics, volume expansion, tissue oxygenation, etc.).
An idioventricular rhythm is a cardiac rhythm characterized by a rate of <50 beats per minute (bpm), absence of P waves and widening of the QRS complex. In cases where the heart rate is  between 50 and 110 bpm, it is known as accelerated idioventricular rhythm and ventricular tachycardia if the rate exceeds 120 bpm. Causes of idioventricular rhythms are varied and can include drugs or a heart defect at birth. It is typically benign and not life-threatening. Etiology
Various etiologies may contribute to the formation of an idioventricular rhythm, and include:
Heart block
Reperfusion after myocardial infarction
Electrolyte abnormalities
Heart diseases present at birth
Certain drugs (eg. digoxin, β-agonists, anaesthetics)

Pathophysiology
The physiological pacemaker of the heart is the sinoatrial node. If the sinoatrial node is rendered dysfunctional, the AV node may act as the pacemaker. If both of these fail, the ventricles begin to act as the dominant pacemaker in the heart. The ventricles acting as their own pacemaker gives rise to an idioventricular rhythm. Diagnosis
An ECG trace is required for diagnosis. Treatment
As this rhythm is not life-threatening, treatment has limited value for the patient. If underlying pathologies are identified, they should be treated appropriately. Antidysrhythmics may be utilised if the patient suffers from dysrhythmias. == References ==