Małopłytkowość poheparynowa

Abstract

Heparin-induced thrombocytopenia (HIT) is a clinical immune-mediated syndrome; symptoms of HIT result from the development of arterial and venous thrombosis and are correlated with the severity of the thrombocytopenia. In all patients receiving heparin preparations in intensive care units, platelet counts should be monitored every 2−3 days throughout therapy, particularly during days 4−14 when HIT is most likely to develop. The major screening tests should always involve a clinical assessment of HIT probability (4Ts or HEP scoring systems) and enzymatic immunoassays (IgG antibodies) for patients with a moderate to high risk of HIT. The full possibilities of such advanced diagnostic procedures are limited in Poland because functional tests are still not widely available. If the diagnosis is questionable, all heparin preparations should be withdrawn and an alternative method of anticoagulation instituted until HIT has been conclusively excluded. The use of new-generation anticoagulants (direct thrombin or Xa factor inhibitors) is currently considered the treatment of choice. Old-generation anticoagulants should not be administered (vitamin K antagonists) as they can aggravate thrombosis. If administered, their action should be reversed by vitamin K once HIT is confirmed. Antithrombotic therapy with "new" anticoagulants should be carried out at least until platelet counts return to the baseline values; the recommended duration of therapy is 4 weeks in patients with isolated thrombocytopenia or 4 months in those with thrombotic complications. Vitamin K antagonists should not be applied until the normal platelet count is restored (usually > 150 G L -1 ). When the therapy with vitamin K antagonists is reintroduced, "old" antagonists should be administered simultaneously with a "new" anticoagulant for at least 5 days due to an initial decrease in protein C concentration concentration, provided that the therapeutic value of INR is maintained (> 2) for at least 2 days.

Pressure Distribution during Negative Pressure Wound Therapy of Experimental Abdominal Compartment Syndrome in a Porcine Model

“…ACS is defined as a sustained elevation of IAP above 20 mmHg (with or without abdominal perfusion pressure (APP) <60 mmHg) that is associated with a new organ dysfunction/failure [ 1 ]. ACS is a life-threatening condition and leaving it untreated leads to multi-organ failure and death.…”

“…There are many temporary abdominal closure (TAC) techniques such as skin only sutures, the application of absorbable meshes, Bogota bag, zipper systems, Wittmann Patch and the different NPWT methods. Open abdomen (OA) complications are well-known and these include entero-atmospheric fistula formation, fluid and protein loss, catabolism, adhesions in the abdominal cavity, fascial retraction among many others [ 1 , 2 , 3 , 7 , 8 ]. According to the WSACS guidelines, NPWT is recommended in the treatment of ACS as it provides superior results to simple packing techniques [ 1 ].…”

“…Surgical intervention is required when these treatment options fail. The basic surgical approach is open abdomen (OA) therapy [ 1 , 2 ].…”

Adverse Drug Reactions in the ICU

“…Heparin-induced thrombocytopenia (HIT) type 2 occurs in 0.5-5 % of patients receiving heparin products [142]. Typically this syndrome is characterized by a 50 % or greater thrombocytopenia from baseline, occurring 5-15 days after initial heparin therapy.…”

“…For moderate or high scores, further testing is recommended, and the patient started on alternative anticoagulation until the diagnosis can be conclusively excluded. The absence of PF4 IgG antibodies has a high negative predictive value and rules out HIT; specificity is poor so positive tests require additional analysis [142][143][144][145]. Serotonin release assay has high specificity (95-100 %) and positive predictive value for HIT; however, the availability is limited.…”