scholarly journals Successful use of N-acetyl cysteine and activated recombinant factor VII in fulminant hepatic failure and massive bleeding secondary to dengue hemorrhagic fever

2014 ◽  
Vol 7 (4) ◽  
pp. 313 ◽  
Author(s):  
EdirisooriyaMaddumage Manoj ◽  
Gayan Ranasinghe ◽  
MK Ragunathan
2003 ◽  
Vol 37 (1) ◽  
pp. e1-e4 ◽  
Author(s):  
Stephen D. Lawn ◽  
Rosalinde Tilley ◽  
Graham Lloyd ◽  
Caroline Finlayson ◽  
Howard Tolley ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-3 ◽  
Author(s):  
Stalin Viswanathan ◽  
Nayyar Iqbal ◽  
P. Philip Anemon ◽  
G. Shyam Kumar

We report a 49-year-old diabetic with dengue hemorrhagic fever who developed fulminant hepatitis, severe coagulopathy, shock, and refractory metabolic acidosis and died on the eighth day of illness. This is the only second report of an adult with fatal fulminant hepatic failure due to dengue, and the first case arising from a primary dengue infection.


2005 ◽  
Vol 50 (6) ◽  
pp. 1146-1147 ◽  
Author(s):  
Venkataraman Subramanian ◽  
Suresh Shenoy ◽  
Anjelivelil J. Joseph

APOPTOSIS ◽  
2006 ◽  
Vol 11 (11) ◽  
pp. 1945-1957 ◽  
Author(s):  
B. San-Miguel ◽  
M. Alvarez ◽  
J. M. Culebras ◽  
J. González-Gallego ◽  
M. J. Tuñón

2008 ◽  
Vol 51 (6) ◽  
pp. 812-813 ◽  
Author(s):  
Satya P. Yadav ◽  
Anupam Sachdeva ◽  
Dhiren Gupta ◽  
Sunil D. Sharma ◽  
Gaurav Kharya

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2086-2086
Author(s):  
Satya Prakash Yadav ◽  
Sunil Dutt Sharma ◽  
Gaurav Kharya ◽  
Dhiren Gupta ◽  
Anupam Sachdeva

Abstract Dengue hemorrhagic fever (DHF) is a potentially lethal complication of mosquito borne viral disease, Dengue Fever. Thrombocytopenia is a constant finding in DHF/Dengue Shock Syndrome (DSS). The cause of thrombocytopenia is not clearly understood and may be due to decreased platelet production, increased peripheral destruction, or both. IV Anti-D is currently licensed to treat immune thrombocytopenia purpura (ITP) in pediatric or adult patients. Unlike other disease states, which may produce ITP, the thrombocytopenia associated with DHF has an acute onset and a high mortality rate if untreated. Use of Intravenous anti D (IV anti-D) for such bleeding has not been documented in the literature which prompted these descriptions Method: We report 2 cases that fulfilled the WHO criteria of DHF: high fever, bleeding, positive tourniquet test, severe thrombocytopenia (<10,000 /mm3) and hemoconcentration (Hematocrit increase> 20%). Case 1: 14-year-old boy was admitted with DHF and hypotension. He was stabilized after a normal saline (NS) bolus and continued on intravenous fluids @3ml/kg/hr. On day 3 of admission he again became hypotensive that responded to NS bolus and increased fluid rate of 5 ml/kg/hr. On day 4 child developed respiratory distress had to be ventilated in view of associated hypotension and deteriorating general condition. Echocardiogram showed global hypokinesia with Left Ventricular Ejection Fraction of 43% so started on inotropes. Few hours later he developed massive pulmonary hemorrhage. The pulmonary hemorrhage continued despite giving 42 units of platelets, 10 units of FFP and 3 units of aphaeresis. Platelet count remained less than 10,000 / mm3 despite repeated platelet transfusions. Recombinant Activated factor VII was given at a dose of 90 ug/kg which corrected coagulation profile to normal but hemorrhage still persisted. KhamRho IV Anti D® 50ug/kg was administered after which child showed dramatic response and bleeding stopped after 4 hr and platelets increased to 30,000 after 6 hr. Over next 48 hrs platelet count rose further. He was gradually weaned off the inotropes and ventilatory support. Case 2: 5-year-old girl admitted with DHF. On admission she was hypotensive and was having massive gastrointestinal bleed. She was given crystalloids/colloids and later started on dopamine infusion. She was intubated in view of deteriorating general condition and hemodynamic instability. She was managed as per the guidelines of dengue shock syndrome after which her hemodynamic status improved but bleeding continued for which she received 16 units of platelet concentrate, 1 unit aphaeresis along with 4 units of FFP and 1 unit cryoprecipitate in view of deranged coagulation profile. Platelet count remained less than 10,000 / mm3 despite platelet transfusion. Despite all these measures her bleeding continued thus a trial of activated factor VII 90 ug/kg two doses 1 hour apart was given but still bleeding persisted. KhamRho IV Anti D®50ug /kg single dose was administered after which child blood pressure stabilized and bleeding stopped after 3 hr. Platelet counts improved and she was gradually weaned off the inotropes and ventilatory support. Conclusion: The response observed in these patients demonstrates that the massive bleeding due to thrombocytopenia associated with DHF responds rapidly to treatment with IV Anti-D. There were no serious adverse events observed in both the patients.


2011 ◽  
Vol 45 (11) ◽  
pp. 1452-1452 ◽  
Author(s):  
Holly B Meadows ◽  
Jill C Krisl ◽  
Charles S Greenberg ◽  
Joseph E Mazur

Objective: To evaluate the use of recombinant activated factor VII (rFVIIa) in a patient with fulminant hepatic failure (FHF) requiring placement of an intracranial pressure monitor. Case Summary: A 21-year-old female with no significant medical history was admitted to an outside hospital with elevated results of liver function tests. Subsequently, the patient was diagnosed with autoimmune hepatitis. Systemic corticosteroids were started, but her condition continued to decompensate. She was transferred to our tertiary care facility 5 days after initial presentation. The liver function test results remained elevated (eg, total bilirubin 27 mg/dL), and international normalized ratio (INR) was 3.57. The medical team decided to place an intracranial pressure monitor, with the neurosurgery team's goal being an INR less than 1.5 before placement of the monitor. After multiple units of fresh frozen plasma (FFP) failed to lower the patient's INR, rFVIIa 40 μg/kg was administered. A rapid decrease of the INR allowed the neurosurgery team to perform the procedure without complications. Discussion: The use of rFVIIa allowed for decrease of this patient's INR after multiple units of FFP had failed to correct it. The utility of INR as a marker of coagulopathy in fulminant hepatic failure has been debated, but it is currently used as the standard laboratory test prior to invasive procedures, as in the case presented here. Conclusions: The use of rFVIta for rapid decrease of INR in a patient with FHF prior to an invasive procedure was safe and efficacious. When considering the use of rFVIIa, clinicians should be aware of the risk of thrombosis. In our experience, and in the limited literature on the matter, rFVIIa 40 μg/kg appears to be an appropriate dose for decrease of the INR. Further studies are needed to confirm this finding.


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