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Course at Global Hospitals:
On arrival here, he was found to be having grade I – II encephalopathy, afebrile, hemodynamically stable with BP: 119/56mmHg, PR: 96/min, bipedal pitting oedema, and icteric.
The abdomen was otherwise normal except for nontender hepatomegaly. He was admitted in the ICU. The provisional diagnosis was acute on chronic alcoholic liver disease likely alcoholic hepatitis with progressive hepatorenal syndrome and progressive jaundice.
On evaluation he was found to have anemia (HB: 6.6gm%), leucocytosis 14000/cumm, Platelets 1.22 lakh/cumm, S. Bil 18.6mg% with a direct component of 11.4mg%, AST / ALT of 65/48 IU/ml, albumin 3.7g%, INR: 2.46, Creatinine 2.6mg%, Urea 69mg%. S.Na was 131mmol/L, K: 3.9mmol/L.
The right IJV was cannulated, and a PA catheter was inserted. This detected a PA pressure of 56/30mmHg. He was planned to stabilize or correct the HRS, improve nutrition and treat the encephalopathy. He was found not to tolerate terlipressin well at the previous hospital and was hence planned to put on octreotide + Albumin + midodrine. Two days later he was again put on trial of terlipressin here which he tolerated well and hence the dose was increased to 1mg every 4 hours along with 20% albumin. He was also put on antimicrobial cover of meropenem, fluconazole and teichoplannin.
He was assessed for the feasibility of a liver transplant but was deferred in view of high PA pressures.
He responded well to the above treatment in the form of increased diuresis, improving mentation, ambulation, improved food intake till 19.10.09. On 19.10.09 morning, he developed fever of 104 F with oliguria, worsening mentation and increase in jaundice accompanied with leucocytosis and a fall in platelet count. This kept on worsening over the next few days despite all adequate supportive measures. The antimicrobial cover was changed to tigecycline + caspofungin + ceftazidime. Routine blood and urine cultures didn’t show any growth. The D dimers were very high with high FDP and low fibrinogen (80mg%) levels suggesting a picture of DIC. Clinically there was bleeding from the previous jugular cannulation site four days after it was removed. By 23rd there was severe oliguria with clinical evidence of fluid overload for which a decision to perform a SLED was taken which necessitated a femoral vein access on the right side. Since then he is requiring daily SLED to remove the excess fluid. He has received several blood products in form packed cells, FFPs, cryoprecipitates including activated factor VII once to correct his coagulopathy.
As on 01.11.09 he is clinically obtunded, icteric, anuric (on SLED daily), worsening liver functions ( S.Bil: 19.3 with direct 15.9mg%, INR 2.94, albumin 5.0), S. Na 147, K: 3.8 , hemodynamically stable without any inotropes, a recent chest x ray shows bilateral diffuse patchy infiltrates. He is presently on BIPAP support (12/5) with a Fi O2 of 0.5. Present antimicrobial cover: meropenem + aztreonam + fluconazole.