Chap. 53 Liver part.2 disease 1/28Infectious disease Pyogenic liver abscess Recurrent Pyogenic Cholangitis Solid Benign Neoplasms Liver cell adenoma Focal nodular hyperplasia Hemangioma Primary Solid Malignant Neoplasm - HCC contents 2/28Pyogenic Abscess Epidemiology Pyogenic liver abscess is now mostly seen in patients in their 50s to 60s and is more often related to biliary tract disease or is cryptogenic in nature. More recent studies from the 1980s through the 2000s have suggested small but significant increases in the incidence of pyogenic liver abscess as high as 22/100,000 hospital admissions A recent population-based study from North America calculated an annual incidence of 3.6 cases/100,000 population. 12 There is no significant gender, ethnic, or geographic differences in disease frequency; Infectious disease Pyogenic abscess Recurrent Pyogenic Cholangitis Solid Benign Neoplasms Liver cell adenoma Focal nodular hyperplasia Hemangioma Primary Solid Malignant Neoplasm - HCC 3/eoplasm - HCC 6/28Pyogenic Abscess Clinical Features Ultrasound and CT are the mainstays of diagnostic modalities for hepatic abscess. Ultrasound usually demonstrates a round or oval area that is less echogenic than the surrounding liver ( The sensitivity : 80% to 95%) CT demonstrates similar findings to ultrasound, and lesions are of lower attenuation than surrounding hepatic parenchyma. ( sensitivity : 95% to 100% ) Infectious disease Pyogenic abscess Recurrent Pyogenic Cholangitis Solid Benign Neoplasms Liver cell adenoma Focal nodular hyperplasia Hemangioma Primary Solid Malignant Neoplasm - HCC 7/28Pyogenic Abscess Treatment broad-spectrum IV antibiotics should be started immediately to control ongoing bacteremia and its associated complications. Blood samples and specimens of the abscess from aspiration should be sent for aerobic and anaerobic cultures Combinations such as ampicillin, an aminoglycoside, and metronidazole or a third-generation cephalosporin with metronidazole are improve with conservative management If intervention is necessary during the acute phase, it must focus on adequate decompression of the biliary tree through open common bile duct exploration or endoscopic papillotomy with stenting. Infectious disease Pyogenic abscess Recurrent Pyogenic Cholangitis Solid Benign Neoplasms Liver cell adenoma Focal nodular hyperplasia Hemangioma Primary Solid Malignant Neoplasm - HCC 12/28Solid Benign Neoplasms Liver Cell Adenoma Liver cell adenoma (LCA) is a relatively rare benign proliferation of hepatocytes in the context of a normal liver. It is predominantly found in young women (aged 20 to 40 years) and is often associated with steroid hormone use, such as long-term oral contraceptive pill (OCP) use. LCAs are usually singular, but multiple lesions have been reported in 12% to 30% of cases Infectious disease Pyogenic abscess Recurrent Pyogenic Cholangitis Solid Benign Neoplasms Liver cell adenoma Focal nodular hyperplasia Hemangioma Primary Solid Mally shows strong hypervascularity in the arterial phase of CT or MRI with central nonenhancing scar The enhancement fades over time, and the lesion becomes isointense to the liver parenchyma in the portal and delayed phases. On occasion, histologic confirmation is necessary, and resection is recommended for definitive diagnosis Fine-needle aspiration for the diagnosis of FNH has been recommended but is often unrevealing Infectious disease Pyogenic abscess Recurrent Pyogenic Cholangitis Solid Benign Neoplasms Liver cell adenoma Focal nodular hyperplasia Hemangioma Primary Solid Malignant Neoplasm - HCC 18/28Solid Benign Neoplasms Focal Nodular Hyperplasia Most FNH tumors are benign and indolent. Rupture, bleeding, and infarction are exceedingly rare, and malignant degeneration of FNH has never been reported. Asymptomatic patients with typical radiologic features do not require treatment. If diagnostic uncertainty exists, resection may be necessary for histologic confirmation. Infectiouselpful in the diagnosis of HCC Infectious disease Pyogenic abscess Recurrent Pyogenic Cholangitis Solid Benign Neoplasms Liver cell adenoma Focal nodular hyperplasia Hemangioma Primary Solid Malignant Neoplasm HCC 23/28Surgical Resection Orthotopic liver transplantation Radiotherapy Combination transarterial and ablative: external beam radiation Ablative Ethanol injection Acetic acid injection Thermal ablation (cryotherapy, radiofrequency ablation, microwave) Systemic Chemotherapy Hormonal Immunotherapy Transarterial Embolization Chemoembolization Hepatocellular Carcinoma Treatment Infectious disease Pyogenic abscess Recurrent Pyogenic Cholangitis Solid Benign Neoplasms Liver cell adenoma Focal nodular hyperplasia Hemangioma Primary Solid Malignant Neoplasm HCC 24/28Hepatocellular Carcinoma Resection Patients with Child-Pugh class B or C cirrhosis or portal hypertension do not tolerate resection. The volume of the FLR is also an important consideration and is associated with postoperat}
* Anatomy - The liver is a solid gastrointestinal organ whose mass (1.2 to 1.6 kg) - The posterior surface straddles the inferior vena cava (IVC)- The large majority of the right liver and most of the left liver are covered by the thoracic cage
* Urine passage : renal pelvis to urethera tip * Obstruction can occur anywhere -> obstructive uropathy : interfere of drainage of urine -> obstructive nephropathy : obstructive uropathy lead to decline in renal function -> Hydronephrosis : dilatation of urinary collecting system
Acute kidney injuryAKI Abrupt decrease in GFR - Accumulation of Nitrogeneous wast product - ability to maintain fluid E’ homeostasisPRERENAL Cause of AKI Reduction of renal perfusion w/o cellular injury Reversible if Underlying cause is corrected Secondary to decreased blood vol. (such as, vomiting, dehydration, hemorrhage) or reduction in the effective arterial blood vol. (such as, CHF, LC) or medication (such as, NSAIDs or RAAS inhibitors)PRERENAL Cause of AKI 40% of hospital-acquired case. Prerenal should be excluded in all case of AKI Therapy : - Reversing Underlying cause - Vol. replacement - discontinuation of offending agentsPOSTRENAL Cause of AKI Obstruction of urine flow Relatively uncommon cause of AKI 3~25% of all case of AKI Divided into renal or extra-renal - Extra renal : prostatic disease, pelvic malignancy - Intra renal : crystal deposition (ethylene glycol ingestion, uric acid nephropathy in tumor lysis syndrome, Cast formation, light chain disease)POSTRENAL Cause of AKI Evaluated with - renal USG - post voiding residual urine in bladder ( 50mL)INTRARENAL Cause of AKI Classified with anatomic location of injury - glomerulus, vasculature, interstitium , tubule Glomerulitis or vasculitis - active urine sediment with red cells and red cell casts Acute interstitial nephritis - pyuria, white cell casts, occastionally hematuriaINTRARENAL Cause of AKI Most case of AKI from interstitial nephritis are - drug related, commonly d/t antibiotics or NSAIDs Recovery - removal of offending agent - short cause of steroids , such as 60-80mg of prednisone for 10 daysINTRARENAL Cause of AKI m/c cause of intrinsic renal failure - acute tubular necrosis (ATN) - cause of ATN : @ prolonged pre-renal azotemia @ hypotension @ sepsis, toxic @ secondary to antibiotics @ chemotherapic agent, contrast mediaINTRARENAL Cause of AKI Sepsis induced AKI m/c cause of AKI in critically ill-patients Renal macrocirculation Resulting from Global renal ischemia, celluar damage, ATN Contrast induced AKI Contrast media cause vasoconstriction medullary ischemia, direct tubular toxicity High risk : pre- excisting renal disease, DM, volume depletedTREATMENT Prevention of contrast-mediated nephrophathy Hydration with isotonic sodium chloride Low or iso-osmolal contrast agent Alkalinization , sodium bicarbonate N- acetylcysteine 1200mg twice daily for 48hrs…..conflicting evidence Statin…..pendingTREATMENT Dopamine - increase GFR, sodium water excretion - increase diuresis Diuresis - convert oliguric into non- oliguric AKI - Loop diuretics , Furosemide - increasing flow rate to flush out tubular cast - high dose - related to ototocixityTREATMENT Atrial natriuretic peptide Increase GFR Glomerular filtration pr. By dilating the afferent arteriole constricting the efferent arterioleHEMODYNAMIC MANAGEMENT Fluid management Crystalloid @ m/c form of vol. replacement @ effect of plasma vol. is limited @ 1 Liter - plasma 200 vol. - intravascular half life is 20 - 30 minHEMODYNAMIC MANAGEMENT Fluid management Colloidal substances @ albumin, dextran, HESs @ macromolecule - better retain intravascular space @ expensive, no difference of renal outcome…..RENAL REPLACEMENT THERAPY Indication The optimal timing of initiation of dialysis is not defined Life threatening conditions @ diuretic- resistant vol. overload @ severe hyperkalemia @ acidosis, azotemia @ overt symptom sign of uremia (e.g. encephalopathy, pericarditis){nameOfApplication=Show}
Management of postoperative liver transplant patientCoagulopathy Thrombocytopenia ESLD patients are hypocoagulable secondary to the loss of synthetic function of the liver operative difficulties that can be encountered that result in massive blood loss to further derange homeostasis. replace the blood that is being lost as a result of the operation and to correct coagulation fresh frozen plasma (FFP) and cryoprecipitate to maintain normal fibrinogen levels.Coagulopathy Thrombocytopenia thrombocytopenia is common in OLT greatly reduced platelet number secondary to multiple factors including ; * sequestration by the spleen resulting in hypersplenism * increased consumption * bone marrow suppression * reduced thrombopoietin levels .Immunosuppression corticosteroids azathioprine mycophenolate mofetil sirolimus cyclosporine tacrolimusImmunosuppression Corticosteroids suppressing antibody and complement binding resulting in a reduced synthesis of immunomodulatory cytokines. Inhibit secretion of IL-1 by macrophages required for antigen presentation and initiation of an acute allograft rejection.Immunosuppression MMF metabolized by the liver into MPA and inhibits cellular proliferation. renders lymphocytes unable to proliferate. antiviral effects with activity against HCV reduce the recurrence of HCV in patients transplanted for this disease.Immunosuppression Cyclosporine and tacrolimus calcineurin inhibitors suppress the immune system by preventing IL-2 production by T cells Tacrolimus also inhibits the formation of IL-2 but is 100 times more potent than cyclosporineop day POD#1 #2 #3 #4 #5 #6 #7 #8 용량 Immunosuppressant Tacrolimus(FK506) *투여 2 시간 전 , 투여후 1 시간 금식 10A, 10P as sheet POD#1 저녁 0.5 mg 으로 시작 renal impairment 시 상의 Steroid Sol 500mg before portal perfusion and after hepatic artery anastomosis Sol 50mg IVP q6hr Sol 40mg IVP q6hr Sol 30mg IVP q6hr Sol 20mg IVP q6hr Sol 20mg IVP q12hr Sol 20mg IVP qd Pd 20mg po qd Pd 20mg po qd ~1 개월 :20mg, ~2 개월 :15mg, ~3 개월 :10mg, ~ 개월 :5mg, ~6 개월 :2.5mg, 6 개월후 stop MMF (myrect) * teratogenic 으로 L-tube 로 granule 형태로 사용 금지 500mg bid 시작하여 증량은 상의 Simulect 20mg on call 20mg ABOi 아니면 모두 투여 , ABOi 는 rituximab(+) 면 투여안함 . mix with D5W or NS 50cc, 20-30 분간 infusionOperative Complications portal vein thrombosis, hepatic artery thrombosis, and bile leaks UCLA ; early primary graft failure, hepatic artery thrombosis, and portal vein thrombosis ; from 0.7% to 6% ; 30% of OLT patients had complications that require reoperation. ; m/c cause of reoperation is bleedingEarly Infectious Complications most common cause of in-hospital death of liver transplant patients is infection increase the risk of bacterial infections ; ischemia-reperfusion injury of the graftEarly Infectious Complications most common cause of in-hospital death of liver transplant patients is infection increase the risk of bacterial infections ; ischemia-reperfusion injury of the graft ; large-volume blood transfusions ; causes of cholangitis including hepatic artery thrombosis and biliary stricturesEarly Infectious Complications trimethoprim-sulfa prophylactically for life to protect against Pneumocystis jirovecii . The liver transplant patient is susceptible to recurrence of the inciting hepatitis virus that resulted in liver failure or HCC They are also at risk of other viral infections that would be uncommon in the general ICU population such as CMV and EBV that may occur as a result of induction immunosuppression therapy.Ampicillin/Sulbactam ( Ambactam ) 3g IV q6hr(AST) 3g q 6h for 24hr(Max.48hr) !!non allergic 인 경우 before and after invasive procedures (for 2-3days) e.g. cholangiography, PTBD, ERBD, Bx 등 *allergy 인경우 1. mild~moderate : cefotaxime 1g 1 8h + vancomycin (10mg/kg)bid(for 24hr), then D/C 2. severe : vnacomycin 10mg/kg gentamycin 2mg/kg q 12h(for 24hr),then D/C Bactrim (Septrin) Diet 진행 후 매주 매일 480g qd Nystatin gargle or swallow 4cc (50 만 iu ) qid{nameOfApplication=Show}
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