Download - Case Study
A CASE OF NONALCOHOLIC STEATOHEPATITISPresentation By: Jennifer Helvey, Dietetic Intern
University of Tennessee, Knoxville
Overview
Patient Profile Background Research Medical History Nutritional Status Treatment Prognosis Team Approach Discharge Recommendations
I. Patient Profile
Age, race, gender: 59 yowf Marital status: married Occupation: homemaker Economic status: disabled, receiving disability Problems affecting health: recurrent UTIs,
cirrhosis secondary to NASH (non-alcoholic steatohepatitis), hypertension, morbid obesity, COPD, anxiety, portal hypertension with variceal bleeding, chronic hepatic encephalopathy, chronic thrombocytopenia, coagulopathy, chronic pain syndrome, intracranial bleed, and seizures
II. Background Research
Pt admitted with abdominal pain and nausea/vomitting
Dx: Cirrhosis secondary to nonalcoholic steatohepatitis (NASH) Fat with hepatocyte changes, inflammation,
and possibly fibrosis1
Etiology of NASH
Not completely understood Several conditions and medication use
have been linked to the development of NASH
“2 hit hypothesis” most accepted etiology 1st hit: hepatic fat accumulation 2nd hit: oxidative injury to hepatocytes
responsible for the transition from bland fatty infiltration to steatohepatitis
Associated Conditions of NASH1,2
Clinical conditions Metabolic syndrome (obesity, type 2 diabetes
mellitus, hyperlipidemia, hypertension) Peroxisomal diseases Polycystic ovarian disease Celiac disease Rare error of metabolism
(abetalipoproteinemia, Wilson disease) Weber-Christian syndrome (hepatic steatosis
feature of this disease)
Associated Conditions of NASH Clinical Conditions Continued
Extensive bowel resection Gastroplasty Biliopancreatic diversion Mitochondrialopathies Rapid weight loss Acute starvation Hypothyroidism Refeeding syndrome Bacterial Overgrowth
Causes of NASH1
Medications Amiodarone Tamoxifen Perhexiline maleate Glucocorticoids Synthetic estrogens Calcium-channel blockers Nucleoside analogues methotrexate
Associated Conditions1
Most common risk factor: Metabolic syndrome 3 or more of the following criteria: 1)
increased waist circumference, 2) hypertriglyceridemia, 3) hypertension 4) high fasting glucose levels, and 5) a low serum level of high density lipoprotein (HDL)
Obesity and metabolic syndrome are strongly linked
NASH is now recognized to be the hepatic manifestation of metabolic syndrome
Nutritional Implications of NASH Exessive oral intake of fats and
carbohydrates Leads to obesity, poorly controlled
diabetes, and dyslipidemia, all of which results in impaired lipid metabolism
Free fatty acids delivered exceeds amount needed for essential functions and results in hepatic fat accumulation Protein-calorie malnutrition, jejunoileal bypass,
and PN Hyperinsulinemia Insulin resistance
III. Medical History
PMH: Cirrhosis secondary to NASH, HTN, dyslipidemia, morbid obsesity, COPD, portal HTN secondary to cirrhosis and subsequent variceal bleeding
Symptoms: left quadrant abdominal pain x 3-5 days, nausea, vomitting, UTI
Hospitalizations
Portal hypertensive bleed with large gastric varices TIPS procedure December 2011
Intracerebral hemorrhage as a result of coagulopathy Hospitalized at Fort Sanders Medical Center from March
27-April 3 Was readmitted because of seizures and cerebral adema
Subsequently admitted to Patricia Neal Rehabiliatation Center
Admitted to Scott County Hospital May 20 for abdominal pain and sent home from there
Admitted to Methodist Medical Center May 25 with abdominal pain
Laboratory Data
Admit Labs: Na-139 K+-3.7 Cl-102 BG-114 H BUN-13 Cr-0.78 AST-50
Laboratory Data
Admit Labs Continued Alk Phos-328 Total bili-1.6 Ca-8.7 Total protein-6.1 Alb-3.2 CO2-30 ALT-23
Laboratory Data
Urinanalysis Small leukocytes Trace bacteria Lipase-27
CT of the abdomen Small plug of fat through the small ventral
hernia left of midline
IV. Nutritional Status
Ht: 64” Wt: 204#/93 kg IBW: 55 kg %IBW: 169 BMI: 35 Morbid obesity Abdominal pain 3-5 days prior to MMC admit Nausea and vomiting prior to admit Constipation, unable to have a bowel
movement Not eating well prior to admit and during stay No appetite prior to admit and during stay Appetite and PO increased enough to discharge
Nutritional Assessment
Nutrition Dx Intake PES: Inadequate energy intake (NI-
1.4) related to poor appetite as evidence by PO <75%.
Clinical PES: Altered nutrition-related laboratory values (NC-2.2) (AST, ALT, Alk Phos, total bili, Cr, BG, K+, and Ca) related to disease process as evidence by values outside of normal ranges.
Nutrition Assessment
I&O Summary Admit to 5/28: Minimal PO 5/28-5/31: 0-25% meals plus 1 Ensure 5/31-discharge: 0-25% breakfast, 100%
lunch and dinner plus 1 Ensure Labs
As PO increases, labs start to stabilize Discharge labs
Diet Prescription
Admit 5/25: Clear liquid 5/27-5/29: 2 g Na plus Enlive
supplement 5/29-discharge (6/1): 2 g Na plus Ensure
Plus and Promod supplements
V. Treatment
Medications
TIPS Procedure
VI. Prognosis
VII. Team Approach
Discharge Recommendations