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