Académique Documents
Professionnel Documents
Culture Documents
SYNOPSIS
By
RTMC no.MED-2015-150-10797
SUPERVISOR
Early studies revealed a 40% prevalence of hypokalemia in cirrhotic patients, irrespective of the
disease stage.2 Patients may be hypokalemic owing to a variety of reasons including low dietary
intake of potassium-rich foods or intracellular shifting of extracellular potassium in the setting of
alkalemia. Alternatively, patients may become hypokalemic, commonly in the setting of potassium
loss with diuretic use, hyperaldosteronism, magnesium depletion (as in the case of chronic
alcoholic liver disease), or vomiting.3 When considering the classic characteristics of cirrhosis
such as vomiting, malnourishment, hypomagnesemia, diarrhea, and diuretic use, the perfect
scenario is set for the activation of renal and extrarenal mechanisms of potassium wasting.4
Operational definition:
A patient will be labelled as having chronic liver disease if patient is child class A or B had
any of the following complications: Ascites, hepatic encephalopathy, hepatorenal
syndrome, esophageal varices along with Abdominal Ultrasound indicating liver cirrhosis
or raised serum bilirubin (more than 2.5 times the upper limit of normal) and prolonged
prothrombin time (prolonged by more than 3 s)
Complications
Ascites: Patient will be labelled as having ascites if he is positive for shifting dullness or fluid
thrill along with a confirmatory ultrasonography finding.
Variceal Bleed: history of hematemesis along with confirmatory endoscopic evidence for
esophageal or gastric varices.
Hypokalemia
Study setting: Department of medicine, Allama Iqbal memorial teaching hospital (AIMTH), Sialkot
Sample size: To determine the sample size, we assumed a confidence level of 95%, with a
precision of 10%. Using a mean prevalence 40% hypokalemia6 in our group of cirrhotic
patients on the basis of previous data; the sample size comes out to be 120
Sample selection
Inclusion criteria
1. Both males and females
2. Patients aged 25-70 years of age
3. Diagnosis of cirrhosis confirmed by clinical, biochemical, and ultrasonographic findings
4. Patients having Hepatitis B or C
Exclusion criteria
1. Patients with hepatocellular carcinoma
2. Patients using diuretics within a 1-month period before admission
3. Patients with cholestatic liver diseases, namely primary biliary cirrhosis (PBC) and primary
sclerosing cholangitis (PSC)
Data Collection
After approval of synopsis, 250 consecutive cases of CLD presenting with complications in the
medicine ward will be offered to enroll in the study. The purpose of the study will be explained in
detail to all the patients and an informed consent will be taken in each case. Ultrasonography, LFTs
and other baseline investigations will be done to evaluate for hepatic decompensation. Serum
electrolytes (for hypokalemia) will be done in turn for every patient admitted. The relevant data
will be collected in a structured proforma containing background information like age, sex, serum
potassium, child class and frequency of different complications observed etc. The patients will be
followed on day to day basis to make sure all the complications that develop during their stay are
documented.
Data Analysis
Data will be analyzed using SPSS version 21.Mean with standard deviation will be calculated
for quantitative variables like Age and Serum potassium levels. In case of qualitative variables
like gender, presence of hypokalemia and different complications seen during liver cirrhosis;
frequency and percentages will be calculated. Data will be depicted in tables and graphs.
Regression analysis would be done and spearman pearson correlation coefficient will be
calculated to check for correlation between hypokalemia and frequency of various
complications seen in CLD.
References
1. Jimnez JV, Carrillo-Prez DL, Rosado-Canto R, Garca-Jurez I, Torre A, Kershenobich
D, Carrillo-Maravilla E. Electrolyte and AcidBase Disturbances in End-Stage Liver
Disease: A Physiopathological Approach. Digestive Diseases and Sciences. 2017 May
13:1-7.
2. Casey TH, Summerskill WH, Bickford RG, Rosevear JW. Body and serum potassium in
liver disease. II. Relationships to arterial ammonia, blood pH, and hepatic
coma.Gastroenterology.1965;48:208215.
3. Adewale A, Ifudu O. Kidney injury, fluid, electrolyte and acid-base abnormalities in
alcoholics. Nigerian medical journal: journal of the Nigeria Medical Association. 2014
Mar;55(2):93.
4. Unwin RJ, Luft FC, Shirley DG. Pathophysiology and management of hypokalemia: a
clinical perspective. Nat Rev Nephrol. 2011;7:7584.
5. Helmy A, Hussein M, Saleh SA, Mostafa AS, Abdella HM, Elaidy D. Serum Electrolytes:
a simple predictive test for grading severity of overt hepatic encephalopathy. International
Journal. 2015;3(7):1342-51.
6. Hayat A, Shaikh N, and Memon F. Identification of Precipitating Factors in Hepatic
Encephalopathy Patients at Liaquat University Hospital Jamshoro, World Applied
Sciences Journal 2010; 8 : 661-6
7. Stephan F, Paillard F: Terlipressin-exacerbated hypokalaemia. Lancet 351:1249-1250,
1998
PROFORMA
Hypokalemia: Yes / No
LFTs
ALT: AST: ALP: Serum Bilirubin:
Complications YES / NO
Ascites
Hepatic encephalopathy
Varix bleeding
Hepatorenal syndrome
Hepatic Hydrothorax
Esophageal varix
Intractable ascites
CONSENT FORM
Medicine Resident), Allama Iqbal memorial teaching hospital, Sialkot for my participation in the
study Frequency of Hypokalemia and its influence on chronic liver disease related
Designation: Professor
Date of submission:
Trainee's Signature
Designation: Professor