Next Best Step in Management
The next best step is to obtain abdominal imaging (ultrasound or CT) to evaluate for biliary pathology, followed by upper endoscopy if imaging is unrevealing, while continuing supportive care and considering discontinuation of Norflox-TZ given the worsening symptoms and hepatic involvement. 1
Immediate Diagnostic Priorities
Imaging to Exclude Structural Pathology
Abdominal ultrasound or CT scan should be performed urgently to evaluate for cholecystitis, choledocholithiasis, or other biliary/pancreatic pathology given the post-prandial pain exacerbation, mild mixed hepatocellular-cholestatic pattern (elevated ALT 78, total bilirubin 1.45, direct bilirubin 0.67), and normal ALP/GGT that argues against extrahepatic obstruction but doesn't exclude intrahepatic or gallbladder disease 1
The post-prandial worsening is a critical clinical clue suggesting biliary or upper GI pathology rather than simple infectious gastroenteritis 1
Consider Upper Endoscopy
If imaging is unrevealing, upper endoscopy should be performed to evaluate for peptic ulcer disease, gastritis, or duodenitis, particularly given the persistent nausea and abdominal pain despite antibiotic therapy 1
The British Society of Gastroenterology guidelines emphasize that functional dyspepsia remains a diagnosis of exclusion after appropriate investigation 1
Medication Management
Reassess Norflox-TZ Therapy
Consider discontinuing Norflox-TZ given that symptoms worsened after eating while on therapy, the negative infectious screen (dengue, typhoid, malaria all negative), and the development of hepatic enzyme elevation 2
Norfloxacin can cause hepatotoxicity with elevated AST/ALT (15.1% and 10.3% respectively in clinical trials) and GI adverse effects including nausea (10%), abdominal pain/cramps (1-3%), and diarrhea (4%) 2
Drug-induced liver injury should be considered given the temporal relationship between antibiotic initiation and worsening symptoms with mild transaminase elevation 3
Symptomatic Management
Initiate proton pump inhibitor (PPI) therapy empirically while awaiting diagnostic workup, as this addresses potential peptic disease and provides symptomatic relief 1
Antiemetic therapy (ondansetron or metoclopramide) should be provided for nausea control 4
Avoid antimotility agents until structural pathology is excluded, as they may worsen outcomes if obstruction or inflammatory bowel disease is present 4
Monitoring and Supportive Care
Fluid and Electrolyte Management
Correct the mild hyponatremia (134 mEq/L) with oral rehydration if tolerated, or IV fluids if oral intake remains poor 4, 5
The hyponatremia is likely secondary to GI losses and reduced oral intake 4
Hemodynamic Monitoring
The tachycardia and hypotension that prompted ER visit require ongoing monitoring, though normal troponin I is reassuring 4
These findings suggest volume depletion rather than primary cardiac pathology 4
Repeat Liver Function Tests
Recheck LFTs in 3-5 days to assess trajectory—rising transaminases would strengthen concern for drug-induced liver injury or evolving hepatobiliary disease 3
The mixed hepatocellular-cholestatic pattern (ALT 78 with elevated bilirubin but normal ALP/GGT) is atypical for simple viral hepatitis and warrants close follow-up 3
Key Clinical Pitfalls to Avoid
Don't Assume Simple Gastroenteritis
The post-prandial exacerbation pattern is NOT typical of infectious gastroenteritis, which usually causes constant or cramping pain unrelated to meals 4, 5
The negative infectious screen (dengue NS1, typhoid IgM/IgG, malaria) makes infectious etiology less likely 4
Don't Continue Empiric Antibiotics Indefinitely
Empiric antibiotic therapy for gastroenteritis has modest benefit and should not be continued beyond 3-5 days without documented bacterial infection, particularly given the risk of C. difficile and drug-induced hepatotoxicity 6
The relative neutrophilia (80.4%) with lymphopenia suggests stress response or early inflammation but does NOT confirm bacterial infection requiring antibiotics 4
Don't Miss Biliary Pathology
Normal ALP and GGT do NOT exclude cholecystitis or choledocholithiasis—these enzymes may be normal early in biliary disease or with cystic duct obstruction 1
The mild direct hyperbilirubinemia (0.67) suggests some degree of cholestasis despite normal canalicular enzymes 3
Alternative Diagnoses to Consider
Functional Dyspepsia
If all structural investigations are negative, functional dyspepsia becomes likely, characterized by post-prandial fullness, early satiety, and epigastric pain 1
However, this remains a diagnosis of exclusion and should not be assumed without appropriate workup 1
Drug-Induced Hepatotoxicity
The hepatocellular pattern (ALT elevation predominant) with mild bilirubin elevation occurring after drug initiation is consistent with drug-induced liver injury 3
Norfloxacin specifically causes hepatic dysfunction including hepatitis in postmarketing surveillance 2