Acute viral hepatitis

Bhuvana¹, Suma², S.J. Sonya Mercy Anbu³, Ruby Ravichandran⁴

¹ER staff nurse, Maa Kauvery, Trichy, Tamil Nadu

²ER Senior staff nurse, Maa Kauvery, Trichy, Tamil Nadu

³Nurse Educator, Maa Kauvery, Trichy, Tamil Nadu

⁴Senior DNS, Maa Kauvery, Trichy, Tamil Nadu

Introduction

Acute viral Hepatitis-A is a contagious liver infection caused by the hepatitis A virus (HAV), primarily transmitted through the fecal-oral route by contaminated food or water or close personal contact. It is commonly seen in areas with poor sanitation and limited access to clean drinking water. The disease mainly affects children and young adults and is usually self-limiting, but it can lead to significant morbidity, especially in adults and those with existing liver disease. Earlyrecognition, proper hygienic measures, and vaccination play a crucial role in preventing the spread of hepatitis A and reducing its public health burden.

Case presentation

A 11-Year-old male childwith H/O intermittent giddiness since last 4yrs of age, on sodium valporate and propranolol, now brought with thec/o fever, vomiting, abdomen pain and high colored urine for 4 days followed by altered sensorium for 1 day. On presenting to the ER child was drowsy, occasionally responding to commands, with a GCS of 14/15. Pupils were equal and reactive to light, and bilateral deep tendon reflexes (DTR) were brisk.

Clinical Findings

Child lethargic and afebrile
Icterus (+)
Pulse volume: good
GRBS: 100mg/dL

Vital signs

Temp: 98.4°F, HR: 62b/mt, RR: 18 b/mt, BP: 100/70mmHg
SpO2: 96 % in RA

Systemic examination

CNS: Lethargic with altered sensorium.
GCS: E4V4M6
Pupils: BL 2mm RTL
Power&GT: 3/5 in all limbs
Tone: Normal in all 4 limbs
DTR: Brisk in all 4 limbs
Plantar: B/L Flexor
Meningeal signs: Absent
No nystagmus
P/A: Soft
Diffuse tenderness present
No guarding/rigidity
No organomegaly
CVS: S1 S2(+) heard, No murmur
RS: Bilateral air entry(+)
No added sounds

Anthropometry	Measurement	Centile
Weight	30kg	25th-50th
Height	156cm	90th-97th
BMI	12.3	less than 3rd
Inference	Underweight

History

Intermittent Giddiness since 4yrs of age, consulted a neurologist and was evaluated for the same, CT Brain and MRI Brain done but reports not available.
He has been on sodium valporate for last 5yrs and propranolol since 2 yrs. EEG done on 29/6/25 was normal.

Antenatal & Birth history

Term / Birth weight: 2.3 kg / LSCS/ Cried immediately after Birth/ No H/O NICU stay

Developmental history

Attained developmental milestones appropriate for age.
Studying 7th std.
Scholastic performance is good.

Immunization history

Immunized up to age
Last vaccination at 10yrs
H/O temper tantrums present.
No other significant behavioral disturbance

Clinical signs and symptoms

Drowsy
Lethargic
Diffused Icterus
Tenderness of abdomen and bilateral brisk
DTR

Lab investigations

Parameter	Results
Ammonia	153 µmol/L
Alanine aminotransferase (ALT/SGPT)	4039 U/L
Aspartate Aminotransferase(AST/SGOT)	3059 U/L
Sodium	138 mmol/L
Urea Serum	14 mg/dL
Gamma - Glutamyl Transferase (GGT)	104 U/L
Alkaline Phosphatase	409 U/L
Hemoglobin	14.2 g/dl
HAV-AB-IgM	Positive (2.54)
Test (APTT)	41.6 Seconds
INR	2.84
T. Bilirubin	6.20
Direct Bilirubin	4.86
Indirect Bilirubin	1.34
T. Protein	6.66
Albumin	3.42
Globulin	3.2

USG Abdomen: Moderate gallbladder edema and minimal free fluid.

Diagnosis

Acute viral Hepatitis-A

Acute liver failure
Hepatic encephalopathy (Grade 3)

Opinion

Pediatric Neurology
Pediatric Gastroenterologist
Pediatric ophthalmologist

Course in the hospital

11years old male childwith the H/Ointermittent giddiness since4 years of age, on sodium valproate and propranolol, now brought with c/o fever, Vomiting, abdomen pain and high colored urine for 4 days followed by altered sensoriumfor last 1day.
On presenting to ER, Child was lethargic and drowsy, occasionally responds to commands, icterus, diffuse tenderness of abdomen and B/L brisk DTRs. Possibility of acute liver failure with hepatic encephalopathy (? Secondary to AcuteViral Hepatitis/ Valproate Induced Hepatotoxicity/ Wilsons disease) wasconsidered.
He was given 3% Nacl IV bolus, Inj vitamin K, IVfluids, NAC infusion, Ursodeoxycholic Acid, Syp. Lactulose, T Rifaximin, Inj. Pantop and Inj. Emeset. Inj. Sodium Valproate and Inj.Propranolol were withheld.
Child was shifted to PICU for neurological monitoring. Blood investigations here showed leukocytosis and normal electrolytes, Hyperbilirubinemia (Direct > Indirect), worsening transaminitis and elevated GGT, mild hypoalbuminemia and hyper ammonemia with deranged coagulation profile. HAV- IgM Ab was positive. Sodium benzoate and L-arginine was added in view of hyperammonemia, and Vitamin K was continued for 3 days. Child sensoriumworsened over next 12 hr.
Child became irritable with inappropriate speech and agitation present. Response to commands were poor. Repeat Ammonia was decreasing in trend, but Sr. Electrolytes showed moderate hyponatremia. Urine output was adequate. No evidence of polyuria. Possibility of Acute liver failure induced Syndrome of Inappropriate Antidiuretic Hormone Secretion was kept. Hence 3% sodium chloride bolus was repeated and started on infusion and one dose of oral tolvaptan was given. Serum sodium improved in next 8 hr and child sensorium also improved, started to interact well. 3% sodium chloride infusion was continued for next 24 hours.
Pediatric gastroenterologist opinion was obtained and advised work up for Wilson disease and Autoimmune hepatitis, serum ceruloplasmin, urine 24hr copper level and serum total IgG were sent and reports are awaited. There were no bleeding manifestations. Repeat LFT showed improving trend of hyperbilirubinemia and transaminitis. Coagulation profile normalized. Pediatric neurologist opinion was obtained for recurrent episodes of giddiness. Child was alert and active, interacting well with parents, tolerated oral feeds and hemodynamically stable. Hence wasshifted to HDU for further care.
Child was hemodynamically monitored in HDU. No further worsening ofsymptoms noted. Paediatric ophthalmologist opinion was obtained and there wasno evidence of KF ring. Serum ceruloplasmin and IgG levels were normal. 24hr urinary copper levels mildly elevated. Child eventually shifted to ward.
Repeat LFT was in improving trend. During ward stay, child remained alert, afebrile, hemodynamically stable andtolerated oral feeds well. Hence child is being discharged with following advice.

Treatment given

1	IV Fluids
2	Inj. Pantocid
3	Inj. Emeset
4	Tab. Rifagut
5	Syp. Duphalac
6	Inj. Vitamin K
7	Sodium benzoate
8	Tab. Udimarin
9	Inj. Cefotaxime
10	Inj. Mannitol
11	Inj. Sodium chloride
12	L - Arginine sachet
13	Inj. N-Acetylcysteine
14	Syp. Potassium Chloride

Lab investigations on discharge

Alanine Aminotransferase (ALT/SGPT)	658 U/L
Gamma - Glutamyl Transferase (GGT)	93 U/L
Alkaline Phosphatase	241 U/L
Haemoglobin	14.2 g/dL
Total Protein	6.82
Albumin serum	3.13
Globulin	3.7

Advice on discharge

Diet advised for adequate calories with protein and carbohydrates and Low fat

S. No	Drug Name	Generic name /Strength	Frequency	Route	Duration
1	Tab. Udimarin	Ursodeoxycholic acid (300mg)	BD	Oral (AF)	1 week
2	Syp. Duphalac	Lactulose	BD	Oral (AF)	1 week

At the time of discharge child was afebrile, hydrated adequately and with good urine output. Child was in a stable condition.Advised the parents to report immediately if baby has excessive dullness, continuous cough, cold, high-grade fever, fast breathing, difficulty in breathing, excessive diarrhea, vomiting, reduced urine output.

Discussion

Hepatitis – A is a contagious liver / infection caused by the hepatitis A viral (HAV) primarily transmitted through the fecal – oral route via contaminated food or water, or close contact with an infected person but is does not cause chronic liver disease like some other hepatitis virus.

Definition

Hepatitis A is defined as an acute viral infectionin Liver caused by the hepatitis A virus (HAV) which leads to inflammation and temporary liver dysfunction.

Nursing Management

Entire team powerfully managed this patient in critical unit, monitored the vital signs closely, medications administered regularly, strictly maintained intake &output chart according and fluid management given to prevent dehydration

Conclusion

This case highlights the potential severity of hepatitis –A infection, which although usually self- limiting, can occasionally progress to fulminant hepatitis with hepatic encephalopathy. Early recognition of symptoms, timely diagnosis, and prompt supportive management are crucial in preventing irreversible liver damage and improving patient outcomes. public health measures such as vaccination, proper sanitation, and awareness about hygiene practices remain key strategies in preventing hepatitis-A infection and its complications. Multidisciplinary ring and multidisciplinary care are essential for optimal recovery and to reduce the risk of long- term hepatic sequelae.

Acute viral hepatitis

Acute viral hepatitis

Bhuvana1, Suma2, S.J. Sonya Mercy Anbu3, Ruby Ravichandran4

Nightingale Journals

Bhuvana¹, Suma², S.J. Sonya Mercy Anbu³, Ruby Ravichandran⁴