An 18-year-old male presented with one week of high fever followed by three days of jaundice, vomiting, and abdominal pain, and six hours of unconsciousness. Physical examination found jaundice and hepatomegaly. Laboratory results showed elevated liver enzymes and hepatitis C positivity. The patient was diagnosed with acute fulminant viral hepatitis based on laboratory findings and treated supportively.

1. CASE PRESENTATION
Dr.Usman Ali,
PGR West Medical Ward,
Mayo Hospital, Lahore.

2. Patient’s Bio data
Name:Shahbaz s/o Abdul Majeed
Age: 18 Years
Sex: Male
Occupation: works in a factory which makes lead based batteries
Address: SHAMKE,KALA SHAH KAKU,SHEIKHUPURA.
D.O.A: 10/10/14
M.O.D: Emergency Department
Ethnicity: Punjabi
Language: Punjabi, Urdu
Religion: Islam

3. Presenting complaints
Fever-7days
Jaundice-3days
vomiting+pain abdomen-3days
ASOC-6hrs
History of presenting illness:
My patient who is neither hypertensive nor diabetic was in usoh
7 days ago when he started having fever which was high
grade(102f-103f) not associated with rigors or chills and
continous (no diurnal variation) ,relieved upon taking
medication.

4. He went to a local quack who gave him some
injections(unknown to attendants) and after that he felt better-fever
reduced.The following day he started having yellowing of
eyes and dark colored urine.this was of sudden onset and also
accompanied by abdominal pain which was severe and
generalized.vomiting also started the same day several
episodes containing food particles but no blood.he remained in
that condition for 2 days and took medication prescribed by Dr
at mayo ER until this morning when he became uncosious.asoc
was of gradual onset not preceded by headache or any focal
neurological deficit.
There is no history of diarrhoea/constipation,sore throat
/cough ,burning micturition.no h/o fits,sob ,bleeding or any
other complaint

5. Past History: •
Suffered from viral encephlitis 2 months back for
which he was treated at NMW and recovered
completely .No H/O surgery, allergies,psychiatric
illness,TB,Asthma or any trauma
Drug History:.
Rx for Encephlitis at NMW(Aclova,ctrox,vanco)
Discharged on PPI,Surbex-z,gravinate
Family History:
No h/o jaundice,viral hepatitis,TB or any serious
infection.

6. Personal History :
no h/o alcohol,smoking or any other drug of
abuse.
Socioeconomic History :
He belongs to poor class . Lives in a joint family of
12 persons in a 10 Marla house .works at factory
making lead based batteries.

7. Systemic Review
Skin: No H/O Rash, redness or itching or any wound yellow tinge+
Eyes: No H/O Eye pain redness, dryness or recent changes in vision.
Ears: No H/O hearing loss, discharge, dizziness or ringing in ear.
Nose: No recent H/O runny nose, stuffy nose or nose bleeds.
Throat: no h/o sore throat,cough,discharge.

8. Neck: No H/O soreness, stiffness , enlarged nodes or lumps on
neck.
Heart: No known H/O of heart problems, hypertension, high
cholesterol, chest pain, palpitations, SOB, orthopnea, PND or
lower extremity edema.
LUNGS: No H/O lung disease, asthma, TB or TB contact,
pneumonia. NO recent H/O cough, sputum, wheezing, SOB
GIT: vomiting+,abd pain+,NO diarrhoea/constipation ,
hematemesis or blood in stool/malena.

9. Urinary: No H/O change in frequency, burning or painful
urination and other lower urinary tract symptoms.
Urine color became dark with onset of jaundice
Genital: Sexually contact -ve. No H/O penile sores, discharge,
testicular pain or enlargement.
Musculoskeletal: No H/O muscle or joint pain, cramps or
stiffness
Neurologic: H/O seizures 2 months back, asoc +,no numbness,
tingling, shooting pain or tremors

10. Endocrine: No H/O diabetes, thyroid problems,
increased thirst, urination, heat or cold intolerance.
Psychiatric: no h/o any psychiatric disesase

11. Summary
An 18 yr old male presented with high grade fever for 7
days followed by sudden onset jaundice,vomiting
,abd pain for 3 days and asoc for 6 hrs.
2 months back had viral encephlitis which resolved
after 2 wk treatment at NMW,MHL.

12. Differential Diagnosis:
Drug/Toxin induced hepatic failure
Acute viral hepatitis
LEPTOSPIROSIS
LYMPHOPROLIFERATIVE DISORDER
HIV
Cerebral Malaria
Hemolysis leading to pre hepatic jaundice
Autoimmune hepatitis
Sepsis leading to organ
failure (liver

13. PHYSICAL EXAMINATION

14. General Survey:
The patient is a normal build, young male who appears his
stated age of 18 and is very irritable. He is drowsy and poorly
oriented to person,place and time. Patient is lying down but
can ambulate with some difficulty . He appears not so well
groomed,dirty clothes and has difficulty communicating with
other people but now better responding well
HR: 90/mint,
BP: 120/80,
RR:17/mit,
Temp: 99 F
Height: 5‘6“,
wt: 51 kg

15. SKIN:
Pallor +ve
Jaundice +ve
Cyanosis –ve
Palmar erythema -ve
slightly warm, humid, normal turgor, . No apparent Skin
Lesion in the exposed area from waist upwards and feet.
NAILS:
Clubbing –ve
Capillary refill 3 seconds
No Nails deformity or pathology in both hands and
feet.

16. Head - normocephalic, no masses /lesions, malar flushing .
Eyes - visual fields intact, PERRLA , conjunctival palor, sclera
icteric, no ptosis
Ears – Hearing appears Normal. No external lesion noted.
Nose - nares patent, no deformity, septal deviation or
perforation.

17. Throat – Pharanx normal, palate rises symmetrically, gag
present.
MOUTH – poor oral hygeine,tongue having yellow
tinge.no other lesion apparent
Neck & Axilla – no LN enlargement,
or thyromegaly/focal lump,
carotid pulses 2+ , no bruits, neck supple , trachea
midline.

18. Back, Thorax & Lungs – N abdomino-thoracic breathing
Chest expansion symmetric, Clear to A&P, Normal
vesicular breathing, eupnoea, no added sounds
Cardiovascular – JVP at 450 not raised,
lInspection: normal,no scars,marks
Palpation: no lifts , heaves or thrill.
.apex beat palpable in 5th ICS, MCL.
Auscultation:
S1- heard best at apex, nl intensity
S2- heard best at base, nl splitting, A2 > P2
no murmurs/S3/S4/friction rub

19. ABDOMEN
Observation: Normal boat shaped abdomen, umbilicus inverted
and situated centrally, no stria, scar marks.
Auscultation: bowel sounds 4-5 cycles/min, no bruits
Palpation: Superficial- tenderness in general,voluntary
guarding +ve, no masses.
Deep- Tenderness more in rt hypochondrium, rebound
tenderness negative, Liver Palpation- liver edge not palpable
Percussion - Size-12 cm in R midclavicular line
Spleen not palpable, B/L Kidneys not palpable
Femoral Pulses: bil equal, no bruit

20. musculoskeletal - gait normal; joints and muscles
symmetric, no
swelling, masses, deformity or tenderness to palpation;
no heat or swelling of joints; muscle
strength 5/5- able to flex against resistance & w/o
tenderness.

21. Nervous – impaired consciousness,Irritable, not very
cooperative previously but now better, sensory -
normal, motor - no atrophy, weakness, tremors or
clonus; tone normal .
DTR's - all + n; Babinski; toes downgoing. gaze
normal;hmf cant be assesed
Cranial Nerves:
All cranial nerves are Intact

23. Differential Diagnosis:
•
Acute viral hepatitis •
Sepsis causing organ failure •
Hemolysis d/t disseminated infection/drug/toxin •
Autoimmune hepatitis •

24. LABORATORY FINDINGS

25. CBC:
wbc 6.3*103
Hb 10.1 mg/dl
HCT 33 %
MCV 84 fL
MCH 26 pg
PLT 157 *103/ ul
Lymp 21 %
Neut 75 %

26. LFT’s:
Ast: 570/619/332
ALT: 664/886/256
TBil: 7.9/13.7 /8.1/
DBIL:1.7
T.P: 6.5
Alb: 3.7
HCV+
RFT’S:
urea: 43
Creat: 1.2
S/E :
Na+ : 133
K+ : 3.9

27. Pt/aptt:normal
HAV BORDERLINE/HEV: NON REACTIVE
CPK:N
LDH :slightly raised-617
U/E : unremarkable
Cxray: Normal
ABG: N
Ultrasound Abdomen : Normal

28. Further Evaluation:
REPEAT HAV SEROLOGY
BLOOD CULTURES
PERIPHERAL SMEAR
LIVER BIOPSY

29. Final Diagnosis:ACUTE FULMINANT VIRAL
HEPATITIS

30. Treatment Given in the ward:
INJ RISEK 40MG iv od
inj flagyl 500mg iv tds
inj 10% d/w+2 amp hepamerz bd
inj gravinate iv tds
mucolator sachet 40 stat then 20sachet6 hrly till
upto 17 doses

31. Discussion:

32. Introduction:
Acute liver failure is an uncommon but serious condition.
The presentation is with progressive deterioration
in liver function and mental changes progressing from
confusion to coma. The syndrome was originally defined
further as occurring within 8 weeks of onset of the
precipitating illness, in the absence of evidence of preexisting
liver disease. This distinguishes it from instances
in which hepatic encephalopathy represents a deterioration
in chronic liver disease

33. ACUTE FULMINANT HEPATIC FAILURE
Massive hepatic necrosis with impaired consciousness occurring within
8 weeks
of the onset of illness.
Causes Infections [viral, including HAV, HBV, HCV (rarely), HDV,
HEV;
bacterial, rickettsial, parasitic],
Drugs and toxins, ischemia (shock), Budd-Chiari
syndrome,
Idiopathic chronic active hepatitis,
acute Wilson’s disease,
microvesicular
fat syndromes (Reye’s syndrome, acute fatty liver of pregnancy).

34. Classification of acute liver failure
Time: jaundice to encephalopathy:
Hyperacute < 7 days,
Cerebral oedema Common
causesViral,
Acute 8–28 days Cerebral
oedemaCommon
causes paracetamol
Cryptogenic
Subacute 29 days–
12 weeks Cerebral
oedema Uncommon drugs
Cryptogenic,
drugs

35. Clinical Manifestations Neuropsychiatric changes—delirium,
personality change,stupor, coma;
Cerebral edema—suggested by profuse sweating, hemodynamic
instability, tachyarrhythmias, tachypnea, fever, papilledema,
decerebrate rigidity(though all may be absent);
Deep jaundice, coagulopathy, bleeding,
Renal failure,
Acid-base disturbance, hypoglycemia,
Acute pancreatitis,
Cardiorespiratory
failure,
Infections (bacterial, fungal)

36. Monitoring in acute liver failure
Cardiorespiratory•
• Pulse•
• Blood pressure•
• Central venous pressure•
• Respiratory rate•
Neurological• Intracranial pressure monitoring •
(specialist units,• Conscious level
• Temperature •

37. Fluid balance
• Hourly output (urine, vomiting, diarrhoea)
• Input: oral, intravenous
Blood analyses
• Arterial blood gases
• Peripheral blood count (including platelets)
• Sodium, potassium, HCO3−, calcium, magnesium
• Creatinine, urea
• Glucose (2-hourly in acute phase)
• Prothrombin time
Infection surveillance
• Cultures: blood, urine, throat, sputum, cannula sites
• Chest X-ray
• Temperature

38. 23.10 Investigations to determine the cause of
acute liver failure
• Toxicology screen of blood and urine •
• HBsAg, IgM anti-HBc •
• IgM anti-HAV •
• Anti-HEV, HCV, cytomegalovirus, herpes simplex, Epstein– •
Barr virus •
• Caeruloplasmin, serum copper, urinary copper, slit-lamp eye •
examination •
• Autoantibodies: ANA, ASMA, LKM, SLA •
• Immunoglobulins •
• Ultrasound of liver and Doppler of hepatic veins •

39. Adverse Prognostic Indicators
• Age <10 or >40,
Certain causes (e.g., halothane,hepatitis C),
Duration of jaundice <7 d before onset of encephalopathy,
Serum bilirubin > 300 mol/L (>18 mg/dL),
Coma (survival <20%),
Rapid reduction in liver size,
Respiratory failure,
Marked prolongation of PT,
Factor V level< 20%.
In acetaminophen overdose, adverse prognosis is suggested by blood
pH< 7.30, serum creatinine > 266 mol/L (>3 mg/dL), markedly
prolonged PT.

40. Acute Hepatic Failure Treatment
Endotracheal intubation often required.
Monitor serum glucose—IV D10 or D20 as necessary.
Prevent GI bleeding with H2-receptor antagonists and antacids
(maintain gastric pH  3.5).
In many centers intracranial pressure is monitored—more
sensitive than CT in detecting cerebral edema. Value of
dexamethasone for cerebral edema unclear; IV mannitol may be
beneficial.
Liver transplantation should be considered in pts with grades III–IV
encephalopathy
and other adverse prognostic indicators.

41. VIRAL HEPATITIS
Acute viral hepatitis is a systemic
infection affecting the liver
predominantly.
Clinically characterized by malaise,
nausea, vomiting, diarrhea, and low-grade
fever followed by dark urine,
jaundice, and tender hepatomegaly;
may be subclinical and detected on
basis of elevated aspartate and alanine
aminotransferase (AST and ALT) levels.

42. CONTINUED:
Hepatitis B may be associated with immune-complex
phenomena,
including arthritis, serum sickness–like illness,
glomerulonephritis, and a polyarteritis nodosa–like
vasculitis.
Hepatitis-like illnesses may be caused not only by
hepatotropic viruses (A, B, C, D, E) but also by other
viruses (Epstein-Barr, CMV,
coxsackievirus, etc.), alcohol, drugs, hypotension and
ischemia, and biliary tract disease

43. TOXIC AND DRUG-INDUCED HEPATITIS
Dose-Dependent (Direct Hepatotoxins) Onset is within 48 h,
predictable, necrosis around terminal hepatic venule–e.g., carbon
tetrachloride, benzene derivatives,mushroom poisoning, acetaminophen,
or microvesicular steatosis (e.g.,
tetracyclines, valproic acid).
Idiosyncratic Variable dose and time of onset; small number of exposed
persons affected; may be associated with fever, rash, arthralgias,
eosinophilia. In many cases, mechanism may actually involve toxic
metabolite, possibly determined on genetic basis—e.g., isoniazid,
halothane, phenytoin, methyldopa, carbamazepine,
diclofenac, oxacillin, sulfonamides

44. Toxic and Drug-Induced Hepatitis Treatment
Supportive as for viral hepatitis;
withdraw suspected agent, and include use of gastric lavage
and oral administration of charcoal or cholestyramine.
Liver transplantation if necessary.
In acetaminophen overdose, more specific therapy
is available in the form of sulfhydryl compounds (e.g., N-acetylcysteine).
These agents appear to act by providing a reservoir of sulfhydryl
groups to bind the toxic metabolites or by stimulating synthesis of
hepatic glutathione.
Therapy should be begun within 8 h of ingestion, but may be
effective even if given as late as 24–36 h after overdose

45. Complications of acute liver failure
Encephalopathy and
cerebral oedema
• Hypoglycaemia
• Metabolic acidosis
• Infection (bacterial, fungal)
• Renal failure
• Multi-organ failure
(hypotension and
respiratory failure)

47. QUIZ: