Jaundice and Liver disease

Warning

Objectives

To guide the rapid assessment and management of jaundice in deployed operational settings, recognising life‑threatening acute liver failure and facilitating timely escalation or evacuation. 

Scope

Applies to adults and children presenting with new‑onset jaundice or abnormal liver biochemistry in Role 1–3 facilities. Definitive hepatology care is outside scope and requires aeromedical evacuation to Role 4 (UK NHS).

Audience

This guideline is intended for use by registered healthcare professionals fulfilling a general role in forward medical locations or in an emergency department in a deployed hospital setting.

Initial Assessment & Management

A typical presentation would be either scleral or cutaneous jaundice, pale stools, dark urine, abdominal pain, or as an incidental biochemical finding. A thorough history must include:

  • past and current alcohol use
  • illicit substance misuse and high risk behaviours for hepatitides including intravenous or other recreational drug use, tattoos, a sexual history
  • new medications or over the counter supplements
  • known liver disease or related conditions such as Gilbert's
  • A full travel history including leisure travel, dietary habits, water exposure and public health practices such as taking malarial prophylaxis, use of mosquito nets etc
  • Painful vs painless; often the most helpful way to delineate between acute obstructive stones or an infected biliary tress (painful, fever) vs painless, more gradual (malignancy/hepatitis)

The history should help to exclude likely exposure to infectious disease pathogens including malaria, leptospirosis, infectious mononucleosis and viral hepatitides. 


Examination should exclude signs of chronic liver disease.  These include

  • Palmar erythema
  • Clubbing
  • Gynaecomastia
  • Ascites
  • Palpable liver or spleen
  • Petechiae or bruising suggesting coagulopathy
  • Confusion or impaired consciousness may represent hepatic encephalopathy due to the accumulation of ammonia, further supported by asterixis or liver flap. 

Investigations should focus on helping to exclude other mimics.  

In endemic areas, A Malarial RDT is critical as jaundice due to haemolysis in falciparum malaria is common and critical to catch early.

On deployment, drugs associated with jaundice can include doxycycline and other anti-malarias and antibiotics, particularly penicillin.

Jaundice can be seen in known Gilbert’s syndrome along with haemolysis from any cause.  Cholestasis caused by sepsis, stones, or extra-biliary obstruction like tumours are all common.  An acute heart failure might lead to congestive hepatopathy.  

In the role 1 context, laboratory tests and imaging will be unavailable, and presentation with features of acute liver failure (Jaundice + encephalopathy and clinical surrogates of coagulopathy such as bruising, petechiae, oozing following needle stick) should prompt urgent evacuation to a higher role.  
Management in role 1 is supportive treating sepsis if suspected with broad spectrum antibiotics, SPB if diffusely tender abdomen. 
Intravenous hydration must avoid hypotonic fluids as these can precipitate cerebral oedema. 

Advanced Assessment & Management

On arrival at role 2/3, A fully history and examination should be re-taken as above. The exact laboratory testing available will be dependent on the deployment.  

  • Biochemical tests (if available): LFTs, FBC, U&Es, INR, glucose, lactate, amylase; serology for Hep A/B/C/E & HIV.  
  • If available, an abdominal ultrasound may be performed for liver size, biliary dilatation, ascites, and portal flow.  These may be identified on Computed Tomography. 

 
Jaundice PLUS encephalopathy and/or INR > 1.5 would equate to Acute Liver Failure, requiring urgent Role 4 evacuation with CCAST; consult hepatology via reach‑back. 

 

  • If cholangitis, SBP or systemic sepsis is suspected, start broad‑spectrum antibiotics as per deployed antimicrobial guidance (typically cefuroxime/metronidazole). 
  • Vitamin K 10 mg IV if coagulopathic; this will be of clinical value if some of the coagulopathy is related to nutritional depletion, common in many cases of jaundice due to malabsorption, but is unlikely to correct coagulopathy due solely to hepatic synthetic dysfunction in liver failure. Pay careful attention to glucose; a falling BM suggests synthetic dysfunction.  
  • Continue isotonic IV fluids (hypotonic fluids could precipitate an osmotic cerebral oedema), monitor neurology, coagulation, glucose and lactate 4‑hourly.
  • Repeat LFTs/U&Es; consider CT if biliary obstruction suspected.
  • Manage cerebral oedema with simple measures such as head elevation, avoidance of hypercapnia and reduce hyperammonaemia with lactulose to aim for 4 bowel movements per day.   
    - Correct coagulopathy with FFP only if bleeding or invasive procedure is required. TEG may be available and will be of greater value in diagnosing and managing true coagulopathy than INR/APTR. 

Prolonged Casualty Care

  • Maintain electrolytes, glucose and strict fluid balance.
  • Lactulose PO/NG to achieve 4 soft stools daily if encephalopathic.
  • Empirical broad‑spectrum antibiotics if worsening.
  • Thiamine 100 mg IV OD in suspected alcohol‑related disease.
  • Low threshold for airway protection if evidence of worsening encephalopathy refractory to initial management.
  • Daily reassessment for evacuation readiness. 

Paediatric Considerations

Typical causes for jaundice or liver failure in children are highly variable depending on age.  Critically, particularly in younger children, systemic jaundice can indicate sepsis.  An initial history must account for the child's vaccination history (Hepatitis A/B status) and Family history for evidence of metabolic or genetic liver disease.

  • Neonates and infants: Physiological jaundice, haemolytic disease, biliary atresia, metabolic disorders, congenital infections.
  • Older children: Viral hepatitis (A, B, E), autoimmune hepatitis, Wilson’s disease, drug-induced liver injury, sepsis.
  • Red flag: Any jaundiced child with altered mental status or hypoglycaemia → treat as acute liver failure and escalate immediately. Deterioration can be rapid. NB Children are more prone to raised intracranial pressure due to the limited intracranial volume.
    • Early airway protection if encephalopathy worsens.
    • Head elevation, avoid hypercapnia,
  • Hypoglycaemia Risk
    • Children have limited glycogen reserves → frequent glucose monitoring and early IV dextrose infusion (10% or higher if hypoglycaemic to maintain blood glucose >4 mmol/L. Careful electrolyte management with an isotonic strategy: a falling sodium will exacerbate elevated intracranial pressures.
  • Children are more prone to raised intracranial pressure.
    • Early airway protection if encephalopathy worsens.
    • Head elevation, avoid hypercapnia, consider mannitol if clinical features severely raised ICP and evacuation is delayed

Last reviewed: 16/02/2026

Next review date: 16/02/2027