High-Risk Livers and Fevered Travelers

Fever after international travel is a common ED presentation.  In this week’s segment, we will highlight practical resources that help you match symptoms, exposures, prophylaxis, exam findings, and destinations to likely pathogens and guide next steps in real time. Next, we will hear from Dr. Tiffany Proffitt and Dr. Jeremy Driscoll,  as they review the progression from healthy liver to cirrhosis, the diagnosis and management of spontaneous bacterial peritonitis, and tips and tricks on performing a bedside paracentesis.

 

Fever in the Returning Traveler

Dr. Geoff Comp, DO, and Dr. Neda Frayha, MD

 

Pearls:

• Focus your differential using four clinical "fever plus" buckets: headache, hemorrhage/petechiae, jaundice, or respiratory symptoms.
• A detailed travel history—including destination, activities, exposures, and prophylaxis—is critical and often more informative than the test results.
• Most patients do well even without a confirmed diagnosis; supportive care and early ID consultation are key.

Background:

• Global travel is increasing, and so is the incidence of imported infectious diseases like malaria.
• Malaria alone had 263 million cases in 2023 worldwide.
• Misattributing tropical illness as “just the flu” can lead to missed diagnoses with serious consequences.

Initial approach:

• Protect first, diagnose second:
• Early identification helps both patient care and staff safety.
• Many infections are droplet or fecal-oral-transmitted; basic hygiene is essential.
• Mask the patient and yourself—use PPE until you can rule out contagious disease.

Diagnostic Framework:  Four “Fever And” Buckets

• When a patient returns from travel reports fever AND another symptom, it should trigger us to think about travel-related diseases. 
• Fever AND headache: Meningitis or cerebral malaria
• Fever AND bleeding/petechiae: Dengue or other hemorrhagic fevers
• Fever AND jaundice: Yellow fever, leptospirosis
• Fever AND respiratory symptoms: TB, viral pneumonitis

 

History: Where did they go, what did they do, and when did they do it?

• Get details on the patient's travel itinerary.
• Where did they travel to?
• Were they in rural areas or in a large city?
• Did they have any layovers in other countries?
• Any exposure to animals, contaminated food, or insect bites?
• Did they seek any medical care while they were abroad?
• Ask about the symptom timeline:
• <1 week: Dengue, flu, yellow fever
• 1–3 weeks: Malaria, typhoid
• 3 weeks: TB, schistosomiasis
• Ask about prophylaxis or vaccination:
• Did they complete their prophylaxis medications?
• People often stop malaria prophylaxis before completion due to side effects.
• Did they get any vaccines before travel, or were any vaccines recommended before travel?

Physical Exam: Let the “four buckets” guide you.

• Skin: Rash, petechiae, jaundice, rose spots
• HEENT: Conjunctivitis, lymphadenopathy
• Cardiopulmonary: Focal crackles, diffuse wheezing, murmurs
• Abdomen: Hepatosplenomegaly
• Neuro: AMS, focal deficits—red flag in any traveler with fever
• Pearl: Petechiae under BP cuff (Rumpel-Leede test) may hint at hemorrhagic fever

Workup and Labs

• Universal: CBC w/ diff, LFTs, renal panel, coags, blood cultures, CXR
• Eosinophilia may point to parasites:
• Based on Presentation:
• LP if concerned about meningitis
• Stool O&P for diarrheal illnesses
• Malaria thick and thin smears (x3 if initial negative)
• Dengue rapid tests; serologies for others
• Involve Infectious Disease consultants early:
• Tests may be hard to order or require special labs
• Let your ID consultant guide any disease-specific testing and result interpretation.

Diagnosis: Don’t Expect One

• In many studies, only 75% of patients with suspected tropical illness receive a confirmed diagnosis—even at referral centers.
• Specific testing may be limited, delayed, or inaccurate.
• Most patients improve with supportive care alone.

 

Management Principles

• Supportive care is the mainstay—hydration, antipyretics, symptom control.
• Avoid empiric antibiotics unless sepsis is suspected.
• Escalate care if red flags (e.g., neuro signs, respiratory failure) develop.
• ICU admission may be needed for severe malaria or decompensation.
• Consider isolation/negative pressure if airborne disease is suspected.

Resources for Real-Time Support  

• CDC Yellow Book
• Country-specific vaccine and disease prevalence data
• Useful for both pre-travel and post-travel risk stratification
• HealthMap
• Live updates on regional outbreaks and infectious alerts
• ID consultation
• Always consult early for guidance on testing and management
• Especially critical when diagnostic resources are limited

Take-Home Points

• Use the “fever plus” buckets to anchor your differential and guide focused workup.
• A meticulous travel and symptom history is more powerful than any lab.
• Don’t get hung up on finding the exact organism—treat the patient, not just the diagnosis.
• Most patients recover with supportive care, but stay vigilant for red flags.

References:

1. CDC Yellow Book
2. Health Map
3. Thwaites GE, Day NP. Approach to Fever in the Returning Traveler. N Engl J Med. 2017;376(6):548-560. PMID: 28177860 
4. Scaggs Huang FA, Schlaudecker E. Fever in the Returning Traveler. Infect Dis Clin North Am. 2018;32(1):163-188. PMID: 29406974
5. World malaria report 2024: addressing inequity in the global malaria response. Geneva:
6. World Health Organization; 2024. [Link]
7. International Society of Travel Medicine
8. Practice Guidelines for Evaluation of Fever in returning Travelers or Migrants
9. GeoSentinel

 

 

The Failing Liver

Tiffany Proffit, DO, and Jeremy Driscoll, MD

 

Pearls:

• Cirrhosis transitions from compensated (no ascites/variceal bleed/encephalopathy/jaundice) to decompensated with a major survival drop after the first decompensating event; ascites is often the first major turning point.
• SBP can be subtle or “silent.”  It is diagnosed by ascitic PMN ≥250 cells/mm³ (regardless of culture).  Do not delay paracentesis due to INR or moderate thrombocytopenia when it’s clinically indicated.
• Ultrasound-guided paracentesis + bedside inoculation of culture bottles improves success.
• Cloudy effluent from a peritoneal dialysis catheter should raise suspicion for peritonitis.

Background:

• Complications of liver disease/cirrhosis are the 9th most common cause of death in the US, and ED clinicians frequently see patients across the spectrum of liver disease—from steatosis to recurrent ascites.
• Cirrhosis can come from many etiologies:
• Viral (notably hepatitis C).
• Alcohol-associated liver disease.
• Metabolic dysfunction–associated liver disease (formerly NASH.)
• Genetic conditions.
• Autoimmune disease.
• Medication/toxin-related injury (e.g. acetaminophen toxicity/overdose).
• Regardless of etiology, cirrhosis results from chronic inflammation leading to scarring and architectural distortion.

Updated Nomenclature:

• NASH → MASH: Metabolic Dysfunction–Associated Steatohepatitis
• NAFLD → MASLD: Metabolic Dysfunction–Associated Steatotic Liver Disease
• These changes were aimed at reducing stigma associated with prior terms.

Prevention:

• ED opportunities exist to intervene earlier (before irreversible cirrhosis) and to rapidly recognize/treat decompensation.
• Where ED clinicians can intervene to prevent progression:
• Alcohol-related disease: counsel on abstinence as a key intervention.
• Viral hepatitis:
• Vaccines exist for hepatitis to help prevent the disease.
• Modern treatments for viral hepatitis can be curative.
• Metabolic dysfunction–associated disease: 
• Emphasize diet and lifestyle modification as meaningful interventions.

Pathophysiology: inflammation → fibrosis → cirrhosis

• Chronic liver injury drives ongoing inflammation.
• Inflammation activates hepatic stellate cells → collagen deposition.
• Progression: fibrosis → bridging fibrosis → distorted liver architecture + nodules = cirrhosis.
• Once cirrhosis develops, it is irreversible.

Clinical presentation: compensated vs decompensated cirrhosis

• Compensated cirrhosis
• No history of ascites
• No variceal bleeding
• No encephalopathy
• Often subtle symptoms (fatigue) or mild lab abnormalities
• Median survival cited: ~10–12 years
• Decompensated cirrhosis
• Development of ascites, variceal bleeding, hepatic encephalopathy, and/or jaundice
• After the first decompensating event, survival is cited as ~2–4 years without transplant

Common outpatient medications you’ll see (and what they signal)

• Portal HTN / variceal bleed prophylaxis
• Nonselective beta blockers (e.g. carvedilol, nadolol, propranolol).
• Used to prevent first decompensation in compensated cirrhosis with clinically significant portal hypertension and reduce variceal bleed risk.
• Ascites /volume management
• Spironolactone + furosemide for uncomplicated ascites.
• Sodium restriction is also used to support diuretics in volume management.
• Refractory/recurrent ascites: 
• Large-volume paracentesis is sometimes needed on a regular basis.
• Consider albumin if performing large volume paracentesis (>5L removed).
• Consider referral to discuss TIPS procedure if the patient requires frequent large-volume paracentesis.
• Hepatic encephalopathy
• Lactulose and rifaximin are the most commonly used medications for hepatic encephalopathy management.
• Lactulose mechanism reviewed:
• Lactulose causes fermentation in gut bacteria, which lowers colonic pH → converts ammonia to non-absorbable ammonium→ ammonium is trapped in the colon and excreted via stool as the osmotic effect of lactulose causes diarrhea.
• Oral and rectal use the same formulation of lactulose.
• Rectal is faster but requires retention enema (often difficult in confused/combative patients).
• An NG tube is a practical ED option when aspiration risk/altered mental status limits oral intake.
• Rifaximin is an antibiotic with broad-spectrum activity against enteric bacteria. Can be an adjunct to lactulose and added if the patient doesn’t respond to lactulose. 
• SBP prophylaxis (high-risk patients)
• Fluoroquinolone (e.g., ciprofloxacin) or TMP-SMX is most commonly used for SBP prophylaxis.
• High-risk features include things like prior SBP, low-protein ascites, or renal dysfunction.
• Albumin: when to consider
• After large-volume paracentesis (>5 L), albumin can be considered.
• Albumin can also be used in refractory cases of hypotension, but should not be used prophylactically in cases where hypotension might develop later.

TIPS procedure: what is it and when should we consider referral?

• TIPS (transjugular intrahepatic portosystemic shunt):
• Creates a low-resistance channel between the portal and hepatic veins → reduces portal pressure
• Helps control refractory ascites and refractory variceal bleeding.
• Also considered in hydrothorax that isn’t controlled with medications.
• Emerging guidance mentioned: earlier/preemptive TIPS in select high-risk variceal bleeds
• Tradeoff: increased risk of hepatic encephalopathy
• Consider referral to hepatology for TIPS consideration when you have a patient with recurrent bleeds/ascites.

Ascites and SBP

• Why ascites is a big deal:
• Often, the first decompensating event.   A major turning point.
•  Associated with higher mortality and complications (variceal bleeding, hepatorenal syndrome).
• SBP vs secondary bacterial peritonitis:
• SBP
• Infection of ascitic fluid without a surgically treatable source.
• Diagnostic threshold: PMN ≥250 cells/mm³ in ascitic fluid (culture can be negative).
• Presentation can be classic (fever, abdominal pain) or subtle (encephalopathy, renal failure, or minimal symptoms).
• Secondary bacterial peritonitis
• Due to surgically treatable intra-abdominal pathology
• Often presents with severe focal peritonitis.
• Clear or identifiable source of infection is present (i.e. perforated appendicitis/diverticulitis, abscess, ischemia).
• Ascitic fluid that suggests secondary process (very high protein, low glucose—mentioned as a clue).
• Requires antibiotics plus surgery involvement.

Peritoneal dialysis (PD)–associated peritonitis

• Can present with cloudy effluent even without pain/fever.
• Diagnostic threshold differs:
• PD peritonitis: WBC >100/mm³ (SBP: PMN >250/mm³)
• Recognize, send appropriate studies, start IV antibiotics if needed
• Coordination with nephrology will be needed for intraperitoneal antibiotics (often not available in typical ED order sets)

Diagnostic Paracentesis: Who, When, Why, and How.

• Why we tap
• Diagnostic paracentesis is recommended in all hospitalized patients with cirrhosis and ascites, even if they are admitted “for something else,” because SBP can be silent and early paracentesis is associated with lower in-hospital mortality. (JAAD)
• ED indications: new-onset ascites, any decompensated cirrhotic with ascites and systemic symptoms (fever, encephalopathy, GI bleed, AKI, hypotension, abdominal pain), or any clinical deterioration with ascites.
• What to send from the tap
• Cell count with differential, albumin, total protein, and culture (inoculate blood culture bottles at bedside).
• Consider glucose, LDH, and amylase if concerned for secondary peritonitis or pancreatic source.
• Technical tips
• Use ultrasound guidance whenever possible to identify a fluid pocket and avoid bowel and vessels; this reduces complications and improves success.
• Typical sites: 2–3 cm medial and cephalad to ASIS, or midline infra-umbilical
• Avoid scars and visible vessels.
• Use a Z-track technique (displacing skin before needle insertion) to reduce post-procedure leak.
• Troubleshooting when the fluid stops draining:
• Commonly bowel/omentum is occluding the catheter tip/ports.
• Check the catheter tip position with ultrasound.
• Roll the patient toward the insertion side to pool fluid.
• You can also apply gentle external pressure to move fluid toward the catheter or use a saline flush to dislodge the obstruction.
• Coags/platelets: don’t let myths delay the tap
• INR
• INR doesn’t reliably predict bleeding risk in cirrhosis due to “rebalanced” hemostasis.
• Both procoagulant and anticoagulant factors are decreased, but INR does not reflect this, making it unreliable.
• INR correction with FFP before low-risk procedures like paracentesis is not routinely recommended.
• Platelets
• Large series and meta-analyses show that major bleeding rates after paracentesis in cirrhotics with coagulopathy are very low (~0.3%), 
• Even with elevated INR and low platelets, especially when ultrasound guidance is used.
• No evidence-based platelet threshold exists where prophylactic transfusion clearly improves outcomes in routine diagnostic or therapeutic taps.
• Routine prophylactic platelets are not recommended in most patients.
• Reasonable caution is advised in patients with active DIC, clinically significant hyperfibrinolysis, or very severe thrombocytopenia (for example, <20k), plus other bleeding risk factor.
• These cases should be discussed with hepatology.
• What to send from ascitic fluid:
• At minimum: Cell count with differential, Albumin, Total protein, Culture
• Inoculate blood culture bottles at the bedside.
• Cultures typically need to be physically walked to the lab (not tubed).
• Post-paracentesis complications and quick fixes
• Possible complications (rare but important):
• Persistent leak from the site, abdominal wall hematoma, intraperitoneal bleeding, pseudoaneurysm.
• Higher risk with multiple needle passes/inexperience.
• Managing a leaking paracentesis site:
• Topical skin adhesive works well. (wall O₂ via nasal cannula can help dry this more quickly).
• If needed: occlusive dressing, purse-string suture, or ostomy appliance for persistent high-output leak.

Summary: Cirrhosis bedside “4 AM” algorithm 

• Step 1: Decide compensated vs decompensated
• Decomp features: ascites, variceal bleed, encephalopathy, jaundice → treat as high short-term risk.
• Step 2: If decompensated + ascites, strongly consider diagnostic paracentesis early
• Especially new/worsening ascites or systemic symptoms; consider empiric antibiotics if SBP suspected.
• Step 3: Treat based on the likely peritonitis type
• Suspected/confirmed SBP → 3rd-gen cephalosporin; consider albumin (particularly with renal dysfunction/jaundice, dosing mentioned: 1.5 g/kg day of presentation).
• Secondary peritonitis → antibiotics + surgery consult.
• PD peritonitis → start IV antibiotics, coordinate intraperitoneal therapy with nephrology.
• Step 4: Don’t delay tap for INR/platelets in typical cirrhotics
• Ultrasound-guided paracentesis is emphasized as safe.
• Step 5: Recognize “failing liver” patterns
• Ascites + SBP + GI bleed + kidney injury + encephalopathy → consider albumin/antibiotics early
• Document the need for hepatology discussion
• TIPS consideration, and transplant pathway when appropriate.

References:

1. Biggins SW, Angeli P, Garcia-Tsao G, Ginès P, Ling SC, Nadim MK, Wong F, Kim WR. Diagnosis, Evaluation, and Management of Ascites, Spontaneous Bacterial Peritonitis and Hepatorenal Syndrome: 2021 Practice Guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021 Aug;74(2):1014-1048. PMID: 33942342.
2. Kaplan DE, Ripoll C, Thiele M, Fortune BE, Simonetto DA, Garcia-Tsao G, Bosch J. AASLD Practice Guidance on risk stratification and management of portal hypertension and varices in cirrhosis. Hepatology. 2024 May 1;79(5):1180-1211. PMID: 37870298.
3. Aithal GP, Palaniyappan N, China L, Härmälä S, Macken L, Ryan JM, Wilkes EA, Moore K, Leithead JA, Hayes PC, O'Brien AJ, Verma S. Guidelines on the management of ascites in cirrhosis. Gut. 2021 Jan;70(1):9-29. PMID: 33067334