Ko e Putupu'u 'o e 'Ate 'o e 'Ate (Hepatic Encephalopathy) mo e Tafe 'a e Toto 'i he Variceal¶

Patients living with chronic liver disease, cirrhosis, or acute liver failure face three life-threatening decompensation emergencies that can erupt without warning at home: ruptured gastroesophageal varices (massive upper gastrointestinal hemorrhage where engorged veins in the lower esophagus burst open), hepatic encephalopathy (acute neuropsychiatric confusion, personality change, flapping hand tremors, and coma caused by ammonia and gut neurotoxins bypassing the scarred liver and swelling the brain), and spontaneous bacterial peritonitis (SBP) (a rapid, life-threatening bacterial infection of the fluid inside a swollen abdomen).

Your immediate responsibilities when caring for a liver patient in crisis are to call emergency medical services immediately, protect the airway by rolling a vomiting or drowsy patient onto their side in the recovery position (as drowning in aspirated blood is a major cause of sudden death in variceal rupture), enforce strict NPO (nothing by mouth) if active bleeding or severe drowsiness is present, test for the telltale "flapping hand tremor" (asterixis) to identify early hepatic encephalopathy, and strictly avoid giving sleeping pills, sedatives, ibuprofen/NSAIDs, or excess acetaminophen.

Fai ʻeni he taimí ni .¶

1. Ta ki he ngaahi sevesi fakafaito'o fakavavevave 'i he taimi pe ko ia: Ta ki ho'o fika fakavavevave fakalotofonua (911 'i he 'Iunaiteti Siteiti mo Kanata, 112 'i he kotoa 'o e 'Iunioni 'Iulope, 999 'i he Pule'anga Fakatahataha, 000 'i 'Aositelelia) pe vakai'i 'emau tohi fakahinohino 'o e ngaahi fika fakavavevave. State clearly that the patient has cirrhosis or liver disease and is either vomiting blood, passing black tarry stools, acting confused/unrousable, or running a fever with belly pain.
2. If vomiting blood or drowsy, place in the side-lying recovery position immediately: Never let a patient who is vomiting blood or drowsy from hepatic encephalopathy lie flat on their back. Roll them onto their left side with their chin tilted slightly downward toward the floor so gushing blood, dark "coffee-ground" vomit, or saliva drains straight out of the mouth rather than choking the lungs.
3. Enforce strict NPO (nothing by mouth) during bleeding or severe drowsiness: Do not give water, milk, food, or oral pills if the patient is vomiting blood, passing black tarry stools, or too drowsy to sit up and converse clearly. Hospital gastroenterologists will need an empty stomach to perform emergency endoscopic variceal band ligation within hours of arrival.
4. Check for the "flapping hand tremor" (asterixis) if the patient seems confused or irritable: Ask the awake patient to stretch both arms straight out in front of them, bend their wrists backward ("like a traffic officer stopping traffic"), and spread their fingers wide apart for 15 to 30 seconds. If their hands and wrists involuntarily drop forward and jerk back up in a rhythmic flapping motion like a bird's wings, they are in acute hepatic encephalopathy.
5. Never give sleeping pills, anxiety sedatives, opioids, or NSAID painkillers: Never give a restless, insomniac, or agitated liver patient benzodiazepines (lorazepam, alprazolam, diazepam), sleep aids (zolpidem, diphenhydramine), opioid painkillers, or NSAIDs (ibuprofen, naproxen, aspirin). Sedatives plunge a patient with hepatic encephalopathy straight into an unrousable coma, while NSAIDs trigger fatal variceal bleeding and immediate kidney shutdown (hepatorenal syndrome).
6. Keep the patient warm and gather all liver medications: Cover the patient with warm dry blankets to prevent hypothermia (which further paralyzes blood clotting in cirrhosis), and collect their bottles of lactulose, rifaximin, beta-blockers (propranolol, nadolol, carvedilol), and diuretics (spironolactone, furosemide) for paramedics.

flowchart TD
    Start["Patient With Cirrhosis or Liver Disease Deteriorates at Home"] --> Triage{"1. Identify the Acute Decompensation Emergency"}
    Triage -->|Vomiting Bright Red Blood, Clots, Coffee Grounds, or Passing Black Tarry Stools| Varices["Ruptured Esophageal Varices: Call 911/112/999 Immediately, High-Mortality Hemorrhage"]
    Triage -->|New Confusion, Reversed Sleep-Wake Cycle, Irritability, Slurred Speech, or Flapping Hands| HE["Hepatic Encephalopathy: Call 911/112/999 or Hepatologist, Check for Hidden Trigger (Bleed, Infection, Constipation)"]
    Triage -->|Swollen Ascites Belly With New Fever, Chills, Belly Tenderness, or Low Blood Pressure| SBP["Spontaneous Bacterial Peritonitis (SBP) / Sepsis: Call 911/112/999 Immediately for IV Antibiotics"]
    Varices --> Airway["2. Roll Patient Onto Side (Recovery Position) Immediately so Blood Drains Out of Mouth, Never Leave Flat on Back"]
    Airway --> NPO["3. Keep Strictly NPO (Nothing by Mouth), Keep Warm with Blankets, Prepare for Emergency Endoscopy"]
    HE --> CheckAwake{"4. Is the Confused Patient Fully Awake and Able to Swallow Safely?"}
    CheckAwake -->|No: Drowsy, Stuporous, or Slurring| Airway
    CheckAwake -->|Yes: Alert Grade 1 or 2 Encephalopathy| Lactulose["Follow Doctor's Sick-Day Lactulose Plan if Prescribed, Never Give Sedatives or Sleeping Pills, Transport to Hospital"]
    SBP --> NPO

Ruptured gastroesophageal varices: why cirrhosis causes catastrophic bleeding¶

In a healthy body, all nutrient-rich blood draining from the stomach, intestines, pancreas, and spleen flows through a large main vessel called the portal vein into the soft, spongy liver to be filtered before returning to the heart. When chronic liver disease (from alcohol, viral hepatitis B or C, metabolic dysfunction-associated steatohepatitis / MASH, or autoimmune disease) replaces soft liver tissue with hard, fibrous scar tissue (cirrhosis), blood can no longer flow easily through the liver.

Pressure inside the portal vein backs up like cars behind a blocked highway tunnel, a condition called portal hypertension. Desperate to find a detour back to the heart, pressurized portal blood forces open tiny, fragile, thin-walled veins lining the bottom of the esophagus (swallowing tube) and the top of the stomach. Over months, these delicate veins balloon into twisted, high-pressure ropes called esophageal and gastric varices.

Two reasons variceal bleeding is far more lethal than a normal stomach bleed¶

1. High portal venous pressure: Unlike a small peptic ulcer, an esophageal varix is under continuous high hydrostatic pressure; when its thin wall ruptures, blood gushes into the esophagus and stomach at rates of 100 to 500 milliliters per minute.
2. Coagulopathy and thrombocytopenia of liver failure: A healthy liver manufactures the body's blood-clotting proteins (prothrombin, fibrinogen, Factors V, VII, IX, X) while an enlarged spleen in portal hypertension traps and destroys blood platelets. Consequently, when a varix bursts in a cirrhotic patient, the blood lacks both the platelets and the clotting factors needed to plug the hole on its own.

Warning signs of ruptured varices (Even before blood is vomited)¶

‘Oku ‘ikai ke lua ma‘u pē ha tokotaha mahaki ‘i he taimi pē ko iá ‘i he taimi ‘oku kamata ke hū ai ha varix ki he keté:

• Hematemesis (Lua toto): Lua ta'e feinga, lahi-volume 'o e toto vai kulokula ngingila, ngaahi toto kulokula kulokula maroon 'a e lahi 'o e palamu, pe me'a 'uli'uli lanumata 'oku hange ha kelekele kofi 'oku 'i ai 'a e vai (toto 'i he kete).
• Melena ('Uli'uli, tarry, foul-smelling stools): Ko e toto 'oku pools 'i he kete pea 'oku paasi hifo 'i he intestines 'oku digested ia 'e he 'esiti 'o e kete mo e gut pecteria ki he jet-'uli'uli, pipiki, ngingila 'a e 'uhiki 'oku hange ha tar 'o e hala pea 'oku 'i ai ha me'a 'oku 'ikai ke fakahala'i, pungentlic metal. Ko e paasi 'a e 'uli'uli tarry stools 'i ha mahaki 'oku 'i ai 'a e cirrhosis ko ha toto 'i 'olunga 'o e GI 'oku ngaue, 'oku fa'a hoko ko e tupu'anga pe 'e taha 'o e puputu'u fakafokifā pe fainting na'a mo e taimi kuo hoko ai 'a e zero vomiting.
• Hematochezia (Maroon pe toto kulokula ngingila mei he rectum): Kapau 'oku vave 'aupito ha toto variceal (laka hake 'i he mililita 'e 1,000), 'oku lele vave 'a e toto 'i he kotoa 'o e intestine 'o 'alu atu mei he rectum 'oku kei sio kulokula fakapo'uli pe maroon, 'o 'alu fakataha mo e dizziness loloto mo e dizziness loloto.
• Painless sudden fainting (Syncope) mo e sweat momoko: Koe'uhi ko e toto 'oku ne fakafonu 'a e kete 'oku ngaue ia ko ha cathartic malohi, 'Oku ongo'i fakafokifā 'e he kau mahaki tokolahi ha fie ma'u fakavavevave ke faka'aonga'i 'a e fale kaukau, lue ki he falekaukau, pea tō ta'e'ilo 'i he faliki 'o e falekaukau kimu'a pea toki fakatokanga'i 'e ha taha 'i loto 'oku nau bleeding.

Tokoni 'uluaki fakasitepu ki he toto 'o e variceal 'oku lolotonga ngaue¶

1. Ui leva 'a e kau toketaa pea fakaava 'a e matapa 'i mu'a: 'Oku lau 'a e miniti kotoa pe; 'oku makatu'unga 'a e mo'ui 'i he falemahaki 'i hono ma'u 'o e ngaahi faito'o konatapu vasoactive 'i he veini (octreotide pe terlipressin ke fakasi'isi'i 'a e 'omi 'o e veini 'o e portal), faito'o fakatupu mate 'i he veini (ceftriaxone), huhu toto fakatokanga, mo e **fakavavevave 'o e endoscopic variceal ligation 'i loto 'i he houa 'e 12.
2. Malu'i 'a e halanga 'ea 'i he Tu'unga Fakaakeake 'o e tafa'aki To'ohema:
3. Fakatakataka'i 'a e mahaki ki honau taha to'ohema 'i he faliki pe mohenga.
4. Kiʻi fakatuliki honau fofongá ki lalo ʻi ha pesini pe taueli koeʻuhí ke lilingi hangatonu mai ʻa e totó mo e ngaahi foʻi huhuʻá mei he kouʻahe ʻi laló.
5. Fakaʻaongaʻi ha louhiʻi nima ʻoku ʻi ai ha toʻukupu ʻoku takaiʻi ʻaki ha tupenu ke tafiʻi ʻaki ʻa e ngaahi foʻi toto lalahi ʻoku hangē ha jelí mei muʻa ʻi he ngutú kapau ʻoku nau gagging. 'Oua 'aupito na'a ke fokotu'u ha mahaki 'oku lua 'o flat 'i honau tu'a, pea 'oua na'a teitei prop kinautolu ke nau tangutu hangatonu kapau 'oku nau 'ohovale pe vaivai, he 'oku fakatupu 'e he tangutu hangatonu 'a e cerebral hypoperfusion mo e syncope fakafokifā mo e aspiration.
6. Tauhi 'a e mahaki ke mafana 'aki ha ngaahi palanikete momoko: Takai'i 'a e sino mo e va'e 'aki ha ngaahi palanikete mafana. Ko e māfana ‘i lalo ‘i he tikilī Selisiasi ‘e 36.0 (tikilī Fālenihaití ‘e 96.8) ‘okú ne ta‘ofi ‘a e ngaahi ‘enisaimi mo e ngaahi peletilet si‘isi‘i ‘oku kei toe ‘a e totó kuo tuku ‘e he tokotaha mahakí.
7. 'Oua 'aupito na'a ke 'oange 'a e vai, 'aisi, antacids, pe ngaahi faito'o toto 'i he ngutu: Neongo kapau 'e kolekole 'a e mahaki ki ha vai ke fufulu 'aki 'a e ifo 'o e toto mei honau ngutu, holoholo'i pe honau loungutu 'aki ha tupenu 'oku 'i ai ha vai. Ko hono ‘oange ‘o e vaí ‘okú ne fakafonu ‘a e keté ‘aki ‘a e vai ‘okú ne fakapo‘uli‘i ‘a e me‘a-faka‘ata ‘a e toketā ‘o e keté pea fakatupunga ai ‘a e toutou lua mo e faka‘amu.

Ko e mahaki ‘ate (HE): ko e hā ‘oku fakatupunga ai ‘e he ta‘elavame‘a ‘a e ‘até ‘a e puputu‘u mo e koma¶

'I he mo'ui lelei, 'oku holoki 'e he fanga ki'i selo 'oku nau nofo 'i loto 'i he kolona 'a e polotini 'o e me'akai pea 'oku nau fakatupu 'a e ngaahi koloa 'o e veve 'o e naitoloseni kona, tautautefito ki he 'amonia (\(NH_3\)), fakataha mo e mercaptans, 'esiti ngako nounou-seini, mo e manganese. Ko e angamahení, ʻoku ʻave ʻe he toto ʻo e veini ʻo e matapaá ʻa e ʻamonia kotoa ko ʻení ʻo hangatonu ki he ʻaté, ʻa ia ʻoku liliu ai ʻe he ngaahi sela ʻate moʻui leleí (hepatocytes) ʻa e ʻamonia kona ki he urea taʻefakatuʻutāmaki ʻo fakafou ʻi he siakale ʻo e urea koeʻuhí ke lava ʻe he ngaahi fatú ʻo fufulu ia ʻi he mimi.

‘I he cirrhosis pe ko e ‘ate ‘oku ‘ikai ke ngaue lelei, ‘oku hala ‘a e ongo me‘a: ‘oku mole ‘a e peseti ‘e 80 ‘o e ngaahi sela ‘o e ‘ate ‘oku ma‘ú ‘o a‘u ki he peseti ‘e 80 ‘o ‘enau malava ke fakama‘a ‘a e ‘amoniá, pea ‘oku fakamālohi‘i ‘e he toto mā‘olunga ‘i he matapaá ‘a e toto ‘o e ‘até ke ne fakalaka faka‘aufuli ‘a e ‘até ‘o fakafou ‘i he ngaahi shunts ‘o e ‘até (pe ko ha tafa ‘oku fokotu‘u TIPS stent intrapalarhe: transjugutic). Ko e ‘amonia ‘oku ‘ikai ke sivi‘í ‘oku tafe hangatonu ia ki he ngaahi halanga toto ‘o e sinó pea kolosi ‘i he ‘ā vahevahe ‘o e totó mo e ‘utó. ‘I loto ‘i he ‘utó, ‘oku feinga ‘a e ngaahi sela poupou ‘o e ‘utó ‘oku ui ko e astrocytes ke faka‘auha ‘a e kona ‘o e ‘amoniá ‘aki hono liliu ‘a e glutamate ki he glutamine. 'Oku ngaue 'a e kulutamine hange ha osmotic sponge 'i loto 'i he astrocytes, 'o toho 'a e vai ki he ngaahi selo 'o e 'uto pea fakatupu 'a e ** edema 'o e 'uto 'oku mafola (fula 'o e 'uto)** mo e ta'ofi 'o e neurokemikale lahi (hepatic encephalopathy).

Ko e Me'afua Fakakalasi 'o e West Haven: 'ilo'i 'a e mahaki 'o e 'ate mei he Kalasi 1 ki he Kalasi 4¶

Ko e kau mēmipa ʻo e fāmilí ʻoku nau nofo mo ha mahaki ʻate ʻoku nau ʻuluaki ʻiloʻi maʻu pē ʻa e Kalasi 1 pe Kalasi 2 hepatic encephalopathy, fuoloa kimuʻa pea toki fakatokangaʻi ʻe ha taha ʻoku ʻikai ke nau ʻiloʻi ha meʻa ʻoku hala. Faka'aonga'i 'a e West Haven Criteria fakavaha'apule'anga ke muimui'i mo lipooti 'a e tu'unga totonu 'o e mahaki:

Founga ke fakahoko 'aki 'a e sivi 'o e "Asterixis" (Flapping Tremor) 'i he tafa'aki mohenga¶

Asterixis 'oku 'ikai ko hono mo'oni ko ha tetetete 'o e ngaahi uoua 'oku fakafetongi; neurophysiologically, ko e myoclonus fakafepaki, ko ha nounou, fakafokifā 50-ki he-200-milisekoni 'uhila tu'u (tāpuni) 'i he ngaahi senitā 'o e cortex 'o e me'alele 'oku nau tauhi 'a e tu'unga 'o e 'atakai 'o e kalavite, 'oku fakatupu 'e he kona 'o e 'amonia.

1. ʻAi ke tangutu hangatonu ʻa e mahakí ʻi hono mohengá pe ʻi ha sea (pe tokoto ʻo poupouʻi hake) pea mafao atu ʻa e ongo nimá ʻo hangatonu ki tuʻa ʻi muʻa ʻi hona fatafatá ʻo hangatonu hona ongo tuliki.
2. Fakahinohinoʻi kinaua ke na punoʻi māsila ʻa e ongo louhiʻi nimá ki mui (dorsiflexion, ʻoku hanga ʻa e ongo nimá ki muʻa ʻo hangē ʻokú na tekeʻi ha ʻā taʻehāmaí) pea mafola hona ongo louhiʻi nimá ʻo mavahevahe.
3. Talaange ke nau mo'umo'ua honau mata pea puke ma'u 'a e tu'unga tonu ko ia 'i he sekoni 'e 30.
4. Ko e hā ha sivi lelei 'oku hā mai: Hili ha latency 'o e sekoni 'e 5 ki he 15, 'oku fakafokifā 'a e ngaahi louhi'i nima mo e louhi'i nima 'oku holo hifo ki mu'a 'i ha ngaahi senitimita si'i 'i he mole 'a e le'o 'o e uoua 'i ha sekoni vahevahe, pea 'oku vave 'a e jerk ki mui ki 'olunga 'i he taimi 'oku puke ai 'e he mahaki 'a e fla**plings (fla ** pings).
5. Sivi kehe ki he kau mahaki vaivai: Kapau 'oku fu'u vaivai 'a e mahaki ke ne pukepuke 'a e ongo nima ki 'olunga 'i he 'ea, tuku ke malolo 'a hona ongo nima mu'a 'i he me'alele pea hiki hake pe hona ongo nima ki 'olunga 'i he louhi'i nima 'i ha sekoni 'e 20, pe kole ange ke na lomi'i tu'uma'u 'a e ongo nima 'o ho ongo louhi'i nima ("milkmaid's grip").

Ko e ngaahi me'a 'e 6 'oku fufuu'i 'oku ne fakavave'i 'a e hepatic encephalopathy .¶

Ko e hepatic encephalopathy ‘oku meimei ‘ikai ke ‘asi mai ia mei he ‘ea manifi ‘i ha tokotaha mahaki cirrhosis na‘e tu‘uma‘u ki mu‘a; ‘i he peseti ‘e 80 tupu ‘o e ngaahi hū ki falemahakí, na‘e fakatupunga ai ‘e ha fakaanga fakafaito‘o fakatu‘utāmaki pau ‘a e ‘alu hake ‘a e ‘amoniá. ‘Oku kumi vave ‘e he kau toketā fakavavevavé ‘a e ngaahi six classic precipitants ko ‘ení (pea ‘oku totonu ke tala ‘e he kau tauhí ki he kau toketā fakafaito‘ó pe ko fē ‘a e ngaahi me‘a na‘e hoko ‘i he houa ‘e 72 kuohilí):

1. Toto Fakalongolongo 'i he Kete (Ko ha "me'akai polotini" lahi 'o e toto): 'Oku fonu 'a e toto 'i he polotini 'o e hemokolopini ('oku 'i he mililita 'e 100 'o e toto 'a e kalami 'e 15 ki he 20 'o e polotini ma'a). ‘I he taimi ‘oku tafe fakalongolongo ai ha varix pe ulcer ‘i he keté ki he halanga me‘akaí, ‘oku kai ‘e he fanga ki‘i pekitilia ‘o e keté ‘a e polotini toto kuo faka‘au‘auhifó pea liliu ia ki ha peau lahi ‘o e ‘amoniá. Sivi ma'u pe 'a e fale kaukau pe 'eke fekau'aki mo e 'uli'uli, tarry stools (melena) 'i ha taimi pe 'oku puputu'u ai ha mahaki 'ate.
2. Infection (Especially Spontaneous Bacterial Peritonitis, UTI, or Pneumonia): Systemic inflammation and bacterial toxins make the blood-brain barrier leaky and multiply ammonia neurotoxicity fivefold.
3. Constipation and missed Lactulose doses: If stool sits inside the colon for 24 to 48 hours instead of being flushed out 2 to 3 times daily, colonic bacteria produce and absorb vastly more ammonia.
4. Ko e 'ikai ke 'i ai ha vai 'i he sino, 'Over-Diuresis, Lua, pe 'Ikai ('Ilekituloiti & Faingata'a'ia 'i he Fatu): Ko hono to'o 'o e fu'u lahi 'o e ngaahi faito'o vai kuo fakahinohino'i (furosemide mo e spironolactone), fufula 'i he vela, pe 'oku 'i ai ha 'uhiki 'i he kete 'oku ne fakatupu 'a e ma'ulalo 'a e fatú (mihypo injury potasiume)**, mo e 'alkalosisi fakametaboliki. Ko e potasiume ma'ulalo 'i he toto 'oku ne faka'ai'ai fakahangatonu 'a e ngaahi fatú ke nau ngaohi 'a e 'amonia lahi ange, lolotonga ia 'oku liliu 'e he alkalosis 'a e ngaahi ions 'amoniume (\(NH_4+\), 'a ia 'oku 'ikai lava ke kolosi ki he 'uto) ki he kasa 'amonia 'oku 'ikai ke totongi (\(NH_3\), 'a ia 'oku kolosi hangatonu ki he 'uto).
5. Central Nervous System Depressant Medications: Taking even a single dose of a benzodiazepine (lorazepam, diazepam, clonazepam), sleeping pill (zolpidem), sedating antihistamine (diphenhydramine, hydroxyzine), or opioid painkiller (oxycodone, morphine, tramadol).
6. Acute Portal Vein Thrombosis or New TIPS Shunt: A fresh blood clot blocking the portal vein or a recently placed liver shunt.

Understanding Lactulose and Rifaximin (And when NEVER to give oral Lactulose)¶

Patients with cirrhosis and prior hepatic encephalopathy are routinely prescribed two daily maintenance medications to clear ammonia from the gut:

• Lactulose (or Lactitol): A thick, sweet, non-absorbable synthetic sugar syrup. When lactulose reaches the colon, beneficial gut bacteria ferment it into lactic acid and acetic acid. This acidification drops the pH inside the colon, which chemically traps diffusible ammonia (\(NH_3\)) by adding a hydrogen ion to turn it into charged ammonium (\(NH_4+\)). Because charged ammonium cannot pass through the intestinal wall into the bloodstream, it remains trapped inside the stool and is flushed out of the body by lactulose's osmotic laxative action. Doctors titrate daily lactulose doses so the patient passes 2 to 3 soft bowel movements every single day.
• Rifaximin: A non-absorbable oral antibiotic that stays strictly inside the intestines and reduces the population of ammonia-producing gut bacteria.

Critical safety rule during an acute encephalopathy crisis at home¶

• If the patient is in early Grade 1 or mild Grade 2 HE (wide awake, sitting up, coughing normally, and able to drink water without choking) and has missed their lactulose or is constipated, calling their hepatologist or emergency dispatch may include giving their prescribed oral sick-day lactulose dose while arranging medical evaluation.
• NEVER pour oral lactulose (or any liquid) into the mouth of a Grade 3 (stuporous/drowsy) or Grade 4 (comatose) patient: Once a patient is drowsy, slurring heavily, or hard to wake up, their gag reflex is blunted. Pouring thick, sticky lactulose syrup into their mouth causes immediate pulmonary aspiration into the lungs. Paramedics and hospital nurses treat Grade 3 and Grade 4 patients safely using lactulose retention enemas or a protected nasogastric tube after securing the airway.

Spontaneous Bacterial Peritonitis (SBP) and tense ascites emergencies¶

Many patients with decompensated cirrhosis accumulate liters of straw-colored fluid inside their abdominal cavity (ascites), causing a tight, swollen, distended belly. Because ascitic fluid has very low levels of protective immune proteins (complement), normal bacteria from the patient's own intestines can migrate microscopically through the bowel wall (bacterial translocation) and infect the belly fluid without any bowel perforation occurring. This life-threatening infection is called Spontaneous Bacterial Peritonitis (SBP) and carries a 20 to 30 percent mortality rate if intravenous antibiotics are delayed by even a few hours.

Red flags of Spontaneous Bacterial Peritonitis (SBP)¶

Unlike surgical peritonitis from a burst appendix (which makes the belly board-hard), the fluid cushion of ascites in a cirrhosis patient prevents the abdominal muscles from feeling rigid. Look for any one of these subtle warning signs in a patient with ascites:

• Any fever above 37.8 degrees Celsius (100.0 degrees Fahrenheit) or hypothermia below 36.0 degrees Celsius (96.8 degrees Fahrenheit), or unexplained shivering chills.
• New diffuse abdominal pain, cramping, discomfort, or tenderness when pressing gently on the swollen belly, or a belly that suddenly feels tighter and more tense than usual.
• New or worsening confusion / hepatic encephalopathy with zero obvious cause (in up to 30 percent of SBP cases, confusion is the only outward symptom, with no fever and no belly pain).
• Unexplained drop in blood pressure, dizziness, or sudden decrease in urine output (hepatorenal syndrome, where SBP infection triggers the kidneys to shut down completely).
• Immediate action: Go straight to an emergency department. Hospital doctors will use a thin needle under ultrasound guidance to draw a small sample of belly fluid (diagnostic paracentesis) to count white blood cells (>250 polymorphonuclear cells per cubic millimeter confirms SBP) and immediately administer intravenous third-generation cephalosporin antibiotics plus intravenous albumin to save the kidneys.

What to do if fluid leaks from an umbilical hernia ("Flood Syndrome")¶

In patients with severe, tense ascites, pressure inside the belly often pushes out the belly button into a thin-skinned umbilical hernia. If the skin over the belly button develops a dark scab or ulcer and suddenly ruptures, liters of clear yellow ascitic fluid can gush out onto the clothes (Flood syndrome).

• Immediate first aid for a ruptured ascitic umbilical hernia:
• Call your local emergency number or transport to the emergency department immediately (if bacteria crawl in through that hole, fatal peritonitis follows within hours, and rapid fluid loss drops blood pressure).
• Have the patient lie flat on their back or tilted slightly so the leaking spot points upward.
• Cover the leaking opening with a thick, sterile gauze dressing or freshly laundered clean towel secured snugly with tape (do not push anything into the hole), and hold gentle external palm pressure until hospital staff can administer intravenous antibiotics, albumin, and surgical repair.

Strict medication safety rules for anyone with cirrhosis¶

A scarred liver metabolizes medications slowly, while portal hypertension makes the stomach lining and kidneys extraordinarily fragile. Every caregiver of a cirrhosis patient should enforce these three household medication rules:

1. Tapui faka'aufuli 'o e ngaahi faito'o NSAID kotoa pe ('Ipupolofeni, Napoloseni, 'Asilini, Melokisikami, Diclofenac): Ko hono to'o na'a mo ha ngaahi fo'i 'akau si'isi'i 'o e ipupolofeni pe naproxen 'i he cirrhosis 'oku ne to'o 'a e ngaahi prostaglandins malu'i mei he fakatou'osi 'a e 'aofi 'o e kete (fakatupu 'a e variceal fakatu'utamaki 'o e kete) (fakatupu 'a e mahaki faka'auha, fa'a fakatupu mate hepatorenal syndrome).
2. Kapuni tu'unga fefeka 'i he 'Asetaminofeni (Paracetamol): Lolotonga 'oku fakatupu 'e he tu'unga ma'olunga 'o e 'Asetaminofeni (>4,000 mg/'aho) 'a e ta'elavame'a 'o e 'ate, 'oku fakatokanga'i 'e he ngaahi fakahinohino 'o e hepatology (AASLD mo e EASL) ki he kau mahaki 'o e cirrhosis tu'uloa 'oku 'ikai ke nau inu 'a e kavamalohi 'oku lahi ange 'i he- 2,000 milikalami (fa 500 mg angamaheni-malohi 'o e ngaahi fo'i 'akau) fakakatoa 'i he houa 'e 24 ki he ngaahi ako nounou 'oku mo'oni 'oku malu ange ia 'i he NSAIDs, tukukehe 'oku 'i he mahaki 'a e **'ate 'o e 'ate 'o e 'ate **, inu malohi 'a e kavamalohi, pe malnourished given/'aukai 'i he taimi 'oku totonu ke ** 'aukai 'a e physic.
3. Puke 'a e ngaahi faito'o faka'auha ("ngaahi faito'o vai") lolotonga 'a e lua, 'u'ua, pe puputu'u: 'Oua 'aupito na'a ke 'oange ha ngaahi faito'o pongipongi 'o e spironolactone pe furosemide kapau 'oku 'ohovale, puputu'u, lua, pe 'oku 'i ai 'a e >4 'o e 'u'ulu 'i he 'aho kae 'oua kuo vakai'i 'e ha toketaa 'enau blood sotinium, possitanium.

Ngaahi fehu'i 'oku toutou 'eke .¶

Kuo vakaiʻi ʻa e ngaahi maʻuʻanga fakamatalá¶

• Kautaha 'Amelika ki he Ako 'o e Ngaahi Mahaki 'o e 'Ate (AASLD) mo e Kautaha 'a 'Iulope ki he Ako 'o e 'Ate (EASL): Ngaahi Fakahinohino ki he Ngaue Fakafaito'o ki he 'Ate 'o e 'Ate 'i he Mahaki 'o e 'Ate (West Haven Criteria), Pule'i 'o e Ascites mo e SpontaPertensi Toto 'i he Silo*.
• Ko e Fakataha Fakatahataha 'a e Baveno VII (Fakatahataha Fakavaha'apule'anga ki he Toto Ma'olunga 'o e Portal): Baveno VII, Fakafo'ou 'a e Fakatahataha 'i he Toto Ma'olunga 'o e Portal mo e Fakaakeake 'o e Toto Ma'olunga 'i he Variceal.
• 'Inisititiuti Fakafonua ki he Mo'ui Lelei mo e Tokanga'i Lelei (NICE) mo e Sosaieti Pilitania 'o e Gastroenterology (BSG, 'Ingilani): Cirrhosis 'i he Ta'u 16: Sivi mo e Pule'i (NG50) mo e Toto 'i 'olunga 'i he Cirrhosis Fakahinohino.
• Kautaha Gastroenterology 'a Mamani (WGO, Fakavaha'apule'anga): Ngaahi Fakahinohino Fakamamani Lahi ki he Ngaahi Varices 'o e Esofageal mo e Hepatic Encephalopathy Triage.

Ngaahi fakahinohino fekau'aki¶

• Toto 'i he kete, lua toto, mo e melena 'uluaki tokoni .
• Sepsis mo e septic shock 'ilo'i mo e tokoni 'uluaki .
• Mo'utaufu'ua mo e circulatory 'uluaki tokoni .
• Ko e kona ‘i he ‘olokaholó, hangover, mo e fefononga‘aki malu ki he fakaakeaké
• Ngaahi fika fakavavevave 'i he fonua