Confusión de insuficiencia hepática (encefalopatía hepática) y sangrado por varices¶

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.

Haz esto ahora¶

1. Llame a los servicios médicos de emergencia de inmediato: Llame a su número de emergencia local (911 en Estados Unidos y Canadá, 112 en toda la Unión Europea, 999 en el Reino Unido, 000 en Australia) o consulte nuestro directorio de números de emergencia. 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. Presión venosa portal alta: A diferencia de una úlcera péptica pequeña, una varice esofágica está sometida a una presión hidrostática alta y continua; cuando su delgada pared se rompe, la sangre brota hacia el esófago y el estómago a velocidades de 100 a 500 mililitros por minuto.
2. Coagulopatía y trombocitopenia de la insuficiencia hepática: Un hígado sano fabrica las proteínas de coagulación de la sangre del cuerpo (protrombina, fibrinógeno, factores V, VII, IX, X), mientras que un bazo agrandado en la hipertensión portal atrapa y destruye las plaquetas de la sangre. En consecuencia, cuando una varice estalla en un paciente cirrótico, la sangre carece tanto de plaquetas como de factores de coagulación necesarios para tapar el agujero por sí sola.

Señales de advertencia de rotura de várices (incluso antes de vomitar sangre)¶

Un paciente no siempre vomita sangre de color rojo brillante inmediatamente cuando una varice comienza a filtrarse hacia el estómago:

• Hematemesis (vómitos con sangre): Vómitos de gran volumen y sin esfuerzo de sangre líquida de color rojo brillante, coágulos de sangre de color rojo granate oscuro del tamaño de ciruelas o material granular de color marrón oscuro que parece posos de café húmedos (sangrado gastrointestinal).
• Melena (heces negras, alquitranadas y malolientes): La sangre que se acumula en el estómago y pasa a través de los intestinos es digerida por el ácido del estómago y las bacterias intestinales en heces de color negro azabache, pegajosas y brillantes que parecen alquitrán y tienen un olor metálico acre e inconfundible. Las heces negras alquitranadas en un paciente con cirrosis son una hemorragia gastrointestinal superior activa, que a menudo es la única causa de confusión o desmayo repentinos, incluso cuando no se han producido vómitos.
• Hematoquecia (sangre granate o rojo brillante del recto): Si el sangrado de una varicea es extraordinariamente rápido (más de 1000 mililitros), la sangre corre por todo el tracto intestinal tan rápido que sale del recto todavía con un aspecto rojo oscuro o granate, acompañado de mareos profundos y shock.
• Desmayos repentinos e indoloros (síncope) y sudor frío: Debido a que la sangre que llena el estómago actúa como un poderoso catártico, muchos pacientes de repente sienten una necesidad urgente de usar el baño, entrar al baño y colapsar inconscientes en el piso del baño antes de que alguien se dé cuenta de que están sangrando internamente.

Primeros auxilios paso a paso para la hemorragia activa por varices¶

1. Llame a los paramédicos inmediatamente y abra la puerta principal: Cada minuto cuenta; la supervivencia hospitalaria depende de recibir fármacos vasoactivos intravenosos (octreótido o terlipresina para reducir la presión de la vena porta), antibióticos profilácticos intravenosos (ceftriaxona), transfusión de sangre cautelosa y ligadura endoscópica urgente con banda de las várices dentro de las 12 horas.
2. Proteja las vías respiratorias en la posición de recuperación lateral izquierda:
3. Gire al paciente sobre su lado izquierdo en el suelo o en la cama.
4. Incline su cara ligeramente hacia abajo sobre un recipiente o una toalla para que la sangre y los coágulos salgan directamente de la parte inferior de la mejilla.
5. Utilice un dedo enguantado envuelto en un paño para barrer los coágulos de sangre grandes y gelatinosos de la parte frontal de la boca si tienen arcadas. Nunca coloque a un paciente que vomita boca arriba y nunca lo coloque sentado si está mareado o se desmaya, ya que sentarse erguido provoca hipoperfusión cerebral y síncope repentino con aspiración.
6. Mantenga al paciente abrigado con mantas secas: Envuelva el torso y las piernas con mantas calientes. La hipotermia por debajo de 36,0 grados Celsius (96,8 grados Fahrenheit) desactiva las pocas enzimas de coagulación y plaquetas que le quedan al paciente.
7. Nunca le dé agua, trocitos de hielo, antiácidos o pastillas para la presión arterial por vía oral: Incluso si el paciente pide agua para quitarse el sabor a sangre de la boca, sólo límpiese los labios con un paño húmedo. Dar agua llena el estómago con un líquido que oscurece la cámara endoscópica del gastroenterólogo y provoca repetidos vómitos y aspiraciones.

Encefalopatía hepática (EH): por qué la insuficiencia hepática provoca confusión y coma¶

En términos de salud, las bacterias que viven dentro del colon descomponen las proteínas de la dieta y producen productos de desecho de nitrógeno tóxicos, principalmente amoníaco (\(NH_3\)), junto con mercaptanos, ácidos grasos de cadena corta y manganeso. Normalmente, la sangre de la vena porta transporta todo este amoníaco directamente al hígado, donde las células hepáticas sanas (hepatocitos) convierten el amoníaco tóxico en urea inofensiva a través del ciclo de la urea para que los riñones puedan eliminarlo en la orina.

En la cirrosis o insuficiencia hepática aguda, dos cosas van mal: las células hepáticas cicatrizadas pierden hasta el 80 por ciento de su capacidad para eliminar el amoníaco, y la hipertensión portal obliga a la sangre intestinal a evitar el hígado por completo a través de derivaciones colaterales (o un stent TIPS colocado quirúrgicamente: derivación portosistémica intrahepática transyugular). El amoníaco sin filtrar fluye directamente hacia las arterias sistémicas y cruza la barrera hematoencefálica. Dentro del cerebro, las células cerebrales de soporte llamadas astrocitos intentan desintoxicar el amoníaco convirtiendo el glutamato en glutamina. La glutamina actúa como una esponja osmótica dentro de los astrocitos, arrastrando agua hacia las células cerebrales y provocando edema cerebral difuso (hinchazón cerebral) e inhibición neuroquímica grave (encefalopatía hepática).

La escala de calificación de West Haven: reconocimiento de la encefalopatía hepática del grado 1 al grado 4¶

Los familiares que viven con un paciente hepático son siempre los primeros en detectar la encefalopatía hepática de grado 1 o 2, mucho antes de que un extraño notara algo malo. Utilice los Criterios de West Haven internacionales para realizar un seguimiento e informar el estadio exacto del paciente:

How to perform the bedside "Asterixis" (Flapping Tremor) test¶

Asterixis is not actually a tremor of contracting muscles; neurophysiologically, it is negative myoclonus, a brief, sudden 50-to-200-millisecond electrical pause (shutoff) in the motor cortex centers that maintain posture against gravity, caused by ammonia poisoning.

1. Have the patient sit upright in bed or a chair (or lie propped up) and extend both arms straight out in front of their chest with their elbows straight.
2. Instruct them to bend both wrists sharply backward (dorsiflexion, palms facing forward as if pushing against an invisible wall) and spread their fingers wide apart.
3. Tell them to close their eyes and hold that exact posture steadily for 30 seconds.
4. What a positive test looks like: After a latency of 5 to 15 seconds, the fingers and wrist suddenly drop forward a few centimeters as muscle tone vanishes for a split second, then immediately jerk back upward as the patient catches it, repeating rhythmically like a bird flapping its wings ("liver flap").
5. Alternative test for weak patients: If the patient is too weak to hold both arms up in the air, let their forearms rest flat on the mattress and simply lift their hands upward at the wrist for 20 seconds, or ask them to squeeze two of your fingers steadily ("milkmaid's grip").

The 6 hidden triggers that precipitate hepatic encephalopathy¶

Hepatic encephalopathy almost never appears out of thin air in a previously stable cirrhosis patient; in more than 80 percent of hospital admissions, a specific acute medical insult triggered the ammonia surge. Emergency physicians search immediately for these six classic precipitants (and caregivers should tell paramedics which ones occurred over the past 72 hours):

1. Silent Gastrointestinal Bleeding (A massive "protein meal" of blood): Blood is packed with hemoglobin protein (100 milliliters of blood contains roughly 15 to 20 grams of pure protein). When a varix or stomach ulcer bleeds silently into the digestive tract, gut bacteria feast on the digested blood protein and convert it into a massive wave of ammonia. Always check the toilet or ask about black, tarry stools (melena) whenever a liver patient becomes confused.
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. Dehydration, Over-Diuresis, Vomiting, or Diarrhea (Electrolyte & Kidney Crisis): Taking too high a dose of prescribed water pills (furosemide and spironolactone), sweating in heat, or having a stomach bug causes acute kidney injury, hypokalemia (low blood potassium), and metabolic alkalosis. Low blood potassium directly stimulates the kidneys to manufacture extra ammonia, while alkalosis converts ammonium ions (\(NH_4^+\), which cannot cross into the brain) into uncharged ammonia gas (\(NH_3\), which crosses straight into the brain).
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. Absolute ban on all NSAIDs (Ibuprofen, Naproxen, Aspirin, Meloxicam, Diclofenac): Taking even a few tablets of ibuprofen or naproxen in cirrhosis strips protective prostaglandins from both the stomach lining (triggering catastrophic variceal or portal hypertensive gastropathy bleeding) and the renal arteries (triggering acute, often fatal hepatorenal syndrome).
2. Strict dose cap on Acetaminophen (Paracetamol): While high-dose acetaminophen (>4,000 mg/day) causes liver failure, hepatology guidelines (AASLD and EASL) note that for chronic cirrhosis patients who do not drink alcohol, low-dose acetaminophen capped strictly at no more than 2,000 milligrams (four 500 mg regular-strength tablets) total per 24 hours for short courses is actually safer than NSAIDs, unless the patient is in acute liver failure, actively drinking alcohol, or malnourished/fasting, in which case zero acetaminophen should be given without direct physician orders.
3. Hold diuretics ("water pills") during vomiting, diarrhea, or confusion: Never give morning doses of spironolactone or furosemide if the patient is dizzy, confused, vomiting, or having >4 loose stools per day until a physician checks their blood sodium, potassium, and creatinine.

Preguntas frecuentes¶

Fuentes verificadas¶

• American Association for the Study of Liver Diseases (AASLD) and European Association for the Study of the Liver (EASL): Clinical Practice Guidelines on Hepatic Encephalopathy in Chronic Liver Disease (West Haven Criteria), Management of Ascites and Spontaneous Bacterial Peritonitis, and Portal Hypertensive Bleeding in Cirrhosis.
• Baveno VII Consensus Workshop (International Portal Hypertension Consensus): Baveno VII, Renewing Consensus in Portal Hypertension and Acute Variceal Hemorrhage Resuscitation.
• National Institute for Health and Care Excellence (NICE) and British Society of Gastroenterology (BSG, United Kingdom): Cirrhosis in Over 16s: Assessment and Management (NG50) and Acute Upper Gastrointestinal Bleeding in Cirrhosis Guidelines.
• World Gastroenterology Organisation (WGO, International): Global Guidelines on Esophageal Varices and Hepatic Encephalopathy Triage.

Guías relacionadas¶

• Gastrointestinal bleeding, vomiting blood, and melena first aid
• Sepsis and septic shock recognition and first aid
• Shock and circulatory collapse first aid
• Alcohol intoxication, hangover, and safe recovery transport
• Números de emergencia por país