GASTRO
In this section, we will go over:
GI Bleed/Hemorrhagic Shock
Acute Liver Failure
ESLD and Cirrhosis
Acute Abdomen
Acute Pancreatitis
GI Bleed/Hemorrhagic Shock
Patients presenting with significant GI bleeding often require immediate resuscitation and interventions to control bleeding sources, which can include endoscopic procedures, embolization, or surgery. GI bleeds can be classified into two main types: upper GI bleeds and lower GI bleeds. Upper GI bleeds originate from the esophagus, stomach, or duodenum, while lower GI bleeds arise from the small intestine, colon, or rectum. The pathophysiology of GI bleeds can vary depending on the location and underlying cause.
Upper GI Bleeds: The most common cause of upper GI bleeds is peptic ulcer disease, which is often associated with Helicobacter pylori infection or the use of nonsteroidal anti-inflammatory drugs (NSAIDs). Other causes include esophageal varices, Mallory-Weiss tears, and gastric erosions. In critically ill patients, stress-related mucosal damage can also contribute to upper GI bleeding.
The pathophysiology of upper GI bleeds involves disruption of the mucosal barrier, leading to exposure of blood vessels and subsequent bleeding. Factors that can contribute to mucosal damage include acid hypersecretion, impaired mucosal blood flow, and decreased production of protective factors such as prostaglandins.
Proton pump inhibitors or histamine-2 receptor antagonists are commonly used to reduce the risk of stress-related mucosal damage and GI bleeding, especially in patients on mechanical ventilation or high dose steroids.
Lower GI Bleeds: Lower GI bleeds can be caused by a variety of conditions, including diverticulosis, angiodysplasia, inflammatory bowel disease, colorectal cancer, and ischemic colitis. The pathophysiology of lower GI bleeds often involves vascular abnormalities, such as arteriovenous malformations or ruptured blood vessels within inflamed or neoplastic tissue.
GI bleeds can also be classified based on the severity and rate of bleeding.
Overt bleeding is visible, while Occult bleeding is not visible to the naked eye and only detected through laboratory tests (such as fecal occult blood testing).
GI bleeds can also be acute (sudden onset of significant bleeding) or chronic (slow and continuous over an extended period, mainly seen outpatient).
Hemorrhagic Shock
Hemorrhagic shock is a life-threatening condition that occurs when there is significant blood loss, leading to inadequate perfusion of vital organs. It can be categorized into four stages: initial, compensatory, progressive, and refractory. In the initial stage, blood loss triggers vasoconstriction (causing the patient to be cool to the touch) and an increase in heart rate to maintain blood pressure. As blood loss continues, the compensatory stage begins, characterized by the activation of the sympathetic nervous system and the release of stress hormones such as epinephrine and norepinephrine. These responses aim to maintain organ perfusion by redistributing blood flow to vital organs.
However, as blood loss worsens, the compensatory mechanisms become overwhelmed, leading to the progressive stage of hemorrhagic shock. During this stage, there is a decrease in blood pressure, impaired tissue perfusion, and the initiation of anaerobic metabolism. The body's attempt to compensate for the lack of oxygen leads to the production of lactic acid, resulting in metabolic acidosis.
The management of hemorrhagic shock in critical care involves a multidisciplinary approach, including resuscitation, hemodynamic stabilization, and addressing the underlying cause of bleeding. Ideally resuscitation is done by giving blood; however, if you are waiting for blood to come to bedside, using IV fluids temporarily is adequate. If left untreated, hemorrhagic shock progresses to the refractory stage, which is characterized by irreversible organ damage and a high mortality rate. The refractory stage is challenging to manage, and prompt intervention during the earlier stages is crucial to prevent its development.
For bleeding in liver failure patients, a TIPS can often help. TIPS is a procedure that involves creating a shunt between the portal vein and the hepatic vein to relieve portal hypertension. It is primarily used in patients with ALF who develop refractory ascites or variceal bleeding. TIPS can help improve symptoms and reduce the risk of complications while awaiting liver transplantation.
ICU Maintstays
In general, the ICU management of both GI bleeds and hemorrhagic shock involves trending a patient’s hemoglobin levels closely, establishing large bore access and maintaining A/B/C’s, A prompt initial GI consult is necessary in order to establish definitive treatment (e.g. colonoscopy or EGD). Often, imaging studies may be needed to determine the source of bleeding. In the setting of severe bleeding, a surgical consult may also be required; working with the GI team on next steps is essential in this case.
Resources to complete:
Marino 3rd ed: Ch. 12, 36
NEJM 2013 UGIB Transfusion Strategy
Emcrit Podcast 30: Hemorrhagic Shock
Pulmcast: GI Bleeds and Hemorrhagic Shock
Acute Liver Failure
Acute liver failure (ALF) is a life-threatening condition characterized by rapid and severe impairment of liver function. It is a complex disorder with various etiologies and pathogenic mechanisms. Understanding the underlying causes and processes involved in ALF is crucial for effective management and improved patient outcomes. ALF can be caused by a wide range of factors, including viral infections, drug-induced liver injury, autoimmune diseases, metabolic disorders, and ischemic liver injury. Viral hepatitis, particularly hepatitis A, B, and E, is a common cause of ALF worldwide. Drug-induced liver injury, often resulting from the use of hepatotoxic medications or overdose, is another significant etiological factor. Acetaminophen overdose is the leading cause of drug-induced ALF in many countries.
The pathogenesis of ALF involves a cascade of events that ultimately lead to severe liver dysfunction. The exact mechanisms can vary depending on the underlying cause, but there are some common pathways involved.
Hepatocyte Injury: The initial insult triggers hepatocyte injury, which can occur due to direct viral infection, drug toxicity, immune-mediated damage, or metabolic disturbances. Hepatocytes play a vital role in liver function, and their dysfunction contributes to the development of ALF.
Inflammation and Immune Response: Hepatocyte injury leads to the release of pro-inflammatory cytokines and chemokines, triggering an inflammatory response. This immune response involves the activation of immune cells, such as Kupffer cells and lymphocytes, which further contribute to liver damage.
Oxidative Stress: The inflammatory process and hepatocyte injury generate reactive oxygen species (ROS), leading to oxidative stress. ROS can cause further damage to hepatocytes and impair liver function.
Disruption of Liver Regeneration: The liver has a remarkable capacity for regeneration. However, in ALF, the regenerative process is often impaired due to the severity of liver injury and the presence of inflammatory mediators. This disruption of liver regeneration contributes to the progression of liver failure.
Patients may present with nonspecific symptoms initially, such as fatigue, malaise, anorexia, and nausea. As the disease progresses, more specific signs and symptoms may develop.
One of the hallmark features of acute liver failure is jaundice, which is characterized by yellowing of the skin and sclerae due to elevated bilirubin levels. Jaundice is often accompanied by dark urine and pale stools. Hepatic encephalopathy is another common manifestation, presenting as altered mental status, confusion, asterixis (flapping tremor), and eventually progressing to coma in severe cases.
Patients with acute liver failure may also exhibit signs of coagulopathy, such as easy bruising, bleeding gums, and petechiae. Hepatomegaly (enlarged liver) and splenomegaly (enlarged spleen) may be present in some cases, depending on the underlying etiology.
The medical management of acute liver failure involves first identifying and treating the underlying cause - often by discontinuing hepatotoxic medication, treating infections or addressing metabolic disorders. For Tylenol overdose, N-acetylcystiene (a drip) is given. Once the underlying cause is treated it is also very important to manage hepatic encephalopthy (e.g. using lactulose and rifaximin), monitor for signs of increased intracranial pressure and manage coagulopathy/bleeding (resulting from impaired synthesis of clotting factors).
The prognostic scoring system we use at Piedmont to assess the severity and predict the prognosis of acute liver failure is called the Model for End Stage Liver Disease (MELD) which looks at three month mortality. This is mainly something the transplant team uses to prioritize liver transplants (with the average MELD of a patient getting a transplant being 30), but the ICU team uses it as a way to recognize how sick someone is. Luckily in EPIC we have a way to quickly calculate this - in your progress note, type “.MELD” and the calculated MELD score will pop up.
Resources to complete:
MedCram: Liver Overview, LFT’s, Liver Disease
LITFL: Acute Liver Failure Overview
ALF Dr. Bhasin PPT
Pulmcast: Cerebral Edema in ALF
ESLD and Cirrhosis
Cirrhosis develops as a result of ongoing liver injury and subsequent attempts at repair. The liver is a vital organ responsible for various functions, including detoxification, metabolism, and synthesis of proteins. In cirrhosis, these functions are impaired due to the replacement of healthy liver tissue with fibrous scar tissue.
The primary cause of cirrhosis is chronic inflammation, which triggers a cascade of events leading to fibrosis. In response to injury, hepatic stellate cells, which are normally quiescent, become activated and transform into myofibroblasts. These myofibroblasts produce excessive amounts of collagen, leading to the deposition of scar tissue within the liver. Over time, the accumulation of scar tissue disrupts the normal architecture of the liver, impairing its function.
Some potential complications of cirrhosis include the following.
Ascites is the accumulation of fluid in the abdominal cavity, resulting from increased pressure within the portal vein system. In cirrhosis, the liver's ability to produce albumin is impaired, leading to a decrease in oncotic pressure and subsequent fluid leakage into the peritoneal cavity. Ascites can cause significant discomfort, abdominal distension, and respiratory compromise. In severe cases, it can lead to spontaneous bacterial peritonitis (SBP), a life-threatening infection. Management of ascites involves sodium restriction, diuretic therapy, and, in refractory cases, paracentesis or the placement of a transjugular intrahepatic portosystemic shunt (TIPS).
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome that occurs as a result of liver dysfunction and the accumulation of toxins, such as ammonia, in the bloodstream. HE can manifest as a wide range of neurological symptoms, including confusion, altered consciousness, personality changes, and even coma. The severity of HE can vary from mild cognitive impairment to profound neurological dysfunction. Management of HE involves identifying and treating precipitating factors, such as gastrointestinal bleeding or infection, and administering medications to reduce ammonia levels, such as lactulose and rifaximin.
Variceal Bleeding: Portal hypertension, a hallmark of cirrhosis, leads to the development of collateral blood vessels, known as varices, in the esophagus and stomach. These varices are prone to rupture, resulting in life-threatening gastrointestinal bleeding. Variceal bleeding is a medical emergency that requires immediate intervention. Initial management involves resuscitation, correction of coagulopathy, and the administration of vasoactive medications, such as octreotide, to reduce portal pressure. Endoscopic therapy, such as band ligation or sclerotherapy, is then performed to control bleeding. In refractory cases, transjugular intrahepatic portosystemic shunt (TIPS) placement or surgical intervention may be necessary.
Spontaneous Bacterial Peritonitis: Spontaneous bacterial peritonitis (SBP) is an infection of the ascitic fluid without an evident intra-abdominal source. It occurs due to bacterial translocation from the gut into the peritoneal cavity, facilitated by impaired immune function in cirrhosis. SBP is associated with significant morbidity and mortality and requires prompt diagnosis and treatment. Patients with cirrhosis and ascites should undergo regular screening for SBP, and those suspected of having the infection should receive empirical antibiotic therapy while awaiting culture results. Third-generation cephalosporins, such as cefotaxime or ceftriaxone, are commonly used as first-line therapy.
Hepatorenal Syndrome: Hepatorenal syndrome (HRS) is a severe complication of cirrhosis characterized by the development of renal failure in the absence of intrinsic kidney disease. It occurs due to the progressive reduction in renal blood flow secondary to severe splanchnic vasodilation and arterial underfilling. HRS is associated with a poor prognosis, and without timely intervention, it can rapidly progress to end-stage renal disease. Management of HRS involves volume expansion with albumin and the administration of vasoconstrictors, such as terlipressin or norepinephrine, to improve renal perfusion. In some cases, liver transplantation may be the only definitive treatment option.
Hepatocellular Carcinoma: Patients with cirrhosis are at an increased risk of developing hepatocellular carcinoma (HCC), a primary liver cancer. HCC typically arises in the setting of chronic liver inflammation and fibrosis. Early detection of HCC is crucial, as it allows for potentially curative treatment options, such as surgical resection, liver transplantation, or local ablative therapies. Surveillance for HCC in cirrhotic patients involves regular imaging studies, such as ultrasound or magnetic resonance imaging, and measurement of serum alpha-fetoprotein levels. The prognosis of HCC in cirrhosis depends on the tumor stage at the time of diagnosis and the availability of appropriate treatment modalities.
End stage liver disease (ESLD) is a condition characterized by the progressive and irreversible damage to the liver, leading to its failure. It is a serious and life-threatening condition that requires critical care management in the ICU. ESLD can result from various causes, including chronic viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, autoimmune hepatitis, and genetic disorders such as hemochromatosis and Wilson's disease.
Liver transplantation is the definitive treatment for patients with ESLD who meet the criteria for transplantation. It offers the best chance for long-term survival and improved quality of life. However, the availability of donor organs is limited, and not all patients are suitable candidates for transplantation. The critical care management of patients awaiting transplantation involves close monitoring of their condition, managing complications, and optimizing their overall health to ensure they are in the best possible condition for transplantation.
Resources to complete:
Intensive Care Network: Chronic Liver Disease Podcast
Cirrhosis, Ascites Dr. Stein and Dr. Rubin PPT’s in new hire folder
Acute Abdomen
Acute abdomen refers to the sudden onset of severe abdominal pain that requires immediate medical attention. It is a common condition encountered in critical care settings and can be caused by a wide range of underlying conditions. The classification of acute abdomen is essential for accurate diagnosis and appropriate management. In this section, we will discuss the causes and classification of acute abdomen in the critical care setting.
Acute abdomen can be caused by various conditions, including both surgical and non-surgical pathologies. Some of the common causes of acute abdomen in critical care include:
Appendicitis: Inflammation of the appendix is a common cause of acute abdomen. It typically presents with right lower quadrant pain, nausea, and fever. Appendicitis requires surgical intervention for removal of the inflamed appendix.
Cholecystitis: Inflammation of the gallbladder, usually due to gallstones, can lead to acute abdomen. Patients may experience severe right upper quadrant pain, fever, and jaundice. Cholecystitis may require surgical removal of the gallbladder.
Perforated Peptic Ulcer: A perforation in the wall of the stomach or duodenum can cause sudden and severe abdominal pain. Patients may also present with signs of peritonitis, such as guarding and rebound tenderness. A quick way to check for pneumoperitoneum (air in the abdomen) is an upright KUB; if you see air on the right side of the abdomen underneath the diaphragm, that is abnormal. A CT scan of the abdomen will also show a perforation. Surgical intervention is necessary to repair the perforation.
Intestinal Obstruction: Blockage of the intestines can lead to acute abdomen. It can be caused by various factors, including adhesions, hernias, tumors, or volvulus. Obstruction can be seen with a CT abdomen pelvis with ideally oral contrast. Intestinal obstruction requires prompt diagnosis and may necessitate surgical intervention.
Diverticulitis: Inflammation or infection of the diverticula, small pouches that develop in the colon, can cause acute abdomen. Patients may experience left lower quadrant pain, fever, and changes in bowel habits. Treatment may involve antibiotics and, in severe cases, surgical intervention.
Ischemic Bowel: Reduced blood flow to the intestines can result in ischemic bowel, which is a medical emergency. It presents with severe abdominal pain, bloody stools, and signs of systemic illness. Often this will result in significant lactic acidosis and requires a CT abdomen with contrast to diagnose. Immediate surgical intervention is necessary to restore blood flow and prevent bowel necrosis.
Pancreatitis: Inflammation of the pancreas can cause acute abdomen. Patients may experience severe epigastric pain that radiates to the back, along with nausea, vomiting, and elevated pancreatic enzymes. Treatment may involve supportive care, IV fluids, pain management, and addressing the underlying cause.
Resources to complete:
ESICM Abdomen Module: High Risk Surgical Patient section
EM Basic Episode 3: Abdominal Pain
Acute Pancreatitis
Acute pancreatitis is a severe inflammatory condition of the pancreas that can lead to significant morbidity and mortality in critically ill patients. It is characterized by the sudden onset of inflammation in the pancreas, resulting in autodigestion of pancreatic tissue and the release of inflammatory mediators. The pathophysiology of acute pancreatitis involves a complex interplay of various factors, including gallstones, alcohol abuse, and metabolic disorders.
The exact mechanisms underlying the development of acute pancreatitis are not fully understood. However, it is believed that the initial insult triggers an inflammatory cascade that leads to tissue damage and systemic complications. The two main pathways involved in the pathophysiology of acute pancreatitis are the premature activation of pancreatic enzymes and the release of inflammatory mediators.
Premature Activation of Pancreatic Enzymes: The pancreas normally produces and stores digestive enzymes, such as amylase and lipase, in an inactive form. In acute pancreatitis, these enzymes become prematurely activated within the pancreatic tissue, leading to autodigestion and tissue damage. The activation of enzymes is thought to occur due to a disruption in the protective mechanisms that normally prevent their activation.
Inflammatory Response: The release of activated pancreatic enzymes triggers an intense inflammatory response within the pancreas. This inflammatory response involves the recruitment and activation of immune cells, such as neutrophils and macrophages, which release pro-inflammatory cytokines and chemokines. These inflammatory mediators further amplify the inflammatory response and contribute to tissue damage.
Several factors can contribute to the development of acute pancreatitis. The most common causes include gallstones and alcohol abuse. However, there are also other less common etiologies that should be considered in critically ill patients.
Laboratory evaluation typically includes measurement of serum amylase and lipase levels. Elevated levels of these enzymes are suggestive of pancreatic injury, although they lack specificity and can be elevated in other conditions such as renal failure or perforated peptic ulcer. Serum amylase levels usually rise within 6-24 hours of symptom onset and return to normal within 3-7 days. Lipase levels remain elevated for a longer duration and are considered more specific for pancreatitis.
Imaging studies play a crucial role in confirming the diagnosis of acute pancreatitis and assessing the severity of the disease.
Abdominal ultrasound is often the initial imaging modality of choice, as it is readily available and can detect gallstones, which are a common cause of pancreatitis. It can also identify other findings suggestive of pancreatitis, such as pancreatic edema or peripancreatic fluid collections. However, ultrasound has limitations in visualizing the pancreas in obese patients or in cases of bowel gas interference.
Computed tomography (CT) scan is the gold standard imaging modality for the diagnosis and staging of acute pancreatitis. It can provide detailed information about the extent of pancreatic inflammation, the presence of necrosis, and the development of complications such as pseudocysts or abscesses. CT scan findings can help guide management decisions, such as the need for surgical intervention or percutaneous drainage.
Endoscopic retrograde cholangiopancreatography (ERCP) may be indicated in patients with suspected biliary pancreatitis or in those with evidence of biliary obstruction on imaging studies. ERCP can both diagnose and treat the underlying cause of pancreatitis, such as gallstone impaction in the common bile duct.
Fluid resuscitation is crucial in the management of acute pancreatitis as patients often present with significant intravascular volume depletion due to third-spacing of fluids. Aggressive fluid resuscitation with crystalloids is recommended to maintain adequate tissue perfusion and prevent organ dysfunction. Close monitoring of fluid balance, urine output, and hemodynamic parameters is essential to guide fluid therapy and prevent fluid overload.
Intravenous antibiotics are not routinely recommended in the management of uncomplicated acute pancreatitis. However, in cases of infected pancreatic necrosis or other evidence of infection, broad-spectrum antibiotics should be initiated promptly to cover the likely pathogens, including gram-negative and anaerobic bacteria. Acute pancreatitis can lead to various complications, including pancreatic pseudocysts, pancreatic abscesses, infected necrosis, and organ failure. These complications can significantly impact the prognosis of patients with acute pancreatitis and may require additional interventions such as drainage procedures or surgical debridement.
Resources to complete: