Week 7 Flashcards
Upper GI bleeds
Patients with acute upper gastrointestinal (GI) bleeding commonly present with hematemesis (vomiting of blood or coffee-ground-like material) and/or melena (black, tarry stools). also postural hypotension, anaemia, petechiae or buccal/facial telangiectasia. The initial evaluation of patients with acute upper GI bleeding involves an assessment of hemodynamic stability and resuscitation if necessary. Diagnostic studies (usually endoscopy) follow.
Hematochezia (red or maroon blood in the stool) is usually due to lower GI bleeding. However, it can occur with massive upper GI bleeding, which is typically associated with orthostatic hypotension.
Potential bleeding sources suggested by a patient’s past medical history include:
●Varices or portal hypertensive gastropathy in a patient with a history of liver disease or excess alcohol use
●Aorto-enteric fistula ( direct communication between aorta and intestinal lumen) in a patient with a history of an abdominal aortic aneurysm or an aortic graft
●Angiodysplasia in a patient with renal disease, aortic stenosis, or hereditary haemorrhagic telangiectasia
●Peptic ulcer disease in a patient with a history of Helicobacter pylori (H. pylori) infection, nonsteroidal anti-inflammatory drug (NSAIDs) use, antithrombotic use, or smoking
●Malignancy in a patient with a history of smoking, excess alcohol use, or H. pylori infection
●Marginal ulcers (ulcers at an anastomotic site) in a patient with a gastroenteric anastomosis (proximal intestine removal)
Peptic ulcer – Upper abdominal pain
●Esophageal ulcer – Odynophagia, gastroesophageal reflux, dysphagia
●Mallory-Weiss tear – Emesis, retching, or coughing prior to hematemesis
●Variceal hemorrhage or portal hypertensive gastropathy: Jaundice, abdominal distention (ascites)
●Malignancy – Dysphagia, early satiety, involuntary weight loss, cachexia
Acid suppression for upper GI bleed
Acid suppression stops rebleeding — Patients admitted to the hospital with acute upper GI bleeding are typically treated with a proton pump inhibitor (PPI). The optimal approach to PPI administration prior to endoscopy is unclear. Options include giving an IV PPI every 12 hours or starting a continuous infusion. Our approach is to give a high-dose bolus (eg, esomeprazole 80 mg) to patients with signs of active bleeding (eg, hematemesis, hemodynamic instability).
Management of upper GI bleeds
Pre-endoscopic management – Prior to endoscopy, patients should receive general supportive measures, including:
- Provision of supplemental oxygen by nasal cannula
- Nothing per mouth
- Two large caliber (18 gauge or larger) peripheral catheters or a central venous line
Nasogastric lavage is NOT a routine part of the management of acute upper GI bleeding.
●Pharmacologic therapy – Medications that should be started prior to endoscopy include a proton pump inhibitor, erythromycin, antibiotics (for patients with cirrhosis), and somatostatin or one of its analogs (for patients with suspected variceal bleeding).
•We suggest that patients admitted to the hospital with acute upper GI bleeding receive an IV proton pump inhibitor (PPI) (Grade 2B). The optimal approach to PPI administration prior to endoscopy is unclear. Our approach is to give a high-dose bolus (eg, esomeprazole 80 mg) to patients with signs of active bleeding (eg, hematemesis, hemodynamic instability). If endoscopy is delayed beyond 12 hours, a second dose of an IV PPI should be given (eg, esomeprazole 40 mg). For patients who may have stopped bleeding (eg, patients who are hemodynamically stable with melena), we give an IV PPI every 12 hours (eg, esomeprazole 40 mg). Subsequent dosing will then depend on the endoscopic findings.
We suggest that erythromycin be given prior to endoscopy to help improve visualization (Grade 2C). A reasonable dose is 250 mg intravenously over 20 to 30 minutes, 30 to 90 minutes prior to endoscopy. Patients receiving erythromycin need to be monitored for QTc prolongation. In addition, drug-drug interactions should be evaluated before giving erythromycin because it is a cytochrome P450 3A inhibitor.
- Patients with cirrhosis who present with acute upper GI bleeding (from varices or other causes) should be given prophylactic antibiotics.
- Somatostatin, its analog octreotide, or terlipressin should be started if variceal bleeding is suspected.
●Blood transfusion – Transfusion is guided by the haemoglobin level and the presence of comorbid conditions:
- The decision to initiate blood transfusion must be individualized (algorithm 1 and table 2). Our approach is to initiate blood transfusion if the hemoglobin is <7 g/dL (70 g/L) for most patients. Higher transfusion thresholds may be indicated for patients at increased risk of adverse events in the setting of significant anemia or those with coronary artery disease. (See “Indications and hemoglobin thresholds for red blood cell transfusion in the adult”, section on ‘Overview of our approach’.)
- It is important to avoid overtransfusion in patients with suspected variceal bleeding because transfusion can precipitate worsening of the bleeding; the blood transfusion goal for variceal bleeding is <7 g/dL (70 g/L).
- For patients with active/brisk bleeding and hypovolemia, decisions about transfusion are guided by hemodynamic parameters (eg, pulse and blood pressure), the pace of the bleeding, estimated blood loss, and the ability to stop the bleeding, rather than by serial hemoglobin measurements.
●Anticoagulants, antiplatelet agents, and coagulopathies – The approach to management of anticoagulants and antiplatelet agents depends on the specific medications being used, the reason they are being used, and how quickly reversal of anticoagulation is needed. Management of coagulopathy depends on the underlying etiology. Hematology input may be advisable.
●Endoscopy – We recommend upper endoscopy within 24 hours for the evaluation and management of patients admitted with acute upper GI bleeding. For patients with suspected variceal bleeding, we perform endoscopy within 12 hours of presentation.
Additional diagnostic tests may be required for some patients. An algorithm providing an overview of the diagnostic approach to patients with suspected upper gastrointestinal bleeding is provided.
●Treatment of the underlying lesion – The approaches to achieve hemostasis for variceal bleeding and bleeding peptic ulcers are discussed separately.
Ulcerative colitis
Ulcerative colitis is characterised by diffuse mucosal inflammation limited to the colon. It is relapsing and remitting. “Distal” disease refers to colitis confined to the rectum (proctitis) or rectum and sigmoid colon (proctosigmoiditis). More extensive disease includes “left sided colitis” (up to the splenic flexure), “extensive colitis” (up to the hepatic flexure), and pancolitis (affecting the whole colon). Sometimes might affect terminal ileum in cases of pancolitis bc incompetent ileocecal valve. Opposite to crohns, smoking decreases risk.
The cardinal symptom of UC is bloody diarrhoea. Associated symptoms of colicky abdominal pain, urgency, or tenesmus may be present. If proctitis will have constipation and rectal bleed. Fever, weight loss, may have tachycardia and hypotension in acute flare.
tenderness, distention, mass. Risk of toxic megacolon. May relate to pyoderma gangrenosum and anterior uveitis. UC is a severe disease that used to carry a high mortality and major morbidity.
Crohn’s disease
Crohn’s disease is characterised by patchy, transmural granulomatous inflammation, which may affect any part of the gastrointestinal tract. It may be defined by location (terminal ileal, colonic, ileocolic, upper gastrointestinal), or by pattern of disease (inflammatory, fistulating, or stricturing). These variables have been combined in the Vienna classification. Also can be termed indeterminate colitis (IC). Gaps are known as skip lesions. Familial link. Average onset age is 15-30 or 50-70. Smoking makes it more likely or worse. Infections and NSAIDS contribute.
Symptoms of CD are more heterogeneous, but typically include abdominal pain, diarrhoea (sometimes bloody and chronic), and weight loss. Systemic symptoms of malaise, anorexia, or fever are more common with CD than UC. CD may cause intestinal obstruction due to strictures, fistulae (often perianal), or abscesses.
Children might grow slowly. Patients on a flare may present anaemic, hypotensive, tachycardic, pyrexia, abdominal mass, ulcers and anal lesions. Extra intestinal signs include clubbing, erythema nodosum, irisitis, arthritis, pyoderma gangrenosum, akylosing spondylitis, fatty liver, cholangitis, cholangiocarcinoma, granulomata, osteomalacia, amyloidosis, calculi.
Both ulcerative and Crohn’s colitis are associated with an increased risk of colonic carcinoma. In CD surgery is not curative and management is directed to minimising the impact of disease. At least 50% of patients require surgical treatment in the first 10 years of disease.
IBD investigations
Sigmoidoscopy
For all patients presenting with diarrhoea, rigid sigmoidoscopy should be performed unless there are immediate plans to perform flexible sigmoidoscopy. Macroscopic features of UC are loss of the vascular pattern, granularity, friability, and ulceration of the rectal mucosa. A rectal biopsy is best taken for histology even if there are no macroscopic changes.
Colonoscopy
For mild to moderate disease, colonoscopy is usually preferable to flexible sigmoidoscopy, because the extent of disease can be assessed, but in moderate to severe disease there is a higher risk of bowel perforation and flexible sigmoidoscopy is safer. It is appropriate to defer investigations until the clinical condition improves. For suspected CD, colonoscopy to the terminal ileum and small bowel barium studies to define extent and site of disease are appropriate. A terminal ileal biopsy performed at colonoscopy documents the extent of examination and may find microscopic evidence of CD.
Other investigations
Double contrast barium enema is usually inferior to colonoscopy because it does not allow mucosal biopsy and may underestimate the extent of disease. Small bowel radiology by follow through or intubation (small bowel enema) is the current standard for assessing the small intestine. Other conditions (including tuberculosis, Behcet’s, lymphoma, vasculitis) may also cause ileal disease. The role of capsule endoscopy is at present unclear. White cell scanning is a safe, non-invasive investigation, but lacks specificity. Ultrasound in skilled hands is a sensitive and non-invasive way of identifying thickened small bowel loops in CD and may identify abscesses or free fluid in the peritoneum. Computed tomography and magnetic resonance imaging, especially of the perineum, help evaluate activity and complications of disease. Laparoscopy may be necessary in selected patients, especially where the differential diagnosis of intestinal tuberculosis is being considered.
FBC, GFR, UE, LFT, ESR, CRP, iron, B12, folate, faecal calprotectin, stool sample for clostridium difficile, often low magnesium and albumin. PANCA in UC, ASCA marker in crohns.
Crohns = cobblestone appearance, ulcerative colitis = red/bleeding fissures.
Ulcerative colitis treatment
Leukophorems/ removal from blood. Avoid antimobility drugs like cardipine, loperamide and antispasmordics- precipitates paralytic ileus and megacolon in those with active phase disease.
Give aminosalicylates like mesalazine 5asa as maintains remission and lowers risk of cancer.
Olsalazine has fewer side effects but diarrhoea is more common- best for left sided uc.
Azathioprine or corticosteroid like prenisolone makes remission. Ciclosporin is the rescue drug for severe refractory colitis. Can also give vedolizumab if extreme.
Crohns treatment
Give either prednisolone, methylprednisolone and iv hydrocortisone.
Adding azathioprine or mercapatopumine to induce remission.
Coeliac Disease
Gluten and prolamine- inflammatory disorder leading to malabsorption. Multigenetic disorder- associated with HLA-DQ2 or DQ8. 1/100.
Might have faltered growth, fatigue, weight loss, mouth ulcers, iron or B deficiency, type 1 diabetes, autoimmune thyroid disease, IBS, metabolic bone disorder, peripheral neuropathy or ataxia, subfertility/miscarriage, raise LFTs, Dental enamel defects, Downs syndrome, turner syndrome.
Often presents with dermatitis herpetiformis, epilepsy, dementia or depression too,
There’s TTG marker for coeliacs and endomysial antibody ema.
Appendicitis
Infection and inflammation of the appendix- common symptoms are abdominal pain, loss of appetite, nausea, vomiting, fever.
It’s caused by blockage of the appendix followed by an invasion of bacteria of the wall of the appendix. Has RLQ pain that was originally central. Common complications= rupture, abscess and peritonitis.
Tests could be FBC, WBC, UE, abxray, barium enema, US, CT, laparoscopy.
Treatments are antibiotics (piperacillin or tazobactam with cefotetan and cefotaxime) and appendectomy.
Dieulafoy lesion
An abnormally large artery in the lining of the GI system. Most commonly in the stomach but also occurs in the SI and LI. Can cause severe and sudden GI bleeding. May give hematemesis, melena, hematochezia, hemoptysis.
May not cause symptoms until the lining of the organ wears away. Until then may only have signs via blood pressure. Associations between it and NSAIDS, alcohol, prior GI surgery.
Treatment is endoscope guided closure and embolism.
Helicobacter pylori
Most common cause of peptic ulcers 95% of duodenals and 70-80% of gastrics. With acute and chronic gastritis, gastric cancer and gastric mucosa associated lymphoid tissue lymphoma.
Tests= urea 13c breath test, stool helicobacter antigen test, lab serology.
Treatment is triple therapy like PPI and amoxicillin and clarithromycin or metronidazole.
Granuloma
A granuloma is an aggregation of macrophages that forms in response to chronic inflammation. This occurs when the immune system attempts to isolate foreign substances.
Diseases with it includes: Tuberculosis Leprosy Schistosomiasis Histoplasmosis Cryptococcosis Cat-scratch disease Rheumatic fever Sarcoidosis Crohn's disease Listeria monocytogenes Leishmania spp. Pneumocystis pneumonia Aspiration pneumonia Rheumatoid arthritis Granuloma annulare Foreign-body granuloma Childhood granulomatous periorificial dermatitis
Occurrence of GI ulcers
Duodenal ulcers occur for the first time usually between the ages of 30 and 50. Stomach ulcers are more likely to develop in people over age 60. Duodenal ulcers occur more frequently in men than women; stomach ulcers develop more often in women than men.
Symptoms of GI ulcers
The most common ulcer symptom is a gnawing or burning pain in the abdomen between the breastbone and the navel. The pain often occurs between meals and in the early hours of the morning. It may last from a few minutes to a few hours and may be relieved by eating or by taking antacids.
Less common ulcer symptoms include nausea, vomiting, and loss of appetite and weight. Bleeding from ulcers may occur in the stomach and duodenum. Sometimes people are unaware that they have a bleeding ulcer, because blood loss is slow and blood may not be obvious in the stool. These people may feel tired and weak. If the bleeding is heavy, blood will appear in vomit or stool. Stool containing blood appears tarry or black.
Diagnosing ulcers, such as performing endoscopic and x-ray examinations, and for testing for H. pylori
Treating GI ulcers
Doctors treat stomach and duodenal ulcers with several types of medicines including H2-blockers, acid pump inhibitors, and mucosal protective agents. When treating H. pylori, these medications are used in combination with antibiotics.
H2-blockers
Currently, most doctors treat ulcers with acid-suppressing drugs known as H2-blockers. These drugs reduce the amount of acid the stomach produces by blocking histamine, a powerful stimulant of acid secretion.
H2-blockers reduce pain significantly after several weeks. For the first few days of treatment, doctors often recommend taking an antacid to relieve pain.
Initially, treatment with H2-blockers lasts 6 to 8 weeks. However, because ulcers recur in 50 to 80 percent of cases, many people must continue maintenance therapy for years. This may no longer be the case if H. pylori infection is treated. Most ulcers do not recur following successful eradication.H2-blockers that are approved to treat both stomach and duodenal ulcers are:
Cimetidine (Tagamet®)
Ranitidine (Zantac®)
Famotidine (Pepcid®).
Acid pump inhibitors
Like H2-blockers, acid pump inhibitors modify the stomach’s production of acid. However, acid pump inhibitors more completely block stomach acid production by stopping the stomach’s acid pump–the final step of acid secretion. The FDA has approved use of omeprazole for short-term treatment of ulcer disease. Similar drugs, including lansoprazole, are currently being studied.
Mucosal protective medications
Mucosal protective medications protect the stomach’s mucous lining from acid. Unlike H2-blockers and acid pump inhibitors, protective agents do not inhibit the release of acid. These medications shield the stomach’s mucous lining from the damage of acid. Two commonly prescribed protective agents are:
Sucralfate (Carafate®). This medication adheres to the ulcer, providing a protective barrier that allows the ulcer to heal and inhibits further damage by stomach acid. Sucralfate is approved for short-term treatment of duodenal ulcers and for maintenance treatment.
Misoprostol (Cytotec®). This synthetic prostaglandin, a substance naturally produced by the body, protects the stomach lining by increasing mucus and bicarbonate production and by enhancing blood flow to the stomach. It is approved only for the prevention of NSAID-induced ulcers.
If H.pylori: Metronidazole 4 times a day
Tetracycline (or amoxicillin) 4 times a day
Bismuth subsalicylate 4 times a day
Acute liver failure
Acute liver failure (ALF) is a rapid decline in hepatic function characterised by jaundice, coagulopathy (INR >1.5), and hepatic encephalopathy in patients with no evidence of prior liver disease.
ALF may be classified as hyperacute, acute, or subacute, depending on the interval from the onset of jaundice to the development of encephalopathy.
Key diagnostic factors presence of risk factors hepatotoxic medication jaundice signs of hepatic encephalopathy
Other diagnostic factors absence of history of chronic liver disease abdominal pain nausea vomiting
Risk factors chronic alcohol abuse poor nutritional status female sex age >40 years
Investigations: liver function tests prothrombin time/INR basic metabolic panel FBC
Investigations to consider viral hepatitis polymerase chain reaction (PCR) studies serum ceruloplasmin serum copper 24-hour urinary copper excretion
Acute liver failure treatments
For hypotension and acute kidney injury, the goal of treatment is maximizing tissue perfusion. Treatment includes IV fluids and usually, until sepsis is excluded, empiric antibiotics. If hypotension is refractory to about 20 mL/kg of crystalloid solution, clinicians should consider measuring pulmonary capillary wedge pressure to guide fluid therapy. If hypotension persists despite adequate filling pressures, clinicians should consider using pressors (eg, dopamine, epinephrine, norepinephrine).
For encephalopathy, the head of the bed is elevated 30° to reduce risk of aspiration; intubation should be considered early. When selecting drugs and drug doses, clinicians should aim to minimize sedation so that they can monitor the severity of encephalopathy. Propofol is the usual induction drug for intubation because it protects against intracranial hypertension and has a brief duration of action, allowing rapid recovery from sedation. Lactulose can cause ileus and produce gas that distends the intestines, which can be problematic if laparotomy is needed (eg, for liver transplantation)
To avoid sudden increases in ICP and avoid decreasing cerebral perfusion pressure: Stimuli that could trigger a Valsalva maneuver are avoided (eg, lidocaine is given before endotracheal suctioning to prevent the gag reflex).
To temporarily decrease cerebral blood flow: Mannitol (0.5 to 1 g/kg, repeated once or twice as needed) can be given to induce osmotic diuresis, and possibly brief hyperventilation can be used, particularly when herniation is suspected. (However, mannitol is contraindicated with acute kidney injury and serum osmolality must be checked before giving a second dose.)
Goals of treatment are an ICP of < 20 mm Hg and a cerebral perfusion pressure of > 50 mm Hg.
Seizures are treated with phenytoin; benzodiazepines are avoided or used only in low doses because they cause sedation.
Infection is treated with antibacterial and/or antifungal drugs; treatment is started as soon as patients show any sign of infection (eg, fever; localizing signs; deterioration of hemodynamics, mental status, or renal function). Because signs of infection overlap with those of acute liver failure, infection is likely to be overtreated pending culture results.
Electrolyte deficiencies may require supplementation with sodium, potassium, phosphate, or magnesium.
Hypoglycemia is treated with continuous glucose infusion (eg, 10% dextrose), and blood glucose should be monitored frequently because encephalopathy can mask the symptoms of hypoglycemia.
Coagulopathy is treated with fresh frozen plasma if bleeding occurs, if an invasive procedure is planned, or possibly if coagulopathy is severe (eg, international normalized ratio [INR] > 7). Fresh frozen plasma is otherwise avoided because it may result in volume overload and worsening of cerebral edema. Also, when fresh frozen plasma is used, clinicians cannot follow changes in PT, which are important because PT is an index of severity of acute liver failure and is thus sometimes a criterion for transplantation. Recombinant factor VII is sometimes used instead of or with fresh frozen plasma in patients with volume overload. Its role is evolving. H2 blockers may help prevent gastrointestinal bleeding.
Nutritional support may be necessary if patients cannot eat. Severe protein restriction is unnecessary; 60 g/day is recommended.
Acute acetaminophen toxicity is treated with N-acetylcysteine. Because chronic acetaminophen toxicity can be difficult to diagnose, use of N-acetylcysteine should be considered if no cause for acute liver failure is evident.
May also give a liver transplant.
Shock
Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death. Mechanisms may involve decreased circulating volume, decreased cardiac output, and vasodilation, sometimes with shunting of blood to bypass capillary exchange beds. Symptoms include altered mental status, tachycardia, hypotension, and oliguria. Diagnosis is clinical, including blood pressure measurement and sometimes measurement of markers of tissue hypoperfusion (eg, blood lactate, base deficit). Treatment is with fluid resuscitation, including blood products if necessary, correction of the underlying disorder, and sometimes vasopressors.
Pathophysiology of shock
Pathophysiology of Shock
The fundamental defect in shock is reduced perfusion of vital tissues. Once perfusion declines and oxygen delivery to cells is inadequate for aerobic metabolism, cells shift to anaerobic metabolism with increased production of carbon dioxide and elevated blood lactate levels. Cellular function declines, and if shock persists, irreversible cell damage and death occur.
During shock, both the inflammatory and clotting cascades may be triggered in areas of hypoperfusion. Hypoxic vascular endothelial cells activate white blood cells, which bind to the endothelium and release directly damaging substances (eg, reactive oxygen species, proteolytic enzymes) and inflammatory mediators (eg, cytokines, leukotrienes, tumor necrosis factor). Some of these mediators bind to cell surface receptors and activate nuclear factor kappa B (NFκB), which leads to production of additional cytokines and nitric oxide (NO), a potent vasodilator.
