Acute upper gastrointestinal (GI) bleeding

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A Case Presentation Of An Acute Gastrointestinal (GI) Bleed Due To The Use Of Nonsteroidal Anti-Inflammatory Drugs(NSAIDS).

Acute upper gastrointestinal (GI) bleeding is one of the most common medical emergencies and most cases require urgent medical assessment. Half of all the cases are due to peptic ulcer.After emergency hospital admission, the main goal is to support the circulation of the shocked patient rather than to identify the source of bleeding. It is vital that all nurses are fully aware of the signs, symptoms, and management of acute upper GI bleeding (Smith, 2004, p. 40).
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Pathophysiology of acute upper GI bleeding

Acute GI bleed as a result of excessive NSAIDs use is mostly due to inflammation of the gastric mucosa resulting in gastritis and the formation of peptic ulcers and in some cases duodenal ulcers.The pathophysiology of an acute GIbleed as a result of NSAID use is as follows; NSAIDs and some other drugs such as aspirinare known to inhibit the biosynthesis of prostaglandins. Due to this inhibitionthere is a decrease in sub-mucosal blood flow, suppression of secretion of mucus and bicarbonate, and gastric acid secretion is enhanced. This results in decreased pH and increased acidity in the stomach or duodenum resulting in mucosal irritation and/or inflammation.In majority of the cases,acid hypersecretion of the gastric acid, by itself, is not the primary reason to cause ulcers. In most of the patients with peptic ulcers, factors in addition to gastric acid need to be present to cause an ulcer. Additionally, NSAIDs can have a direct effect on the mucosa that can result in mucosal irritation (Lehne,2012,p. 986). Our female patient had a significant history of high dose NSAIDs use to alleviate severe dental painthat contributed to the patient’s admitting diagnosis of gastritis and possible peptic ulcer secondary to the usage of NSAIDS.

The risk factors contributing to diagnosesin our patient were vomiting of large quantities of dark brown liquid followed by dark brown liquid diarrhea after a month long use of high dose of NSAIDS.Furthermore, the patient’s admission physical assessment suggested that she was pale(anemic/shock),blood pressure(BP) was102/55(In young, athletic and or pregnant females the systolic blood pressure could be normal), she was tachycardic (pulse>110bpm). JVP was not mentioned in the case history.The respiratory rate was 26-28 breaths/min suggesting she was hyperventilating.SaO2 values (96%) suggested normal oxygen saturation in her blood.

The clinical signs and symptoms of pathology that warranted close monitoring in our patient washypovolemia and recurrence of bleeding. For that purpose patient was given IV fluids, her BP, CVP and urine output was closely monitored. Hemoglobin(Hb) had to be >10g/dl for that purpose transfusion was given. AdditionallyProton pump inhibitors (PPIs) omeprazole 40mg IV was started.Fluid replacement was monitored as dictated by BP, CVP,and urine output. Initially hourly then the frequency is decreased to 4hrly if patient is haemodynamically stable(Longmore, 2007, p.244).The patient did not require high flow oxygen as her SaO2 values(96%) were well within normal limits. Furthermore,table.1 displays additional management for hypovolemic shock and upper GI bleeding to manage and stabilize the patient.
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A risk assessment score (Rockall score) had been established for patients with acute GI bleeding. A series of independent risk factors is scored and the total score predicts clinical outcome.

Laboratory and test values

Table.2Lab assessments

Laboratory TestsValueReference Range Adults
Hematocrit (%)19.437.0-47.0
Hemoglobin (g/dl)7.212.0-15.0
White blood count (x 103/µL)9.84.8-10.8
Blood urea nitrogen (BUN) mg/ml278-21
Platelet (x 103 / µL)223150-400

 

The lab values in table.2suggest that our patient’s hematocrit, hemoglobin and BUN values were out of range. This is a classic case of upper GI bleed,however, the other labs includingprothrombin time, international normalized ratio, creatinine, sodium, potassium, phosphorus, magnesium, calcium, total protein, albumin, were all within normal ranges.The low hemoglobinvalue suggests decreased tissue perfusion and oxygen-carrying capability, which can affect every organ system in the body(Praskash& Zuckerman, 2003, p.330).That is why acute upper GI bleeding calls for vigilant nursing assessment and intervention.The lab values that would need close monitoring in this patient will be FBC, U&E,LFT,and blood clotting. Any changes would require adjustment in management plans.A patient who is bleeding slowly may have a very low haematocrit, yet have no change in vital signs (Hines, 2000, p. 20).

The elevated BUN level and normal creatinine level in this patient suggested an upper GI bleeding source.Hypovolemia due to acute blood loss causes a rise in BUN; however other factors such as digestion of blood proteins in the small intestine, the absorption of nitrogenous waste products, and dehydration can also lead to rise in BUN levels(Avunduk, 2008,p.85).

The Coombs’ test is used to detect antibodies that act against the surface ofan individual red blood cells. The presence of these antibodies indicates a condition known as hemolyticanemia, in which the blood does not contain enough red blood cells because they are destroyed prematurely.There are two types of Coombs’ tests: direct and indirect. The direct Coombs’ test, also known as the direct antiglobulin test, is the test usually used to identify hemolyticanemia(“Coombs’ test,” 2009,n.p.).

This autoimmune hemolyticanemia could be the reason our patient had a complicated delivery with hemorrhage that same pregnancy requiring hysterectomy and multiple transfusions in the past.

Medication Management.Acetaminophen, ibuprofen, and,vicoprofen belong to a group of drugs known as NSAIDs.As previously mentioned NSAIDS act by inhibiting the biosynthesis of prostaglandins.In doing so they can decrease submucosal blood flow, suppress secretion of mucus and bicarbonate, and promote secretion of gastric acid. Additionally, NSAIDs can irritate the mucosa directly. NSAID-induced ulcers are most likely with long-term, high-dose therapy(Lehne, 2012, p. 986).

Prophylaxis.For patients with risk factors for ulcer development (e.g., age over 60, history of ulcers, high-dose NSAID therapy), prophylactic therapy is indicated. Histamine2 receptor blockers and proton pump inhibitors are preferred. If possible, the offending NSAID should be discontinued, so as to accelerate healing. According to the author if the NSAID cannot be discontinued, a proton pump inhibitor is the best choice to promote healing(Lehne, 2012, p. 987).

Mechanism of action.Omeprazole is a prodrug that undergoes conversion to its active form within parietal cells of the stomach. The active form then causes irreversible inhibition of H1,K 1-ATPase (proton pump), the enzyme that generates gastric acid.Because it blocks the final common pathway of gastric acid production, omeprazole can inhibit basal and stimulated acid release. Partial recovery occurs 3 to 5 days after stopping treatment. Full recovery may take weeks(Lehne, 2012, p. 992).

Side effects of omeprazole.Headache,diarrhea, nausea, vomiting,Pneumonia(alteration of upper GI flora (owing to reduced gastric acidity) and impairment of white blood cell function), fractures in long-term therapy, especially in high doses, rebound Acid hypersecretion,hypomagnesaemia with long-term use, Clostridium difficile Infection and gastric cancer.The prescribeddose of 40 mg IV bid is within the normal range for acute GI bleed prophylaxis for this patient since this patient is not been given a bolus dose.There is no evidence that high-dose I.V. PPI therapy is beneficial in patients with GI bleeding from an ulcer that has a low risk of rebleeding (i.e., a clean-based ulcer on endoscopy). In these patients, oral PPI therapy can be instituted after the patient has recovered from the endoscopy. (Lauritsen,1985; McFarland, 1990; Marks, 1991).Sertraline (Zoloft) blocks reuptake of 5-HT, relieve symptoms of major depression,causes CNS stimulation rather than sedation, andhave minimal effects on seizure threshold and the electrocardiogram (ECG).

Mechansim of action.Sertraline is slowly absorbed following oral administration. Food increases the extent of absorption. In the blood, the drug is highly bound (99%) to plasma proteins. Sertraline undergoes extensive hepatic metabolism followed by elimination in the urine and faeces. The plasma half-life is approximately 1 day(Lehne, 2012, p. 362).

Side effects of sertraline.Headache, tremor, insomnia, agitation, nervousness, nausea diarrhea, weight gain and sexual dysfunction are some of this drugs side effect. Treatment may also increase the risk of suicide. Because of the risk of serotonin syndrome, sertraline must not be combined with MAOIs and other serotonergic drugs.mg/mL). To initially treat depression, the adult daily dosage is 50 mg, administered in the morning or evening. After 4 to 8 weeks, the dosage may be increased by 50-mg increments to a maximum of 200 mg/day. When discontinuing the drug, dosage should be reduced gradually. However it can be taken with vitamins(Lehne, 2012, p. 362).Our patient would need drug counselling and her anxiety and drug related queries should be addressed such that she should not be discouraged to take NSAIDS in the near future, however she should be advised not to take high quantities or dosage of NSAIDs as it could lead to recurrence of ulcers.

Nursing Interventions in support of plan of care

In our case the patient hadpositive direct Coomb’s test for warm autoantibodies and the hospital was preparing 2 units of leukoreduced packed red cells for transfusion.Leukoreduced red Blood cell units contain leukocytes in a specifically reduced amount. In the United States, Blood processing centers use filtration to make leukoreduced red Blood cell units. Indications are for patients who have experienced two or more non-haemolytic febrile transfusion reactions. They are usually effective in preventing non-haemolytic febrile transfusion reactions for most patients and prevention of CMV transmission or HLA alloimmunization (“Leukoreduced red blood cells,” 2013,n.p.). If there is a transfusion reaction blood samples from the person getting the transfusion and from the donor are tested to find thecause and transfusion can be stopped.Mild symptoms such as back pain,bloody urine, chills, fainting, fever and flushing of the skin may be treated with Acetaminophen, and fluids given through a vein (intravenous) and other medicines to treat or prevent kidney failure and shock(“Transfusion reaction,”2015, n.p.). Additionally the patient is vigilantly monitored and evaluated constantly as mentioned in table 3.

Table.3.Montioring and Evaluation of patient while undergoing blood transfusion (“Blood transfusion therapy,”2015, n.p.)

  1. The patient maintains normal breathing pattern.
  1. The patient demonstrates adequate cardiac output.
  1. The patient reports minimal or no discomfort.
  1. The patient maintains good fluid balance.
  1. The patient remains normothermic.
  1. The patient remains free of infection.
  1. The patient maintains good skin integrity, with no lesions or pruritus.
  1. The patient maintains or returns to normal electrolyte and blood chemistry values.
 

Once all these measures are undertaken and the patient is stable while she undergoes endoscopy a good prognosis can be anticipated.

References:

  1. Avunduck, C. (2008). Manual of Gastroenterology: Diagnosis and Therapy (4thed). (Lippincott Manual Series (Formerly known as the Spiral Manual Series)).
  2. Blood transfusion therapy. (2015).www.nursingcrib.com. Retrieved from: http://nursingcrib.com/nursing-notes-reviewer/blood-transfusion-therapy/.
  3. Coombs’ test. (2009).Medline Plus. US National Library of Medicine and National Institutes of Health. Retrieved from: http://www.nlm.nih.gov/MEDLINEPLUS/ency/article/003344.htm
  4. Delle F-G, Annibale B, Franceschi M, Quatrini M, Cassetta MR, Torsoli A.(1992). Omeprazole versus famotidine in the short-term treatment of duodenal ulcer disease. Aliment PharmacolTher, 6:469-78.
  5. Hines, S. E. (2000). Current management of upper GI tract bleeding. Patient Care, 30(2), 20.
  6. Hotz J, Kleinert R, Grymbowski T, Hennig U, Schwarz JA.(1992). Lansoprazole versus famotidine: efficacy and tolerance in the acute management of duodenal ulceration. Aliment PharmacolTher, 6:87-95.
  7. Lauritsen K, Rune SJ, Bytzer P, Kelbaek H, Jensen KG, Rask M-J,et al.(1985). Effect of omeprazole and cimetidine on duodenal ulcer. A double-blind comparative trial. N Engl J Med, 312:958-61.
  8. Lehne, R.A. (2012). Pharmacology for Nursing Care (8th ed.). St.Louis, MO. Elsevier.
  9. Leukoreduced red blood cells.(2013).www.bloodbank.com. Retrieved from: http://www.bloodbook.com/products.html#Leukoreduced.
  10. Longmore, J. M. (2007). Oxford handbook of clinical medicine. Oxford: Oxford University Press.
  11. Marks IN, Danilewitz MD, Garisch JA. (1991). Omeprazole 20 mg qd and ranitidine 150 mg bid in the treatment of benign gastric ulcer. Italian Cooperative Group on Omeprazole. Hepatogastroenterology, 38:400-3.
  12. McFarland RJ, Bateson MC, Green JR, O’Donoghue DP, Dronfield MW, Keeling PW,et al. (1990). Omeprazole provides quicker symptom relief and duodenal ulcer healing than ranitidine. Gastroenterology, 98:278-83.
  13. Praskash, C., & Zuckerman G. R. (2003). Acute small bowel bleeding: A distinct entity with significantly different economic implications compared with GI bleeding from other locations. GastrointEndosc, 58(3), 330.
  14. Smith, G.D. (2004).The management of upper gastrointestinal bleeding. Nursing Times,100: 26, 40-43.
  15. Transfusion reaction. (2015).www.nlm.nih.gov. Retrieved from: http://www.nlm.nih.gov/medlineplus/ency/article/001303.htm

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