upper gi - Nursing Case Study

Pathophysiology

• Primary mechanism: Acid secretion imbalance in the stomach leads to mucosal damage. Parietal cells overproduce hydrochloric acid due to stimuli like stress, NSAID use, or Helicobacter pylori infection, compromising the protective mucosal barrier and causing gastritis or peptic ulcers.

• Secondary mechanism: Impaired mucosal defenses fail to neutralize gastric acid, exacerbating tissue damage. Bicarbonate secretion and mucus production decrease, further reducing the stomach's ability to protect itself against acidic injury.

• Key complication: Chronic exposure to gastric acid can result in peptic ulcer disease, characterized by deep lesions in the gastric or duodenal lining, which may lead to bleeding, perforation, or gastric outlet obstruction if untreated.

Patient Profile

Demographics:

56-year-old male, construction worker

History:

• Key past medical history: Chronic gastritis, hypertension, type 2 diabetes

• Current medications: Omeprazole, Lisinopril, Metformin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Persistent abdominal pain and nausea

• Key symptoms: Epigastric pain, bloating, intermittent vomiting, melena, fatigue

• Vital signs: Blood pressure 148/92 mmHg, heart rate 105 bpm, respiratory rate 22 breaths/min, temperature 99.1°F, oxygen saturation 95% on room air

Section 1

During the initial assessment, the clinical team noted that the patient's abdominal pain was localized to the epigastric region and intensified after meals. Physical examination revealed mild tenderness upon palpation of the upper abdomen, without guarding or rebound tenderness, suggesting potential peptic ulcer involvement rather than acute perforation. Auscultation of bowel sounds was normal, but the patient's intermittent vomiting and melena raised concerns about potential upper GI bleeding. The patient's vital signs indicated a mildly elevated blood pressure of 148/92 mmHg, tachycardia with a heart rate of 105 bpm, and mild fever, all suggestive of stress response or possible infection.

Laboratory tests were ordered to further evaluate the patient's condition. Complete blood count results showed a hemoglobin level of 10.5 g/dL, indicating mild anemia, likely secondary to chronic gastrointestinal blood loss from the suspected ulcer. The patient's hematocrit was also low at 32%, reinforcing the suspicion of ongoing bleeding. Serum electrolytes revealed hyponatremia and hypokalemia, likely due to frequent vomiting and potential volume depletion. A Helicobacter pylori test was conducted, with results pending, to determine the underlying cause of the mucosal damage.

Given these findings, the team initiated a plan to manage the patient's complications. Intravenous fluids were started to address dehydration and correct electrolyte imbalances. A proton pump inhibitor was continued to reduce gastric acid secretion and promote healing. The patient's glycemic control was closely monitored due to his type 2 diabetes, and adjustments to his Metformin regimen were considered to minimize gastrointestinal side effects. The team prepared for an upper endoscopy to directly visualize the gastric mucosa, assess the extent of the ulceration, and potentially identify the source of bleeding. These actions aimed to stabilize the patient and prevent further deterioration while awaiting diagnostic confirmation of H. pylori infection, which would guide the long-term management plan.

Section 2

As the clinical team proceeded with the management plan, they carefully monitored the patient's response to the interventions in place. Initial rehydration efforts with intravenous fluids showed some improvement in the patient's vital signs. The heart rate gradually decreased to 98 bpm, and blood pressure stabilized to 140/88 mmHg, suggesting a positive response to fluid resuscitation. However, the patient's mild fever persisted, warranting further investigation into the potential sources of infection or inflammation.

The upper endoscopy was performed, revealing a large gastric ulcer with visible stigmata of recent bleeding, confirming the source of the patient's anemia and melena. The endoscopic team successfully applied endoscopic hemostatic therapy to control the bleeding. Biopsies were taken from the ulcer margin to rule out malignancy and to test for Helicobacter pylori. Meanwhile, the proton pump inhibitor therapy was intensified to promote ulcer healing and prevent rebleeding.

Despite these interventions, the patient's hyponatremia and hypokalemia persisted, with sodium levels at 130 mmol/L and potassium at 3.0 mmol/L. This raised concerns about ongoing losses or insufficient replacement. The clinical team adjusted the electrolyte replacement strategy, considering the patient's continued vomiting and potential underlying renal involvement due to his diabetes. They also initiated antiemetic therapy to control nausea and prevent further electrolyte imbalances. The pending biopsy results and H. pylori test would guide the long-term management strategy, but immediate attention was required to stabilize the patient's electrolyte status and prevent further complications. This situation demanded careful clinical reasoning to balance the management of acute symptoms while preparing for potential chronic treatment adjustments.

Section 3

As the clinical team continued to manage the patient's condition, a new complication emerged that required immediate attention. Over the course of the next 24 hours, the patient developed worsening abdominal pain and distension. Vital signs indicated a mild tachycardia at 105 bpm, and while the blood pressure remained stable, the respiratory rate increased to 24 breaths per minute, suggesting an element of respiratory compensation. On examination, the abdomen was tender to palpation, particularly in the epigastric region, with decreased bowel sounds. These findings raised the concern for a possible perforation or obstruction, necessitating further diagnostic imaging.

A stat abdominal CT scan was performed, revealing free air under the diaphragm, indicative of a perforated gastric ulcer. This finding explained the sudden change in the patient's clinical status and underscored the urgency for surgical intervention. The surgical team was consulted immediately, and preparations for an emergent laparotomy were initiated. Meanwhile, the patient was kept nil per os (NPO), and broad-spectrum intravenous antibiotics were started to prevent the risk of peritonitis, alongside continued intravenous proton pump inhibitors.

The clinical reasoning had to swiftly pivot from managing a bleeding ulcer to addressing a perforation, highlighting the dynamic nature of gastrointestinal complications. The team discussed the potential impacts of the patient's diabetic status on wound healing and infection risk, planning for close post-operative monitoring. This change in status required a coordinated multidisciplinary approach, emphasizing the importance of timely surgical intervention to prevent further deterioration and to stabilize the patient’s condition.

Section 4

As the surgical team prepared for the emergent laparotomy, the nursing staff continued to monitor the patient's vital signs closely. Despite the administration of IV antibiotics and fluids, the patient began to exhibit signs of hemodynamic instability. The heart rate increased to 118 bpm, and the respiratory rate rose to 28 breaths per minute, with the patient appearing visibly more distressed. The blood pressure, previously stable, now showed a slight downward trend at 98/60 mmHg, raising concerns about potential septic shock secondary to the perforation.

The latest laboratory results returned, revealing a white blood cell count of 18,000/mm³, indicating an ongoing inflammatory response. Serum lactate levels were elevated at 3.5 mmol/L, further supporting the suspicion of sepsis and prompting the addition of vasopressor support to maintain adequate perfusion. Blood cultures were drawn to identify any specific infectious agents, though results would take time to process. The team recognized the critical need for rapid surgical intervention and confirmed that the operating room was ready to receive the patient.

In the interim, the multidisciplinary team evaluated the patient's diabetic management, given the increased risk of complications in the context of infection and stress on the body. Tight glucose control was deemed essential to optimize recovery and reduce the risk of wound complications post-surgery. An endocrinologist was consulted to provide input on adjusting the patient's insulin regimen, ensuring that blood glucose levels remained within the target range. The team remained vigilant, understanding that the upcoming surgery would be a pivotal moment in stabilizing the patient's condition and preventing the progression of septic shock.

Section 5

As the surgical team prepared for the procedure, the nursing staff continued to closely monitor the patient's condition, keenly aware of the potential for new complications. Despite the introduction of vasopressor support, the patient's condition did not stabilize as expected. The heart rate increased further to 126 bpm, and the blood pressure dropped to 92/58 mmHg, signaling worsening hemodynamic instability. The patient's skin became cool and clammy, and capillary refill time lengthened, indicating inadequate peripheral perfusion. These changes heightened concerns that the patient was slipping deeper into septic shock, necessitating immediate attention.

Simultaneously, a repeat assessment of the patient's abdominal status revealed increased distention and rigidity, with the patient reporting severe, diffuse abdominal pain. These findings were consistent with the progression of peritonitis, likely exacerbated by the underlying perforation. The nursing team noted that the patient's oxygen saturation had decreased to 90% on supplemental oxygen via nasal cannula, prompting escalation to a non-rebreather mask to ensure adequate oxygen delivery.

As the multidisciplinary team regrouped to evaluate these developments, the patient's blood glucose level was noted to be 280 mg/dL, despite insulin adjustments. This hyperglycemia further complicated the clinical picture, as elevated glucose levels can impede immune response and exacerbate infection. The endocrinologist recommended an intravenous insulin drip to achieve tighter glucose control. The urgency of surgical intervention became increasingly apparent, with the team understanding that prompt resolution of the perforation and source control were critical to reversing the cascade of sepsis and stabilizing the patient's condition.