gi bleed - Nursing Case Study

Pathophysiology

• Primary mechanism: Mucosal erosion or ulceration in the gastrointestinal tract, often due to conditions like peptic ulcer disease or gastritis, leads to damage of blood vessels and subsequent bleeding. This erosion is frequently exacerbated by factors such as NSAID use or H. pylori infection.

• Secondary mechanism: Variceal bleeding, primarily resulting from portal hypertension due to liver cirrhosis, causes dilated veins (varices) in the esophagus or stomach that are prone to rupture and bleed.

• Key complication: Hypovolemic shock may occur if the bleeding is significant, leading to decreased blood volume, reduced cardiac output, and impaired oxygen delivery to tissues, requiring immediate medical intervention.

Patient Profile

Demographics:

58-year-old male, construction worker

History:

• Key past medical history: History of peptic ulcer disease, hypertension

• Current medications: Lisinopril 10 mg daily, Omeprazole 20 mg daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Dark, tarry stools for the past two days

• Key symptoms: Fatigue, dizziness, abdominal pain

• Vital signs: Blood pressure 92/60 mmHg, heart rate 112 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F, oxygen saturation 94% on room air

Section 1

As the healthcare team begins the initial assessment, they note the patient's pallor and cool, clammy skin, indicative of potential hypovolemic shock. The patient's orientation is slightly altered, with slowed responses and mild confusion, likely secondary to decreased cerebral perfusion. On auscultation, heart sounds are tachycardic, consistent with compensatory mechanisms aiming to maintain cardiac output despite falling blood volume. Abdominal examination reveals generalized tenderness, particularly in the epigastric region, without rebound tenderness or guarding, which could suggest peritoneal irritation or perforation.

Recognizing signs of significant blood loss, the team quickly initiates intravenous access and begins fluid resuscitation with isotonic crystalloids to stabilize hemodynamics. Blood work is prioritized, revealing a hemoglobin level of 8.2 g/dL, hematocrit at 25%, and blood urea nitrogen/creatinine ratio suggestive of pre-renal azotemia, supporting the diagnosis of acute blood loss anemia. The patient's lactate level is elevated at 3.5 mmol/L, indicating tissue hypoperfusion. A nasogastric tube is inserted, returning bright red blood, confirming ongoing upper gastrointestinal bleeding.

Despite initial fluid resuscitation, the patient's blood pressure remains borderline at 96/62 mmHg, and heart rate is persistently elevated at 118 bpm, reflecting inadequate volume replacement and ongoing bleeding. The patient is prepared for urgent endoscopic evaluation to identify and control the source of bleeding. The medical team considers the potential need for blood transfusion and proton pump inhibitor infusion to stabilize the gastric environment. As the situation evolves, the team must remain vigilant for further complications such as worsening shock or the development of coagulopathy, necessitating rapid, coordinated interventions.

Section 2

As the patient undergoes urgent endoscopic evaluation, the gastroenterologist identifies a large, actively bleeding peptic ulcer in the duodenum, which is successfully cauterized using endoscopic techniques. Despite this intervention, the patient's hemodynamic status does not stabilize as anticipated. The team notes that although the heart rate has decreased slightly to 112 bpm, the blood pressure remains precariously low at 90/60 mmHg, and the patient continues to exhibit signs of inadequate perfusion, including tachypnea and worsening confusion, now with a Glasgow Coma Scale score of 13.

New laboratory results reveal a further drop in hemoglobin to 7.6 g/dL, prompting the decision to initiate a transfusion of packed red blood cells. Concurrently, the patient's coagulation profile is assessed, showing an international normalized ratio (INR) of 1.8, slightly elevated from baseline, indicating potential coagulopathy. The team discusses the possibility of administering fresh frozen plasma or other clotting factors if the coagulopathy progresses. As part of ongoing management, the patient is also started on a high-dose proton pump inhibitor infusion to reduce gastric acid secretion and prevent further bleeding.

The patient's clinical course is complicated by the development of mild acute kidney injury, with serum creatinine rising from 1.2 mg/dL to 1.8 mg/dL, reflecting ongoing hypoperfusion despite aggressive resuscitation efforts. The healthcare team considers the need for additional fluid support, balanced with the risk of fluid overload, given the patient's borderline respiratory status. Continuous monitoring and reassessment are essential as the team remains alert to the potential for further complications, including recurrent bleeding or the need for surgical intervention if conservative measures prove insufficient. The interdisciplinary team collaborates closely to refine the management plan and prioritize the patient's stabilization and recovery.

Section 3

As the transfusion of packed red blood cells progresses, the team closely monitors the patient's response. Initially, there is a modest improvement in the patient's hemodynamic status, with blood pressure slightly increasing to 95/65 mmHg and heart rate decreasing to 106 bpm. However, the patient's mental status does not show significant improvement, with the Glasgow Coma Scale score remaining at 13. This prompts the team to reassess the patient's oxygenation and perfusion status. Arterial blood gas analysis reveals a pH of 7.32, indicating a mild metabolic acidosis likely due to lactate accumulation from ongoing tissue hypoperfusion.

Further laboratory tests reveal a rising lactate level, now at 3.5 mmol/L, which suggests that the patient's organs are not receiving adequate oxygen and nutrients despite the transfusion. The team also notes that the patient's urine output has decreased to 20 mL per hour, further indicating potential renal impairment. In light of these findings, the team considers augmenting the patient's fluid status cautiously, potentially utilizing colloid solutions to enhance intravascular volume without exacerbating the risk of fluid overload.

The team also decides to initiate discussions with the nephrology and critical care teams to explore additional supportive measures for the acute kidney injury and to evaluate the need for more aggressive interventions such as renal replacement therapy if the patient's renal function continues to deteriorate. Meanwhile, the patient is kept under continuous monitoring in the intensive care unit to quickly detect any signs of recurrent bleeding or further deterioration, with plans to escalate care as needed to address these complex, interrelated complications effectively.

Section 4

As the patient remains under intensive care, the team notes a subtle yet concerning change in the patient's status. Over the next few hours, the patient's heart rate begins to rise again, reaching 118 bpm, while blood pressure drops slightly to 90/60 mmHg. These changes signal potential ongoing instability, prompting further evaluation. Concurrently, the patient exhibits increasing confusion, with a Glasgow Coma Scale score now at 12, indicating a worsening mental status. This decline urges the healthcare team to reassess potential causes, suspecting that the initial transfusion did not fully address the underlying issues or that new complications are arising.

New diagnostic results return, revealing a hemoglobin level that has decreased again to 7.2 g/dL, suggesting possible recurrent bleeding or inadequate response to the prior transfusion. Coagulation profiles show a prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), raising concerns about coagulopathy, possibly linked to liver dysfunction or dilutional effects from resuscitation efforts. Additionally, the patient's lactate level continues to rise, now at 4.2 mmol/L, underscoring the persistence of tissue hypoperfusion and the potential for further organ dysfunction.

In response to these findings, the team escalates care by administering additional units of packed red blood cells and considers the administration of fresh frozen plasma to address the coagulopathy. They also initiate vasopressor support to stabilize the patient's hemodynamics, carefully balancing interventions to prevent exacerbating cardiac or renal stress. Continuous monitoring and collaboration with multidisciplinary teams remain crucial as they work to stabilize the patient, address the underlying causes, and prevent further decline. The evolving situation highlights the complexity of managing gastrointestinal bleeds with concurrent organ dysfunction, demanding precise clinical reasoning and timely intervention to navigate the patient's precarious condition.

Section 5

As the critical care team continues to manage the patient's condition, they observe a further change in status that heightens concern. The patient's heart rate, which had been elevated, now shows an erratic pattern, with occasional episodes of tachycardia reaching 130 bpm, interspersed with brief periods of bradycardia at 50 bpm. Blood pressure remains unstable, with readings fluctuating between 85/55 mmHg and 95/65 mmHg. This hemodynamic instability suggests a potential cardiovascular complication, possibly related to the stress of ongoing bleeding or the effects of vasopressor support.

Further complicating the situation, the patient's respiratory rate increases to 28 breaths per minute, and arterial blood gas analysis reveals a worsening metabolic acidosis with a pH of 7.25 and a bicarbonate level of 18 mmol/L. The rising lactate, now at 5.0 mmol/L, corroborates the persistence of systemic hypoperfusion and suggests that the current interventions are insufficient to reverse the underlying shock state. Simultaneously, the patient exhibits decreased urine output, with only 15 mL over the past hour, raising suspicions of acute kidney injury secondary to hypoperfusion or possible nephrotoxic effects from medications.

In light of these findings, the healthcare team intensifies their focus on optimizing cardiac output and ensuring adequate perfusion to vital organs. They consider adjusting the vasopressor regimen and increasing fluid resuscitation cautiously to avoid fluid overload. Additionally, they initiate renal protective strategies, including the careful monitoring of renal function and consideration of diuretics or renal replacement therapy if necessary. The team collaborates with cardiology and nephrology specialists to refine the management plan, recognizing the critical balance required to address the multifaceted complications now presenting in the patient's clinical picture. This juncture underscores the need for ongoing vigilance and adaptive clinical reasoning to navigate the complex interplay of gastrointestinal bleeding and multi-organ dysfunction.