gastroparesis - Nursing Case Study
Pathophysiology
• Primary mechanism: Impaired gastric motility due to vagus nerve dysfunction leads to delayed gastric emptying. Damage to this nerve disrupts the signals needed for stomach muscles to contract and propel food into the small intestine.
• Secondary mechanism: Dysfunctional interstitial cells of Cajal (ICCs) reduce gastric pacemaker activity, further impairing coordinated peristalsis and exacerbating gastric stasis.
• Key complication: Resultant chronic gastric retention can cause severe nausea, vomiting, and malnutrition, significantly impacting patient quality of life and increasing the risk of bezoar formation and subsequent gastric outlet obstruction.
Patient Profile
Demographics:
45-year-old female, nurse
History:
• Key past medical history: Type 1 diabetes mellitus for 20 years, hypothyroidism, and previous gastric ulcer
• Current medications: Insulin glargine, insulin lispro, levothyroxine, metoclopramide, ondansetron, and omeprazole
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Severe abdominal pain and persistent nausea
• Key symptoms: Vomiting, early satiety, abdominal bloating, weight loss, fatigue, and erratic blood glucose levels
• Vital signs: Blood pressure 88/58 mmHg, heart rate 118 bpm, respiratory rate 22 breaths per minute, temperature 100.4°F, oxygen saturation 93% on room air
Section 1
As the healthcare team progresses with the evaluation, the initial assessment findings reveal several critical insights. The patient exhibits signs of dehydration and electrolyte imbalances, as evidenced by dry mucous membranes, decreased skin turgor, and laboratory results showing hyponatremia (sodium level at 128 mmol/L) and hypokalemia (potassium level at 3.0 mmol/L). Her blood glucose levels are erratic, with readings fluctuating between severe hyperglycemia and hypoglycemia, complicating her diabetic management. The abdominal examination reveals distension and tenderness in the epigastric region, with hypoactive bowel sounds suggesting decreased gastrointestinal motility. Given her hypotension and tachycardia, there is concern for potential hypovolemic shock, necessitating immediate intervention.
In response to these findings, the medical team initiates intravenous fluid resuscitation with isotonic saline and electrolyte replacement to address her dehydration and correct the imbalances. Anti-emetic therapy is adjusted to better control her nausea and vomiting. Despite these efforts, her condition remains precarious as her blood pressure continues to struggle to stabilize, and her heart rate remains elevated. The patient's persistent abdominal pain and bloating raise suspicion of further complications, such as a gastric bezoar or worsening gastric outlet obstruction, necessitating urgent imaging studies.
The evolving clinical picture highlights the complexity of managing gastroparesis in the context of her longstanding diabetes and other comorbidities. The team must carefully balance fluid management with the risk of exacerbating her gastric retention, while vigilantly monitoring for signs of potential complications such as aspiration pneumonia or acute renal injury due to ongoing nausea and vomiting. The next steps involve a multidisciplinary approach, possibly including gastroenterology consultation, to explore advanced therapeutic options or consider surgical interventions if mechanical obstruction is confirmed.
Section 2
New Diagnostic Results:
Following the suspicions of a gastric bezoar or gastric outlet obstruction, the healthcare team proceeds with an urgent abdominal CT scan and an upper GI endoscopy. The CT scan reveals the presence of a large gastric bezoar, which is contributing to gastric outlet obstruction. The bezoar appears to be composed of indigestible material, likely exacerbated by the patient's impaired gastric motility. The endoscopy confirms these findings, showing a large, dense mass in the stomach with evidence of inflammation and irritation of the gastric mucosa. Additionally, the endoscope reveals delayed gastric emptying, consistent with severe gastroparesis.
Concurrently, laboratory results show a worsening renal function with elevated creatinine levels of 2.1 mg/dL and blood urea nitrogen (BUN) of 45 mg/dL, indicating acute kidney injury likely secondary to prolonged dehydration and electrolyte imbalances. Blood cultures are performed due to persistent hypotension and tachycardia, revealing a low-grade bacteremia, raising concerns for possible aspiration pneumonia or another source of infection. The patient's blood pressure remains labile, hovering around 85/55 mmHg, despite aggressive fluid resuscitation, and her heart rate remains tachycardic at 115 beats per minute.
These findings necessitate immediate action to address the bezoar and potential infection. The medical team decides to initiate broad-spectrum antibiotics to cover for possible aspiration pneumonia and considers endoscopic or surgical procedures to remove the bezoar to relieve the gastric obstruction. The complexity of her condition is compounded by her fluctuating glucose levels, requiring continuous monitoring by the endocrinology team to prevent further metabolic derailments. The decision-making process now involves weighing the risks and benefits of surgical intervention against the backdrop of her unstable hemodynamics and renal impairment, while closely collaborating with gastroenterology and surgery to determine the most appropriate course of action.
Section 3
Following the initiation of broad-spectrum antibiotics and the decision to proceed with endoscopic intervention, the patient's condition begins to evolve. Despite the administration of antibiotics, her vital signs remain unstable. Her blood pressure further drops to 80/50 mmHg, and her heart rate increases to 120 beats per minute, indicating a worsening of her hemodynamic status. The nursing team notes that her urine output has significantly decreased over the past three hours, now registering at 15 mL per hour, raising concerns of worsening acute kidney injury. Additionally, the patient begins to exhibit signs of altered mental status, becoming increasingly lethargic and disoriented, which suggests potential hypoperfusion to the brain or worsening sepsis.
In light of these developments, the critical care team conducts a thorough reassessment. Her repeat laboratory results show further elevations in creatinine, now at 2.5 mg/dL, and BUN at 52 mg/dL, confirming the progression of renal impairment. Arterial blood gas analysis reveals a metabolic acidosis with a pH of 7.25, HCO3 of 18 mEq/L, and a lactate level of 4.2 mmol/L, indicating tissue hypoxia and potential septic shock. The need for urgent intervention becomes clear, as the team debates the initiation of vasopressor support to stabilize her hemodynamics while continuing to address the underlying gastric obstruction and infection sources.
The decision to proceed with endoscopic removal of the bezoar is complicated by her current instability. The gastroenterology team is consulted to consider the potential benefits of a less invasive endoscopic procedure with the understanding that surgical intervention may pose significant risks given her current state. This situation requires careful balancing of the risks of delayed gastric clearance against the potential for worsening systemic complications, necessitating close interdisciplinary collaboration and continuous monitoring to adaptively manage her rapidly changing clinical status.
Section 4
As the critical care team deliberates on the next steps, the patient's condition takes an unexpected turn. Despite the initiation of vasopressor support with norepinephrine at 5 mcg/min to stabilize her declining blood pressure, her hemodynamic status remains precarious. Her blood pressure momentarily stabilizes at 90/60 mmHg, but her heart rate continues to climb, now reaching 130 beats per minute. The team observes that her extremities are becoming cool and mottled, a concerning sign that peripheral perfusion is diminishing. Furthermore, the patient's respiratory rate increases to 28 breaths per minute, and her oxygen saturation begins to drop, hovering around 88% on 4 liters of oxygen via nasal cannula, suggesting the development of respiratory compromise potentially secondary to metabolic acidosis or evolving pulmonary edema.
In parallel, new diagnostic imaging results arrive. A CT scan of the abdomen, ordered to further evaluate the extent of the gastric obstruction, reveals significant gastric distention with air-fluid levels and a possible perforation, an alarming finding that complicates her management further. This revelation escalates the urgency for intervention, as the risk of peritonitis adds another layer to her already critical condition. Blood cultures, drawn earlier, return positive for gram-negative bacilli, confirming a bloodstream infection and solidifying the diagnosis of septic shock, likely secondary to the gastrointestinal source.
Faced with these developments, the interdisciplinary team, including gastroenterology, infectious disease, and surgery, debates the feasibility and timing of endoscopic versus surgical intervention. The potential for a minimally invasive approach remains alluring to avoid the physiological stress of surgery, yet the risk of a perforated viscus necessitates urgent attention. As the patient’s mental status further declines, with a Glasgow Coma Scale dropping to 10, the team is pressed to decide on a course of action that balances the immediate need for stabilization with long-term recovery prospects, prompting a reassessment of priorities and a recalibration of their intervention strategy. The evolving clinical scenario underscores the critical need for rapid, informed decision-making and highlights the complexity of managing such a multifaceted case.
Section 5
As the critical care team grapples with the patient's deteriorating condition, new diagnostic results add complexity to the clinical picture. A repeat arterial blood gas analysis indicates a worsening metabolic acidosis, with a pH of 7.22, bicarbonate of 16 mEq/L, and a pCO2 of 32 mmHg, suggesting uncompensated metabolic acidosis likely due to lactic acid accumulation from both septic and hypoperfusion-related etiologies. Concurrently, her lactate levels have climbed to 4.5 mmol/L, underscoring the severity of her shock state. The laboratory panel further reveals acute kidney injury, with serum creatinine rising to 2.3 mg/dL from a baseline of 0.9 mg/dL, and a decline in urine output to less than 20 mL/hour, indicative of renal hypoperfusion and failure to maintain adequate organ perfusion.
In light of these findings, the intensivist increases the norepinephrine infusion to 12 mcg/min in an attempt to improve mean arterial pressure and organ perfusion. However, despite this adjustment, the patient's hemodynamic stability remains elusive, with blood pressure fluctuating between 85/55 mmHg and 92/58 mmHg. The patient's respiratory status continues to decline, necessitating escalation from nasal cannula to high-flow oxygen therapy, yet her oxygen saturation stubbornly lingers around 86%. Given these developments and the risk of impending respiratory failure, the team considers the need for intubation and mechanical ventilation to secure her airway and optimize oxygen delivery.
As the situation evolves, the surgical team prepares for potential exploratory laparotomy, weighing the risks of surgery against the pressing threat of peritonitis and further hemodynamic collapse. The patient's altered mental status, evidenced by a further reduction in her Glasgow Coma Scale to 8, presses the urgency of intervention. The team faces the formidable challenge of orchestrating a multifaceted management approach that addresses the overlapping crises of septic shock, potential gastrointestinal perforation, and multi-organ dysfunction, all while remaining nimble to the rapidly changing dynamics of her critical illness.