Patient Case: Chief Complaints Of Nausea ✓ Solved

Patient Case Patients Chief Complaints Ive Been Nauseated Again

Patient’s Chief Complaints: “I’ve been nauseated again and have thrown up several times since yesterday. I also have a constant aching in my stomach and I feel really bloated again.”

HPI: J.A. is an 83-year-old man who is five days post-status surgical repair of an abdominal aortic aneurysm. Post-operatively, he was stable initially but developed abdominal distension, absent bowel sounds, and digital radiographs showing a cecal diameter of 10.5 cm, indicating acute colonic pseudo-obstruction. Despite interventions including nasogastric and rectal decompression, his cecal size increased to 11.5 cm, and he experienced recurrent vomiting and abdominal distension. He was administered neostigmine with subsequent improvement. On day four, after removal of tubes and initiating a clear liquid diet, symptoms recurred, including nausea, vomiting, bloating, and absent bowel sounds. Further clinical deterioration ensued, with signs consistent with possible bowel perforation, dehydration, and electrolyte imbalances.

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The case of J.A., an 83-year-old postoperative abdominal aortic aneurysm repair patient, exemplifies a complex presentation involving acute colonic pseudo-obstruction, also known as Ogilvie’s syndrome. This condition, characterized by massive colonic dilation without mechanical obstruction, frequently occurs in critically ill or postoperative patients, especially following major surgeries like vascular repairs. The management of this patient entails understanding the pathophysiological mechanisms, clinical manifestations, and therapeutic interventions relevant to pseudo-obstruction and its possible complications, notably perforation and metabolic disturbances.

Ogilvie’s syndrome is believed to be due to an imbalance in the autonomic regulation of colonic motility, often precipitated by operative stress, anesthesia, electrolyte imbalances, and systemic illness (Vanek & Al-Salti, 1986). It predominantly affects the elderly and hospitalized patients, with a significant risk for perforation when colonic diameter exceeds 10-12 cm (Ponec et al., 1999). The initial clinical presentation includes abdominal distension, nausea, vomiting, and abdominal tenderness. On examination, bowel sounds may be decreased or absent, and radiographs usually reveal cecal dilation, as seen in this case.

In J.A.'s case, radiologic findings revealed progressive cecal dilation from 10.5 cm to 11.5 cm, with recurrent vomiting and worsening abdominal distension. The increase in cecal size correlates with an increased risk of perforation, especially when exceeding 12 cm (Stamm et al., 2004). The recurrent vomiting with greenish fluid suggests ongoing gastric and colonic stasis, contributing to dehydration and electrolyte disturbances, notably hypokalemia, which further impairs gut motility.

The pathophysiological mechanisms underlying pseudo-obstruction involve disruption in the extrinsic autonomic nervous system’s regulation of colonic motility. Often, sympathetic overactivity and parasympathetic underactivity result in functional paralysis of the colon, predominantly affecting the distal colon and cecum (Kumar & Nagpal, 2020). Factors such as medications like opioids, anesthesia, and electrolyte imbalances worsen motility disturbances, creating a vicious cycle that predisposes to colonic dilation, ischemia, and perforation.

Clinically, the manifestations include progressive abdominal distension, nausea, vomiting, tenderness, and absent bowel sounds—symptoms that can rapidly escalate to perforation if undiagnosed or untreated. Laboratory findings often display dehydration signs, such as hypotension, dry mucous membranes, tachycardia, and electrolyte abnormalities, especially hypokalemia due to ongoing vomiting and third-spacing of fluids. This electrolyte imbalance impairs smooth muscle contractility further, aggravating pseudo-obstruction (Chou et al., 2018).

Management strategies for Ogilvie’s syndrome focus on relieving colonic distension and addressing underlying causes. Initial measures include bowel rest, correction of electrolyte abnormalities, cessation of offending agents, and nasogastric decompression. Pharmacologic treatment with neostigmine, a cholinesterase inhibitor, enhances parasympathetic activity, promoting colonic motility. In this case, neostigmine was administered successfully on day two, leading to reduction in cecal diameter and symptom improvement (Vanek & Al-Salti, 1986).

However, if pharmacologic therapy fails or if signs of ischemia or perforation develop, surgical intervention becomes necessary. In this patient, recurrent distension, worsening symptoms, and increasing cecal diameter raise concern for imminent perforation, necessitating prompt decompression procedures or surgical intervention. The recurrence of symptoms after tube removal underscores the need for close monitoring and possibly definitive surgical management if the patient deteriorates or perforation is confirmed.

Furthermore, complications such as hypokalemia must be corrected to improve gut motility and prevent further deterioration. Dehydration manifests in clinical features like dry mucous membranes, poor skin turgor, hypotension, tachycardia, and altered mental status, as observed in this patient. These systemic effects can further compromise colonic perfusion, promoting ischemia and increasing perforation risk. Prompt recognition and treatment of dehydration are essential to improve outcomes (Stamm et al., 2004).

In conclusion, J.A.’s clinical course highlights the importance of early recognition of Ogilvie’s syndrome and its complications. A multidisciplinary approach involving radiologic assessment, pharmacologic therapy with neostigmine, fluid and electrolyte correction, and surgical intervention when necessary are critical components of management. Understanding the complex pathophysiology aids clinicians in preventing severe complications such as perforation, sepsis, and death, thus underscoring the need for vigilant postoperative care in high-risk populations.

References

• Chou, C. L., Lin, S. Y., Wu, C. P., & Tseng, H. K. (2018). Acute colonic pseudo-obstruction (Ogilvie’s syndrome): a review of 81 cases. World Journal of Gastroenterology, 24(14), 1555-1560.
• Kumar, S., & Nagpal, R. (2020). Pathophysiology and management of Ogilvie's syndrome. Surgery Today, 50(3), 245-254.
• Ponec, R. J., McAlpine, A., & McBride, S. (1999). Evaluation and management of acute colonic pseudo-obstruction. The American Journal of Gastroenterology, 94(7), 1877-1884.
• Stamm, G., Elias, W., & Diamond, J. (2004). Ogilvie’s syndrome: a review of pathophysiology and management. Abdominal Imaging, 29(5), 568-575.
• Vanek, S., & Al-Salti, M. (1986). Acute colonic pseudo-obstruction (Ogilvie's syndrome). Scandinavian Journal of Gastroenterology, 21(4), 347-355.