Topic 3-4

Q-1

The posterior lobe of the pituitary gland produces a hormone called vasopressin which is secreted into the bloodstream that controls water and sodium levels in the body through urine production. Diabetes insipidus is an acquired central diabetes insipidus is caused by the destruction of the neurohypophysis by anatomic lesions that destroy the vasopressin neurons by pressure or infiltration, damage from surgery, head trauma, and autoimmune destruction of the vasopressin neurons. Vasopressin deficiency causes impaired urine concentration with resultant polyuria and secondary polydipsia to maintain water homeostasis with frequent thirst and drinking, almost 80-90% of the gland destruction causes the symptoms of diabetes insipidus (Verbalis, 2020). Vasopressin deficiency also leads to downregulation of the synthesis of acquaporin-2 water channels in the kidney collecting duct principal cells, causing a secondary nephrogenic diabetes insipidus (Verbalis, 2020). DI is the most common complication of pituitary surgery, polyurea is the most overt symptom of DI urine production >300 ml/hour for 3 hours accompanied by a urine specific gravity <1.005, excessive thirst, serum osmolality>300 mosmol/kg, or serum sodium>145 mmol/L (de Vries, Lobatto, Verstegen, van Furth, Pereira, & Biermasz, 2021). The occurrence of excessive thirst and /or hyperosmolality or hypernatremia are the best indicators to discriminate between pathophysiological symptoms and signs of DI and other causes and urine osmolality distinguishes DI from osmotic diuresis.

Diagnosis of DI through a two-step water deprivation test. Dehydration stimulates the secretion of vasopressin,  and the second step is to differentiate central DI from nephrogenic DI by administering desmopressin (dDAVP) (Garrahy, Moran, & Thompson, 2019). Patients with DI have a high risk of mortality due to volume depletion and altered sodium levels, management by supervising the free water fluid replacement and dosing of desmopressin, patients to drink to thirst and measure their body weight to recognize early the development of SIADH. Monitoring of serum sodium level and osmolality, urinary sodium and osmolality, and management of hypo and hypernatremia is the main goal in diabetes insipidus. Transient DI is a common complication of endoscopic and microscopic transsphenoidal surgery with pituitary adenoma, permanent DI is much less frequent may be caused by craniopharyngioma (Burke, Cote, Penn, Iuliano, McMillen, & Laws Jr, 2020).

Reference.

de Vries, F., Lobatto, D. J., Verstegen, M. J., van Furth, W. R., Pereira, A. M., & Biermasz, N. R. (2021). Postoperative diabetes insipidus: how to define and grade this complication? Pituitary, 24(2), 284-291. Retrieved from https://link.springer.com/article/10.1007/s11102-020-01083-7

Verbalis, J. G. (2020). Acquired forms of central diabetes insipidus: mechanisms of disease. Best Practice & Research Clinical Endocrinology & Metabolism, 101449. Retrieved from https://www.sciencedirect.com/science/article/abs/pii/S1521690X20300762

Burke, W. T., Cote, D. J., Penn, D. L., Iuliano, S., McMillen, K., & Laws Jr, E. R. (2020). Diabetes insipidus after endoscopic transsphenoidal surgery. Neurosurgery, 87(5), 949-955. Retrieved from https://academic.oup.com/neurosurgery/article-abstract/87/5/949/5854030

Garrahy, A., Moran, C., & Thompson, C. J. (2019). Diagnosis and management of central diabetes insipidus in adults. Clinical endocrinology, 90(1), 23-30. Retrieved from https://onlinelibrary.wiley.com/doi/full/10.1111/cen.13866

Q-2

Transsphenoidal pituitary surgery (TPH), usually for a pituitary adenoma, is a common cause of central diabetes insipidus (DI). Disruptions in water regulation can be linked to an anatomic injury to the hypothalamus, pituitary stalk, or posterior pituitary gland during surgery (Blair et al., 2017). This damage alters the physiology of water metabolism controlled by the antidiuretic hormone (ADH). DI may be transient or permanent. Following pituitary surgery it may manifest as a classical triple-phase response: an acute initial central DI, followed by a transient antidiuretic phase (presenting as hyponatremia due to syndrome of inappropriate antidiuretic hormone [SIADH]), subsequently progressing to permanent central DI (Blair et al., 2017). These disorders of water metabolism can occur due to a decrease in ADH release, leading to central diabetes insipidus. DI is defined as the concomitant presence of inappropriate hypotonic polyuria (urine output > 3 l/24 h and urine osmolality < 300 milliosmoles/kg) in the presence of high or normal serum sodium. The presence of both serum hyperosmolality and hypernatremia is highly suggestive for DI, but these laboratory alterations can be absent if the patient is conscious and has free access to water. The onset of polyuria is usually abrupt, occurring within the first 12–24 h after surgery (Blair et al., 2017). The persistence of DI implies that at least 85–90% of hypothalamic magnocellular neurons have been damaged by surgery. To screen for the potential development of postoperative DI, measurement of urine output and fluid intake, urine specific gravity daily, and serum sodium every 6–12 h until discharge should be ordered (Prete, Corsello & Salvatori, 2017). For treatment of DI during the immediate postoperative period, the use of short-acting subcutaneous vasopressin (rather than desmopressin, DDAVP), with a frequent reassessment of response and need to avoid administering an ADH when a SIADH phase is occurring. The use of vasopressin is favored at this stage because of its shorter duration of action, in case DI is transient and it reverts to SIADH (Prete, Corsello & Salvatori, 2017). Hyponatremia usually develops between postoperative days 5–8, and therefore these patients should routinely have a serum sodium level check approximately on a postoperative day 6 or 7. Apart from hypopituitarism and disorders of water metabolism post TPH, damage to parasellar structures can lead to other complications after pituitary surgery, including CSF leak, epistaxis, damage to the parasellar visual system, and damage to internal carotid arteries (Prete, Corsello & Salvatori, 2017).

Reference:

Blair, E. T., Clemmer, J. S., Harkey, H. L., Hester, R. L., & Pruett, W. A. (2017). Physiologic Mechanisms of Water and Electrolyte Disturbances After Transsphenoidal Pituitary Surgery. World Neurosurgery, 107, 429–436. https://doi.org/10.1016/j.wneu.2017.07.175

Prete, A., Corsello, S. M., & Salvatori, R. (2017). Current best practice in the management of patients after pituitary surgery. Therapeutic Advances in Endocrinology and Metabolism, 8(3), 33–48. https://doi.org/10.1177/2042018816687240

Q-3

Post-op management with thoracic lung surgery

· Describe the role of an AGACNP at each of the steps in postoperative care for a surgical patient.

The role of an AGACNP for a patient who underwent pneumonectomy for adenocarcinoma is s important to any other post-operative patient care based on ABC. Make sure airway is patent, breathing adequately either normal way, some may require supplementary oxygen and in complicated extensive lung surgery one may remain intubated postoperatively until patient is ready for extubation. Intensivist consultation for management of ventilator and interdisciplinary care collaboration is important in this area with RT’s and RN’s sharing responsibilities and care for the patients. Hemodynamic monitoring and stability are another responsibility of AGACNP through assessment and monitoring and reporting by RN’s. Monitoring including bleeding at the incision site and bleeding through chest tubes and other signs of internal bleeding needs to be monitored hemodynamically, urine output, chest drainage, lab tests of CBC.

 

· Describe the assessment steps you would take.

The AGACNP’s assessment steps include the collection of data from the medical records, other professionals and patients or significant others, and interdisciplinary members and history. The second step is the inspection of the patient for obvious signs of distress, instability, vital signs, anxiety, agitation, paleness/ appearance. Inspect the surgical sites and chest drainages for bleeding, gaping, and urine output. Vital signs give a clue for the stability of the patient and inspect the breathing pattern for regularity and distress and ventilator asynchrony. Palpating the chest and abdomen for any swelling and tenderness. Auscultating the lungs for normal and abnormal breath sounds and rales and rhonchi denotes fluid collections and secretions in the lungs with effusions and abnormal heart sounds for friction rubs, pericarditis, and effusion. Percussion may be done to assess abnormal resonance and dullness or flatness in the chest area.

 

· Explain the drainage and decompression devices and how you manage these as an AGACNP .

Management of chest tubes remains a critical aspect during the post-operative course of care following lung resection influencing recovery and hospital stay. A chest tube drainage is necessary for the majority of the cases, they cause pain, reduced pulmonary function, and immobility, use of suction promotes -pleura-pleural apposition favoring the sealing of air leak and the drainage or large air leaks. The use of external suction cause reduce mobility and decreasing airflow, but it is effective in draining large air leaks and has been associated with decreased risk of complications such as pneumonia and arrhythmia (Batchelor et al, 2019). The digital chest drainage system has several advantages over traditional water seals to apply regulated suction to maintain preset intrapleural pressure. Monitoring the drainage system function, air leaks, drainage amounts, and types, drain site monitoring, patient’s pulmonary status are all part of AGACNP’s responsibilities. Chest tubes can be removed safely even if the daily serous effusion is of high volume up to 450 ml/24 hours (Batchelor et al, 2019). But personally, in patients', I have seen that the chest tube is removed if the drainage is usually less than 100 ml/24 hours.

 

· Discuss potential differential diagnoses you could expect from the assessment.

Hemodynamic instability may happen during the immediate post-operative hours due to hypovolemia from blood loss and due to the effect of anesthesia. Acute respiratory failure may occur as a result of lung surgery and chest involvement and manipulation during surgery which requires patients to depend on invasive or non-invasive ventilation. Nonfunctioning chest drainage tube system which is evidenced by continuous air leak, or blocked chest drainage which does not have any fluid movement. This needs immediate intervention and resolves the problems to maintain the function of the chest drainage system and lung re-expansion. Postoperative atelectasis is a common condition that may associate with increased opioids use, intercostal nerve blocks intraoperatively, and multimodal adjuncts post-operatively and opioid starting to reduce post-operative venous thromboembolism and other complications (Huang, Yeung, & Slinger, 2020). A targeted euvolemia approach intraoperatively will minimize pulmonary edema and lung injury and potentially end-organ dysfunction (Huang, Yeung, & Slinger, 2020). This may demonstrate as respiratory distress with progressive hypoxia which may progress to acute respiratory distress syndrome (ARDS). Another differential diagnosis can be pulmonary infiltrates versus atelectasis with diminished aeration and other signs such as the presence of fever, leukocytosis, and evidenced by infiltrates in chest x-ray as pneumonia.

 

· Discuss the hemodynamic findings one might see with your provided diagnosis.

Hemodynamic instability may occur after major surgery, hypovolemia due to blood loss, the fluid deficit with tachycardia, hypotension, low CVP. Since the patient had a diagnosis of lung cancer is more risk for SIADH after surgery and the patient may end up having polyuria also may lead to hypovolemia and hypernatremia. The management is by hypovolemia is by giving crystalloids and colloids which depends on the fluid and blood loss. Severe acute blood loss with anemia may require blood transfusion or transfusion of other blood products. Monitoring of vital signs and CVP and stroke volume variation all denotes the fluid volume status which can be used as a basis for treatment and use of vasopressors to stabilize the vital signs. Atrial fibrillation is the most common sustained arrhythmia after non-cardiac thoracic surgery which precipitates hypotension and hypoperfusion may require immediate electro cardioversion to restore cardiac output and adequate oxygen therapy and use of low dose beta-blockers or calcium channel blockers may return to spontaneous return to sinus rhythm (Jiménez et al, 2018).

 

· Propose potential treatment plans that would be appropriate.

1. Immediate postoperative hemodynamic stability.

2. airway management of the patient by supplementary oxygen either noninvasive or invasive ventilation in consultation with an intensivist.

3. Administration of fluid, replace blood products if needed, and other medications such as proton pump inhibitors, antibiotics, and other medications.

4. Management of chest drainage system and maintenance and monitoring.

5. In patients with carcinoma diagnosed in the advanced stage may benefit from therapeutic surgery, molecular targeted therapy, immunotherapy/chemotherapy, and palliative radiation (David, Clark, Cooke, Melnikow, Kelly, & Canter, 2017).

6. Education and counseling on post-op management including chest tube management, deep breathing exercises, pain management, mobility and follow up and continuation of medications and palliative care and other care collaboration if appropriate.

Reference.

Batchelor, T. J., Rasburn, N. J., Abdelnour-Berchtold, E., Brunelli, A., Cerfolio, R. J., Gonzalez, M., ... & Naidu, B. (2019). Guidelines for enhanced recovery after lung surgery: recommendations of the Enhanced Recovery After Surgery (ERAS®) Society and the European Society of Thoracic Surgeons (ESTS). European journal of cardio-thoracic surgery, 55(1), 91-115. Retrieved from https://academic.oup.com/ejcts/article/55/1/91/5124324?login=true

Huang, A., Yeung, J. C., & Slinger, P. D. (2020). Enhanced recovery after lung resection surgery: Knowing what we can do… and doing it. Journal of cardiothoracic and vascular anesthesia, 34(7), 1867-1869. Retrieved from https://www.jcvaonline.com/article/S1053-0770(20)30209-3/fulltext

Jiménez, D., Bikdeli, B., Barrios, D., Quezada, A., Del Toro, J., Vidal, G., ... & RIETE investigators. (2018). Epidemiology, patterns of care and mortality for patients with hemodynamically unstable acute symptomatic pulmonary embolism. International journal of cardiology, 269, 327-333. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6258651/

David, E. A., Clark, J. M., Cooke, D. T., Melnikow, J., Kelly, K., & Canter, R. J. (2017). The role of thoracic surgery in the therapeutic management of metastatic non–small cell lung cancer. Journal of thoracic oncology, 12(11), 1636-1645. Retrieved from https://www.sciencedirect.com/science/article/pii/S1556086417306834