Balaji, G (2012) Prospective Study of Evaluation of the Role of Vasopressin in the Management of Hypernatremia in Clinically Brain Dead Patients. Masters thesis, Madras Medical College, Chennai.
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Abstract
INTRODUCTION: In response to a traumatic brain injury or physiological “insult” to the brain (e.g., hemorrhagic or ischemic stroke), some patients suffer global and irreversible loss of brain stem function, leading to a diagnosis of brain death. Some of these patients may be candidates for organ and tissue donation, a decision mediated by the patient’s previously expressed wishes, sometimes in the form of an advance directive or organ donor card, and the preferences of the patient’s family. Patients with irreversible brainstem dysfunction are potential candidates for organ donation. As the awareness regarding organ donation and the frequency of donation are increasing with time, organ preservation strategies and protocols should be followed meticulously to improve the outcome of donation programme. After the diagnosis of brain death the focus of patient care shifts from interventions aimed at saving the patients (donor) life to interventions aimed at maintaining viability of potentially transplantable organs. As the brainstem dysfunction evolves the there occurs so many alterations in the normal physiology. The resultant changes in the cell homeostasis can adversely affect the donor organ viability which in turn affect the graft function. By understanding the pathophysiology of brain death we can manage the adverse changes reasonably, which may improve the survival of the grafted organs. Among the major changes endocrine changes are worth mentioning. Diabetes insipidus is the most common endocrine abnormality seen in the brain-dead patients, manifests earlier or later during the process(1)(2). One of the effects of diabetes insipidus is hypernatremia, defined as serum sodium level >145mEq/L(3). Organs commonly harvested are kidneys, liver, heart/heart valves, cornea etc. Donor organs affected by hypernatremia are liver, kidneys, heart. Of these liver grafts are more prone to early rejection. Effects are more when the sodium levels are > 155mEq/L particularly when it is a persistent one for longer duration before procurement(3). Various studies have showed the relationship between the serum sodium level and the graft survival and explained the adverse effects of hypernatremia. So managing the hypernatremia can improve the survival of transplanted organs especially the liver. Which is the theme of this study. There are many approaches for managing the hypernatremia. Among them I have chosen the exogenous vasopressin administration to replace the reduced serum vasopressin level as the treatment of choice because it also has potent vasopressor property which will be useful in maintaining hemodynamic stability in these patients due to the frequently accompanying autonomic failure. Other derangements also have to be corrected with fluid replacement, dopamine, thyroxine, methyl prednisolone, insulin-KCL regimen, antibiotics etc. In this study I have attempted to evaluate the role of vasopressin in the management of hypernatremia in clinically brain-dead patients, by comparing the serum sodium levels before and after initiating the vasopressin infusion therapy. AIM OF THE STUDY: To evaluate the role of vasopressin in the management of hypernatremia in clinically brain-dead patients using intravenous vasopressin infusion at a dose of 0.01-0.04U/min in 40 clinically braindead patients. MATERIALS AND METHODS: It was a prospective a study of evaluation of the role of vasopressin in the management of hypernatrmia in clinically braindead patients, conducted in Government General Hospital, Chennai. Study Design: Prospective, interventional. After obtaining institutional ethical committee clearance, 40 clinically braindead patients with hypernatremia were selected using following criteria: Inclusion Criteria: 1. Clinically braindead patients (ASA PS 6). 2. Traumatic injury. 3. Serum Na+ level > 145 meq/L. 4. Urine output > 4ml/kg/hr. Exclusion Criteria: 1. Braindead patients with serum Na+ < 146meq/L. 2. Urine output < 1.5-2ml/kg/hr. 3. Patients with known renal pathology. 4. Allergy to vasopressin group of drugs. MATERIALS: 1. 18G venflon. 2. Heparin. 3. ABG analysis source. 4. intra venous fluids (5%D,RL,1/2NS). 5. Monitors- Monitors: ECG, Pulse oximetry, Capnography, NIBP. 6. Vasopressin injection. STUDY METHOD: After receiving information from any ward, patientswere visited and examined (History and clinical examination) thoroughly. Investigations were evaluated and if not complete instructions were given. After confirming the existence of hypernatremia and verifying inclusion criteria, consent was obtained from patient’s attenders and vasopressin infusion was started at a dose of 0.01U/min or 10mU/kg/hr. 20units vasopressin in 500ml NS (1ml =0.04U). Above mentioned parameters were monitored at specified time intervals for 6 hours. RESULTS: 1. Serum Na+ reaches the target value. 2. Decreased but not to the target level. 3. No change in serum Na+ level. 4. Persistently increasing levels noted. Interpretation of results. Response to vasoprssin. 1. PRESENT- if there was decrease in serum Na+ level (to target level or decrease >10 to 15% from baseline). 2. NOT- if there was no change or increasing levels. Statistics: Statistical analysis was done to determine the significance (Friedman test and paired t test were used). SUMMARY: This was a prospective study conducted in 40 clinically braindead patients with hypernatremia. Trauma patients were chosen. After confirming hypernatremia with baseline serum sodium values and inclusion criteria vasopressin infusion was started at a dose of 0.01U/min. Hourly serum sodium, serum potassium, urine output, blood urea, serum creatinine, blood pressure, heart rate and blood sugar were monitored for 6 hrs. Blood pressure was monitored – every 15 minutes during 1st hour, every 30 minutes during 2nd & 3rd hour, every hour for next three hours. Observed parameters were evaluated for statistical significance. Statistical analysis was done with appropriate tests. It shows that the effect of vasopressin in decreasing serum sodium was statistically significant. It's effects in decreasing urine output and maintaining hemodynamic stabily were also significant. CONCLUSION: As endocrine and autonomic failure both are common in braindead patients, vasopressin at a dose of 0.01-0.04U/min will be superior to other options in managing hypernatremia in these patients as it handles both hypernatremia and hypotension. Other options include desmopressin (lacks vasopressor effect) and using sodium free IV fluids or IV fluids with high free water clearance.
| Item Type: | Thesis (Masters) |
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| Uncontrolled Keywords: | Vasopressin ; Management ; Hypernatremia ; Clinically Brain dead Patients ; Prospective Study. |
| Subjects: | MEDICAL > Anaesthesiology |
| Depositing User: | Subramani R |
| Date Deposited: | 22 Apr 2018 09:59 |
| Last Modified: | 22 Apr 2018 12:41 |
| URI: | http://repository-tnmgrmu.ac.in/id/eprint/7211 |
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